Lovenox in NSTEMI

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Written by: Terese Whipple, MD (NUEM PGY-3) Edited by: Andrew Ketterer, MD (NUEM Alum ‘17) Expert commentary by: Michael Macias (NUEM Alum ‘17)

The Case

 A 64 year old female with history of diabetes and hypertension is brought to your emergency department (ED) by EMS for “acid reflux.” She has new T wave inversions in leads II, III, and aVF with a troponin of 0.12.  The patient is given aspirin, nitroglycerine, and ticagrelor, but before signing your heparin drip order, you ask yourself:

 Would enoxaparin (LMWH) be a better option?

 The Recommendation:

 The AHA and ACC guidelines state, “In patients with NSTE-ACS, anticoagulation, in addition to antiplatelet therapy, is recommended for all patients irrespective of initial treatment strategy. Treatment options include:

  • Enoxaparin: 1 mg/kg subcutaneous every 12 hours, continued for the duration of hospitalization or until PCI is performed. An initial IV loading dose is 30 mg (Level of evidence A)

  • Unfractionated heparin (UFH) IV: initial loading dose 60 IU/kg (max 4000 IU) plus 12 IU/kg/h (max 1000 IU/h) adjusted per activated PTT in according to specific hospital protocol (Level of evidence B)”[2]

  • Bivalirudin/Fondaparinux- These are other options outside the scope of this post

The Evidence:

So why is the evidence for enoxaparin Level A and UFH level B? Multiple randomized controlled trials have examined this issue:

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  • The ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events) trial was the first major RCT to demonstrate the efficacy of enoxaparin over UFH. Although it was conducted in the late 90s, before GIIb/IIIa inhibitors or early invasive intervention were commonplace, it demonstrated a statistically significant decrease in the risk of death, MI, or recurrent angina in those randomized to treatment with enoxaparin (16.6%) v. UFH (19.8%) (p=.019). Incidence of major bleeding was similar in both groups.

  • TIMI-II: Enoxaparin was found to be superior with no increase in hemorrhage. Outcomes measured were death, MI, and urgent revascularization at 8 and 43 days, respectively, for enoxaparin (12.4%, 17.3%) and UFH (14.5%, 19.7%) (P=.048).

  • SYNERGY: In patients undergoing early PCI, enoxaparin was not inferior to UFH in the treatment of NSTEMI. However, enoxaparin was associated with more major bleeding (3.7% v 2.5%, p=.028). Both bleeding and efficacy were potentially confounded by crossover from LMWH before randomization to UFH upon randomization and vice versa … more below.

  • A to Z: Studied the efficacy and safety of enoxaparin and tirofiban compared w/ UFH and tirofiban. Incidence of death, MI, refractory ischemia with enoxaparin (8.4%) v. UFH (9.4%) were similar with similar bleeding incidences. Enoxaparin was found to be not inferior to UFH.

  • A systematic review conducted in 2004 of approximately 22,000 patients extending across the evolution of ACS treatment from conservative management to early PCI, demonstrated that enoxaparin is more effective than UFH in preventing MI and death.

It may seem that as treatment of NSTEMI has evolved to include antiplatelet therapy and early invasive intervention, the superiority of enoxaparin has been negated. However, both the SYNERGY and A to Z trials were potentially confounded by the fact that a majority of patients received pre-randomization therapy. A subgroup analysis performed on those patients who received only enoxaparin in the SYNERGY trial and no pre-treatment anticoagulation demonstrated the superiority once again of enoxaparin over UFH in regards to the combined outcome of death and MI (13.3% vs. 15.9% , p= 0.004).  The bleeding risk also seemed to be increased by pre-randomization therapy. The subgroup analysis showed no significant difference in major bleeding between UFH and enoxaparin when the patients received enoxaparin only (OR 1.04, CI 0.83-1.3).


If changing anticoagulation potentially increases bleeding risk, what about those destined for PCI?

The practices and procedures involved in PCI are beyond the scope of emergency medical practice, however the medications that we choose in the ED have downstream effects on patient care. Therefore, if we chose to use enoxaparin in the ED, we need to make sure that it won’t interfere with the ability of the patient to undergo PCI, and that it won’t increase their risk of adverse outcomes. Fortunately, this has been evaluated in controlled trials:

  •  STEEPLE (Safety and Efficacy of Enoxaparin in PCI patients, an international randomized evaluation). This trial examined the safety and efficacy of IV bolus (0.5 mg/kg or 0.75 mg/kg) of LMWH at time of PCI.[7]

    • Bleeding: Incidence of non-CABG-related bleeding complications in first 48 hours - 5.9% with 0.5 mg/kg enoxaparin (p=0.01 vs. UFH), 6.5% with 0.75 mg/kg enoxaparin (p= 0.051 vs. UFH), and 8.5% with UFH.

