Author Archives: Bryan Darger

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]

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.

Faking it: How to detect malingered psychosis

This was an amusing and interesting article shown to me by one of our consulting psychiatry faculty — in it, the authors Drs. Resnick and Knoll lay out their approach to determining whether someone might be feigning madness for secondary gain. This is, sadly, something we see very frequently in the emergency department — not so much specifically the faking of psychosis, but more often things like suicidality, which some patients (whose unfortunate lives are such that they would prefer being stuck in the emergency department on an “involuntary” hold to being out in the streets, or often those who were just arrested and are now on their way to jail) will endorse knowing that it results in a cascade of CYA consultations that result in a longer LOS and often a sandwich / sometimes psychotropic medications, or alcohol withdrawal. In the case of arrested patients, sometimes they can avoid a trip to jail by diverting to the hospital which will lead the officer to write them a ticket instead of arrest them. Sometimes this population also endorses psychotic symptoms such as command hallucinations, and the subjective nature of these complaints makes them very difficult to determine as being organic or not.

Malingering, defined by the authors as “the intentional production of false or grossly exaggerated physical or psychological symptoms, motivated by external incentives” is obviously a diagnosis of exclusion, particularly in our most vulnerable populations such as the homeless or incarcerated. However, one must also consider the patients whose care is being delayed by beds occupied by those without true illness, and the resources allocated to sussing out those actually at risk from those who are angling for secondary gain. There is also a very strong “Peter and the Wolf” phenomenon that can result from dealing with the same patients every day who come in claiming suicidality, only to recant after they sober up, or who are found to have conditional suicidality that hinges on things like being fed, housed, or given controlled substances such as pain medications or benzodiazepines — meaning, there is a risk that it could both degrade one’s index of concern for true suicidal ideation, and one’s empathy for other patients presenting with concern that they are a danger to self.

So what do they recommend? Some highlights:

Asking about improbable symptoms, which are rarely seen even in the most severely disabled patients, e.g. “When people talk to you, do you see the words they speak spelled out?” or (my personal favorite) “Have you ever believed that automobiles are members of an organized religion?”

Focusing on incongruities between the way they are presenting or endorsing symptoms and the circumstances they were in before arrival, or the way they behave when the examiner is not present, e.g. endorsing having active auditory and visual hallucinations yet showing no evidence of being distracted or attending to internal stimuli.

Critically evaluate reported hallucinations, particularly visual ones which are less often seen in true psychosis than reported in malingering. True visual hallucinations also are usually of “normalized people” and seen in color, rather than dramatic or atypical things such as giant monsters or devils, or flashes of light/color, which is more associated with neurologic disease or drug intoxication than psychosis.

They close by advising clinicians to “avoid direct accusations of lying, and give the suspected malingerer every opportunity to save face. For example, it is preferable to say, ‘You haven’t told me the whole truth'”, rather than directly confront them as malingering or lying.

All in all, this was an interesting diversion regarding a very difficult population and a sad phenomenon seen in the ED. Worth the 10 minutes it takes you to read, even if it doesn’t ultimately stop you from consulting psychiatry.

 

Transient Hypotension in the Emergency Department

An interesting technicality in the use of the PERC rule to rule out pulmonary embolism is the tachycardia component — it asks not whether the patient is tachycardic at the time of the application of the rule, or whether tachycardia was sustained throughout the emergency department stay, but instead whether the patient had (as described by Jeff Kline in his great review article on PE diagnosis and risk stratification): “3. Pulse <100 beats/min during entire stay in ED”.  Meaning, even transient tachycardia may suggest a life-threatening diagnosis, even if it resolves while the patient is in the emergency department, and we’re probably PERCing out a whole bunch of patients inappropriately, at least according to Kline (who, notably, testifies a whole bunch as an expert witness in cases of missed pulmonary emboli).

I recently had a handful of patients in whom concerning blood pressures were measured and documented, which then resolved when vital signs were re-checked or after a small quantity of fluid or repositioning. I was wondering whether anyone had looked at the prognostic significance of ED hypotension, and whether these momentary dips in blood pressure should be something that concerns me. I did a quick search and found two studies that addressed this question in two different populations:

First we have, from the Rick Bukata school of title writing: “Emergency department hypotension predicts sudden unexpected in-hospital mortality: A prospective cohort study.”  This study, by Alan Jones and Jeff Kline out of (and formerly out of) Carolinas, prospectively enrolled 4,790 adult ED patients admitted to the hospital for reasons other than trauma. Patients were divided into those with and without systolic BPs below 100 mmHg at any time during their ED visit and followed through their hospitalization for the primary outcome of in-hospital mortality. Secondary outcomes included “sudden and unexpected death”, the relationship between the degree and the duration of hypotension measured and mortality, and the test characteristics of hypotension as a test for predicting in-hospital mortality.

Their conclusions are illustrated well in this graph:

hypotension

As they concisely summarize in the article’s conclusion:

Patients exposed to hypotension had a threefold increased risk of in-hospital death and a 10-fold increased risk of sudden, unexpected in-hospital death. Patients with any one SBP < 80 mm Hg had a sixfold-increased incidence of in-hospital death, and patients with a SBP < 100 mm Hg for > 60 min had almost a threefold-increased incidence of in-hospital death.

The second article from the same group echoes this conclusion in a different population of patients. This article, “The significance of non-sustained hypotension in emergency department patients with sepsis” is a secondary analysis of the above data set which looks specifically at the prognostic value of non-sustained hypotension defined as one or more occurrence of SBP < 100 mmHg in patients with sepsis as defined by the receipt of antibiotics in the ED + at least two SIRS criteria.

774 patients met their inclusion criteria for sepsis, and after 74 were excluded for “overt shock” (sustained hypotension or use of pressors). They examined the remaining patients for a primary outcome of in-hospital death.  They found, as one might expect, that hypotension predicts worse outcomes in this sub-population of patients — including when patients had non-sustained hypotension. Again, there seemed to be a “dose-dependent” relationship, with an inverse relationship between the nadir of the ED SBP and the frequency of in-hospital death, as shown here:

sepsishypotension

Another important finding (though taken in context of a fairly small sample) was the statistically similar incidence of the primary outcome in both the groups with transient and sustained hypotension. Both groups of patients had a 2.5-3x higher risk of in-hospital mortality when compared to patients without any hypotension.

Without belaboring the point, these two studies underscore the prognostic significance of even transient hypotension in the undifferentiated emergency department patient, and (as is better known to have implications in terms of severity) in patients diagnosed with sepsis. Like the previous post regarding lactate, or the well-known pearl about tachycardia at discharge, this is a number that should get your attention and which demands evaluation and possible intervention / escalation of care.

References

Marchick MR1, Kline JA, Jones AE. The significance of non-sustained hypotension in emergency department patients with sepsis. Intensive Care Med. 2009 Jul;35(7):1261-4. PMID: 19238354. [PubMed] [Read by QxMD]
Holler JG1, Bech CN1, Henriksen DP2, Mikkelsen S3, Pedersen C4, Lassen AT1. Nontraumatic hypotension and shock in the emergency department and the prehospital setting, prevalence, etiology, and mortality: a systematic review. PLoS One. 2015 Mar 19;10(3):e0119331. PMID: 25789927. [PubMed] [Read by QxMD]