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]

Scooped yet again! Teaching Point on a Non-Traditional IO Application

One of my senior residents, now graduated and a fancy informatics fellow and general badass at Stanford, Christian Rose and I used to discuss how we wondered if in extenuating circumstances one could use an intraosseous drill / needle to trephine a skull and drain a rapidly-expanding intraaxial hematoma in a crashing patients. Like most emergency medicine doctors, I find life-saving procedures interesting and cool and even though I would never want the lifestyle that accompanies neurosurgery, being able to do these interventions in a resource-limited setting is something I aspire to if it had to be done. (I’ve seen a burr hole and clot evacuation done once by an ED physician who had been trained in the military and done them abroad in forward operating theaters — he borrowed a drill from the ortho OR. It was successful, appeared fairly easy, and saved a life.)

This was all just theoretical until I read this post from the EMCore conference blog by Peter Kas. He relates a story recently published as a case report in Injury of using an EZ-IO drill and a 25 mm 15 ga intraosseous needle to drain a rapidly-expanding epidural hematoma in a pedestrian who was struck by an auto who presented and had a rapid decline in GCS and clinical signs of herniation. This procedure took about 8 minutes — shaving and sterilizing the scalp, and was done in the anesthesiology prep area while the neurosurgeons prepped for a craniotomy. They were able to aspirate ~ 30 mL of blood, with resulting improvement in the pupillary exam. A formal craniotomy was completed, and the patient had a good outcome. 

The authors note that this is unlikely to provide definitive management, given that most significant hematoma requiring craniotomy are of a more solid consistency that would be difficult to drain entirely via this route, but that it might be utilized by ED providers needing to transfer a patient over a long distance to definitive care. They specifically describe how they envision the procedure:

We propose the site of insertion should be the point of maximal clot depth and therefore localisation of the insertion point would be on a case by case basis. Most extradural haematomas requiring emergency craniotomy are of sufficient size that we postulate that failure to place the needle into the haematoma is unlikely but a potential complication.

Anyway, fun fact of the day, and perhaps someday (hopefully this will never come up) a last-ditch hail mary move that is a little easier and possibly safer/faster than borrowing a drill from your local orthopod and hoping you don’t go too deep.

References

Bulstrode H1, Kabwama S2, Durnford A3, Hempenstall J4, Chakraborty A5. Temporising extradural haematoma by craniostomy using an intraosseous needle. Injury. 2017 May;48(5):1098-1100. PMID: 28238447. [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]

Photoplethysmographic pulsus paradoxicus!

Say that three times fast.

We had a challenging case in our emergency department recently involving a patient with a self-inflicted stab wound to the anterior chest, which resulted in a pericardial effusion, prompting concern for the development of tamponade. A challenging element of the case involved thinking about the patient’s stability, and the urgent/emergent need for operative intervention v percutaneous intervention v observation — how could we determine whether this patient was, in fact, in cardiac tamponade or on their way towards developing this condition?

A classic teaching is to assess for a pulsus paradoxus, or an exaggerated decrease in the arterial blood pressure with inspiration. Traditionally this is done using a stethoscope and manual blood pressure cuff (I will not try to spell the S-word). If the difference in BP between the first expiratory Korotkoff sound and the first Korotkoff sound that no longer disappears with inspiration (the pulsus) is greater than 10 mmHg, a pulsus paradoxus is present.

Has anyone ever checked for one of these, or has this technique become like with many other physical exam findings, something that people are aware of but don’t really know how to check for? I’m not sure — I personally have never checked for one, and reach for the ultrasound when trying to risk stratify patients with pericardial effusions. Is there an easier way, or one that doesn’t require PoC echo?

These authors evaluate the utility of pulse oximetry, or plethysmography in the assessment of tamponade. They suggest that the difference between the inspiratory decrease in the magnitude of the waveform and the expiratory increase has been shown to correlate with intraarterially measured pulsus paradoxus. Unfortunately it turns out that this finding is not pathognomic for cardiac tamponade — it is linked to a number of other conditions (e.g. elevated intrathoracic pressures from asthma), and may be absent in patients who actually have tamponade physiology.

The most relevant article to this particular case is probably the study from Stone et al., “Respiratory changes in the pulse-oximetry waveform associated with pericardial tamponade.” from 2006, when they measured phasic respiratory variability in the pulse-oximetry waveform of patients undergoing aspiration of pericardial effusions. They found that the degree of respiratory variability in the pulse-oximetry waveform was significantly increased in these patients compared to effusion-less patients, and increased with the hemodynamic consequences of the tamponade. When the effusions were aspirated and drained, the variability disappeared.