    • Conclusion: IV bolus 0.5 mg/kg enoxaparin associated with reduced rates of bleeding, 0.75 mg/kg associated with similar bleeding risk to UFH. For the combined end point of bleeding and ischemic events, both doses of LMWH were non-inferior to UFH.

    • 1-year mortality rates were comparable between patients receiving enoxaparin and UFH (2.3% for 0.5 mg/kg, 2.2% for 0.75 mg/kg, 1.9% for UFH)

  • CRUSADE (Can rapid risk stratification of unstable angina patients suppress adverse outcomes with early implementation of ACC/AHA guidelines). This trial studied the efficacy and safety of LMWH compared with UFH in high risk NSTEMI patients also receiving early GPIIb/IIIa inhibitor therapy.

    • In patients who underwent PCI within 48 hours the ORs for risk of death and reinfarction were similar for LMWH compared to UFH (OR 0.93, CI 0.67-1.31).

    • In patients who underwent PCI >48 hours into hospitalization, LMWH therapy was associated with reduced rates of death or reinfarction (OR 0.57, 95% CI = 0.44-0.73) and transfusion (OR 0.66, 95% CI = 0.52-0.84).

    • Conclusion:  Early invasive management with LMWH and GP IIb/IIIa inhibitor in NSTEMI is safe and doesn’t result in increased bleeding complications. In fact, it actually improves outcomes for those who don’t undergo PCI within 48 hours. 9


Take Home Points:

  1. Enoxaparin has been proven to be at least non-inferior and likely even superior to UFH when it comes to reducing the risk of death and MI in the setting of NSTEMI.

  2. Bleeding risk with enoxaparin compared to UFH appears to be equal (with the exception of the Synergy trial).

  3. Enoxaparin is safe and efficacious for use during PCI.

  4. Dialogue should occur between ED providers and interventional cardiologists to ensure their comfort with enoxaparin use and to prevent bleeding complications. If everyone is on board with using enoxaparin, it will likely get your patient anticoagulated more expediently than they otherwise would while waiting for pharmacy to mix up your heparin drip.

Expert Commentary

 Dr. Whipple, thank you for an excellent review of the literature supporting the use of lower molecular weight heparin (LMWH) for Non-ST-Elevation Myocardial Infarction (NSTEMI). There are two important points to discuss here before we even talk about LMWH, specifically: (1) What is the evidence behind good ole unfractionated heparin (UFH) in patients with NSTEMI? (2) Based on the evidence for UFH, is there a subgroup of patients who are likely to benefit more than others?


What is the evidence behind good ole unfractionated heparin (UFH) in patients with NSTEMI?

If you look at the AHA/ACC guidelines, UFH is listed as a Class I recommendation. Like any recommendations in guidelines, it is always important to look back at the data behind it. Specifically with respect to UFH, this data is weak but unfortunately is the best we have. Many of studies supporting the use of UFH in NSTEMI involved patients with “unstable angina” in the era before modern laboratory diagnostics (most studies used creatinine kinase), dual anti-platelet therapy (DAPT),  GpII/IIIa inhibitors, early invasive strategies, and revascularization [10]. This is a very different population than NSTEMI patients today. In general, these studies did find a strong trend in reduction of composite endpoints (mainly recurrent angina, death or MI) however this was only during hospitalization (short term endpoints) and this is the main crux of the AHA/ACC guideline recommendations. Further in the guidelines favor, the Cochrane review also concluded that UFH in NSTEMI reduces the rate of MI with a relative risk of 0.4 (0.25-0.63) [11]. However what both the guidelines and Cochrane review failed to consider is the benefits of UFH to our patients at a later time point. Deeper analysis of the Cochrane review reveals that the majority of their data points came from the FRISC study, which used only a six-day end point for their outcomes. A meta-analysis performed by Oler in 1996, took into account a time period beyond the UFH treatment duration (2-12 weeks) and found no significant difference in outcomes:

“Because the anticoagulant effects of heparin are brief, any benefit of therapy is unlikely to last beyond the duration of treatment.  Consistent with this theory, we found no reduction in the risk of MI or death between 2 and 12 weeks following randomization in patients with unstable angina who received heparin and aspirin compared to those who received aspirin alone.  This result underscores that heparin is a short-acting, temporizing therapy, and not an intervention that alters underlying atherosclerotic disease. - Oler et al. 1996”

 Not only do the studies that the guidelines base their data off fail to consider more later end points, they also include a different patient population, in a different era of acute coronary syndrome management. Since heparin has now become the standard of care for management of NSTEMI, no further placebo- controlled trials of heparin will ever exist.


Based on the evidence for UFH, is there a subgroup of patients who are likely to benefit more than others?