So, is this something to hang your hat on? Probably not useful entirely for ruling OUT pericardial tamponade, but in a patient with an effusion if you’re asked by the consultant you wake up in the middle of the night whether you’ve checked for a pulsus yet, this might be an easier way than busting out your manual BP cuff and Googling how to check one the traditional way.

References

Clark JA1, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004 Jan;158(1):48-51. PMID: 14706958. [PubMed] [Read by QxMD]

Sunglasses Sign

I came across this piece from a 2008 issue of Neurology recently, and wanted to keep it here for posterity. The conclusions of the study were clearly communicated by the title: “The “sunglasses sign” predicts nonorganic visual loss in neuro-ophthalmologic practice.”

In this seminal article, Bengtzen and colleagues performed a prospective analysis of all patients wearing sunglasses in clinic, and patients receiving diagnoses of “non-organic vision loss”, which was a technical term new to me. They report on a number of co-variates of this diagnosis, including the wearing of sunglasses inside the exam room, alongside “highly positive review of systems, workers’ compensation claim, disability, and lawsuit”.

Specifically, the reported sensitivity of wearing sunglasses for non-organic vision loss (NOVL) was 0.46 (95% CI 0.33 to 0.59). The prevalence of NOVL in the entire study population was 4.3% but  79% in sunglasses-wearing patients. The specificity of sunglasses for the diagnosis of NOVL was 0.995 (95% CI 0.989 to 0.998).

I found this interesting if only because it supports existing stereotypes about the wearing of sunglasses indoors. The article does not comment on why this relationship exists, nor does it suggest that the performance characteristics of this finding allow you to use it to rule in or rule out true vision threats, but it does shed some light on the patterns that shape our practice and color our perceptions.

References

Bengtzen R1, Woodward M, Lynn MJ, Newman NJ, Biousse V. The “sunglasses sign” predicts nonorganic visual loss in neuro-ophthalmologic practice. Neurology. 2008 Jan 15;70(3):218-21. PMID: 18195266. [PubMed] [Read by QxMD]

Predictors of Central Dizziness

I’m rotating through a community emergency department this month, in which it seems like 40% of the patients I’m seeing have dizziness as some element of their constellation of chief complaints. This is one of the most difficult chief complaints to evaluate in emergency medicine — not only because people use the term “dizziness” to describe a multitude of subjective experiences, e.g. vertigo, syncope/presyncope, generalized weakness, anxiety, ataxia, or any sort of disturbance in mentation. Add in the barriers to effective communication that can accompany elder patients visiting an ED, such as language barriers + hearing/vision issues that accompany aging (imagine a translator on a video phone screaming at a patient who is extremely hard of hearing) and this becomes a tricky subject indeed.

To that end, I reviewed a paper published by a Korean group evaluating dizzy patients in their emergency department: Characteristics of central lesions in patients with dizziness determined by diffusion MRI in the emergency department, by Lee et al.

This was a retrospective review of 902 patients presenting to a single ED with a chief complaint of dizziness over six months. They looked closely at 645 patients (!) who recieved MRI imaging as part of their workup, which showed 23 patients (3.6%) having strokes, the majority in the posterior circulation. The authors then examined the characteristics that best predicted the presence of a central lesion.

Their findings? Predictably, advancing age brought with it a higher likelihood of central etiologies: the rate of central lesions on DWI was 3.9% and 3.5% in patients in their 50s and 60s respectively; 7.4% in 70s and 16.7% in their 80s! Hypertension was more common in patients with strokes (69% versus 36%). Atrial fibrillation was more common. 77% of patients with a central cause reported a more vague non-whirling dizziness compared to 40% in patients without central lesions. Other associated neurologic symptoms were present in about 46% of patients with a central cause, compared to only 3% in those who were MR-negative.

So while this study had all the drawbacks of most retrospective, single-center publications, and may not generalize exactly to the populations I work with, I felt it was useful in terms of giving me at least *some* numbers to use to estimate what proportion of these patients are hiding badness. I will have a much lower threshold to MRI patients who are in their 70s-80s, those with AF who aren’t anticoagulated (though the sensation of palpitations or the diminished cardiac output can contribute to the sensation of dizziness as well), or those who report a “vague non-whirling” sense of dizziness. That last point stands in contrast to what I’ve read in other studies that suggested that the character of dizziness was *not* useful, so that was interesting. When this study was reviewed on EMRAP another thing that Sanjay and Mike mentioned was that older patients often have difficulties cooperating with the exam, accurately reporting/describing their symptoms, and that our threshold for obtaining further diagnostic imaging in these patients should be lower.

More on dizziness to come soon, I’m sure.

References

Lee DH1, Kim WY2, Shim BS3, Kim TS4, Ahn JH5, Chung JW5, Yoon TH5, Park HJ5. Characteristics of central lesions in patients with dizziness determined by diffusion MRI in the emergency department. Emerg Med J. 2014 Aug;31(8):641-4. PMID: 23722117. [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.

Goal-directed Hemostatic Resuscitation of Trauma-induced Coagulopathy: Time for TEG?

Along with the usual suspects in the world of emergency medicine / FOAMed podcasts, I’ve tried to start listening to the educational podcasts being generated by those outside of our specialty — the Eastern Association for the Surgery of Trauma, EAST, recently had a great episode of their podcast (“Traumcast”) that featured Dr. Gene Moore, chief of trauma at Denver Health reviewing a single-center RCT comparing the use of viscoelastic coagulation assays to traditional coagulation testing such as INR and PTT in guiding resuscitation of trauma patients.

I went to medical school in Houston and did my clinical rotations at Memorial Hermann, where John Holcomb did his work looking at the use of rotational thromboelastography, including the development of a very robust system for getting TEG results to the trauma team within 15 minutes of the arrival of a patient to the trauma bay. The system they developed also provided automated guidance for the administration of specific blood products based off of the TEG assay, and is described in the second article linked below from Blood: How I treat patients with massive hemorrhage, on which Dr. Holcomb is the coordinating author.

I felt like this made a ton of sense — in the often coagulopathic trauma patient, we have shown over and over again that saline is not the resuscitative fluid of choice, and have more recently demonstrated in large, prospective, pragmatically-designed trials the superiority of using more physiologic (or “balanced”, as many surgeons refer to them) protocols for transfusing bleeding patients. Why not use more dynamic information to help inform the choice of which product goes first to fix the specifically broken link in the cascade of coagulation, as these viscoelastic testing assays seem to offer?

In this study, patients requiring massive transfusion activation were randomized in a block fashion to either have transfusion of blood products guided by TEG or by traditional coagulation assays. MTP activation was based on the Resuscitation Outcome Consortium criteria: SBP <70 mm Hg or SBP 70–90 mm Hg with heart rate > 108 beats/min, in addition to any of the following injury patterns: penetrating torso wound, unstable pelvic fracture, or FAST suspicious of bleeding in more than one region.

One hundred eleven patients were included in an intent-to-treat analysis, evenly split between the groups. Survival in the TEG group was significantly higher than the conventional MTP group (log-rank P = 0.032, Wilcoxon P = 0.027); 20 deaths in the control group (36.4%) compared with 11 in the TEG group (19.6%) (P = 0.049). Most deaths occurred within the first 6 hours from arrival (21.8% CCA group vs 7.1% TEG group) (P = 0.032).

Keeping in mind that TEG is a diagnostic tool rather than a treatment, and the relatively small numbers in this single central study, I don’t know that anyone could definitively say that the use of TEG is responsible for the increased survival seen here, but the results are impressive. Given the additional information conveyed by the TEG or other functional coagulation assays, I think that more broad deployment (including outside the OR, as they have at Memorial Hermann, where the TEG is the first test run off of the trauma activation patient, and where the results– along with a computerized interpretation of the graph with a recommendation for transfusion– print off on a laser printer in the trauma bay automatically) makes a lot of sense.

We should all be learning how to interpret these assays, especially in EM where we are often initiating the massive transfusion and resuscitation of these sick trauma patients (or other exsanguinating patients — I think it stands to reason that functional clotting assays would be much more useful in patients with other kinds of coagulopathy, e.g. liver failure or and sepsis) — I think this is now reaching a broader audience, as just recently Josh Farkas covered the use of TEG in sepsis-induced coagulopathy on PulmCrit and an article in EM Resident magazine covered the basics of TEG. Hopefully as more and more people learn about these technologies, we’ll see wider deployment and utilization, resulting in better care and smarter transfusion strategies.

References

Gonzalez E1, Moore EE, Moore HB, Chapman MP, Chin TL, Ghasabyan A, Wohlauer MV, Barnett CC, Bensard DD, Biffl WL, Burlew CC, Johnson JL, Pieracci FM, Jurkovich GJ, Banerjee A, Silliman CC, Sauaia A. Goal-directed Hemostatic Resuscitation of Trauma-induced Coagulopathy: A Pragmatic Randomized Clinical Trial Comparing a Viscoelastic Assay to Conventional Coagulation Assays. Ann Surg. 2016 Jun;263(6):1051-9. PMID: 26720428. [PubMed] [Read by QxMD]
Johansson PI1, Stensballe J2, Oliveri R3, Wade CE4, Ostrowski SR3, Holcomb JB4. How I treat patients with massive hemorrhage. Blood. 2014 Nov 13;124(20):3052-8. PMID: 25293771. [PubMed] [Read by QxMD]