Based on the discussion above, there isn’t strong evidence to support UFH use in all comers with NSTEMI however based on its mechanism of action, it is likely to benefit those with high risk NSTEMI (TIMI Risk Score), or those who will undergo coronary intervention or revascularization. Intuitively this makes sense and jives with the evidence in the AHA/ACC guidelines. Patients who are placed on UFH and bridged to PCI/revascularization will benefit from the theoretical plaque stabilization. Those who are observed without any intervention will not, as once heparin is discontinued, their ongoing plaque burden and coronary anatomy will be unchanged, placing them at risk for a “rebound” event.

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In the emergency department we are burdened with making decisions with minimal initial information and only a few hours of observation. That being said, making a confident decision about which NSTEMI patients will need PCI/revascularization (and therefore will benefit from UFH) may prove very difficult. Therefore it may be more prudent to consider when certain situations make intervention less likely. These situations may include:

  • Patients without ACS symptoms but with elevated troponin:

    • Renal disease

    • hypotension

    • Sepsis

    • Toxic ingestion

    • Significant metabolic derangement

    • Anemia

    • Heart failure (without suspicion for ischemic etiology)

    • Supraventricular tachycardia (SVT)

    • Other presentations where troponin elevation is suspected to be related to a supply/demand issue

  • Patients with atypical history and high bleeding risk

The best course of action in these situations is to discuss the utility of UFH with the consulting cardiologist or admitting hospitalist about what is right for your patient based on the risk and benefits of anticoagulation, as well as your clinical suspicion for true acute coronary syndrome.



Now that we have a better understanding of the utility of UFH in NSTEMI, the use of LMWH becomes more clear. The same considerations just discussed should be similarly applied to the use of LMWH. As your literature review demonstrates, LMWH appears to be as good (if not better) than UFH with a similar bleeding risk profile. It is also easier to administer, requires less monitoring and has a lower risk of accidental supra-therapeutic anticoagulation. While it seems that it may be an obvious decision to switch to LMWH, remember that there is always a significant time lag between evidence and its incorporation into clinical practice. Therefore as you mentioned in your take home points, clear communication with other services is key. Before you go rogue giving LMWH to all your NSTEMI patients, I recommend having a evidence based discussion with your cardiologists and hospitalists to ensure everyone is on the same page.


Michael Macias, MD

NUEM Alumus 2017

University of California, San Diego

How To Cite This Post

[Peer-Reviewed, Web Publication] Whipple T, Ketterer A. (2019, March 18). Lovenox in NSTEMI [NUEM Blog. Expert Commentary by Macias M]. Retrieved from

Other Posts You May Enjoy


  1. Antman EA, et al. Enoxaparin prevents death and cardiac ischemic events in unstable angina/non-Q-wave myocardial infarction results of the TIMI 11B trial. Circulation. 1999; 100: 1593-1601.

  2. Amsterdam EA, et al. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes. Circulation. 2014;000:000–000. DOI:10.1161/CIR.0000000000000134

  3. Blazing MA, et al. Safety and efficacy of enoxaparin v unfractionated heparin in patients with no-ST-segment elevation acute coronary syndromes who receive tirofiban and aspirin: a randomized controlled trial. JAMA. 2004; 292: 55-64.

  4. Cohen et al. A comparison of Low-Molecular-Weight Heparin with Unfractionated Heparin for unstable coronary artery disease.  N Engl J Med. 1997; 337: 447-52.

  5. Harvey et al. Efficacy and safety of enoxaparin compared with unfractionated heparin in high-risk patients with non-ST-segment elevation acute coronary syndrome undergoing percutaneous coronary intervention in the Superior Yield of the New Strategy of Enoxaparin, Revascularization, and Glycoprotein IIb/IIIa inhibitors (SYNERGY) trial. Am Heart J 2006; 152: 1042-50. Doi: 10.1016/j-ahj.2006. 08.002

  6. Montalescot et al. Enoxaparin versus unfractionated heparin in elective percutaneous coronary intervention. N Engl J Med. 2006; 355: 1006-1017.  DOI: 10.1056/NEJMoa052711

  7. Montalescot, et al. Enoxaparin versus unfractionated heparin in elective percutaneous coronary intervention: 1 year results from the STEEPLE Trial. J Am Coll Cardiol Intv 2009; 2: 1083-91.

  8. Peterson JL, et al. Efficacy and bleeding complications among patients randomized to enoxaparin or unfractionated heparin for antithrombin therapy in non-ST-Segment Elevation Acute Coronary Syndromes. JAMA. 2004;292:89-96.

  9. Singh KP, et al. Low-molecular-weight heparin compared with unfractionated heparin for patients with non-ST-segment elevation acute coronary syndromes treated with glycoprotein IIb/IIIa inhibitors: results from the CRUSADE initiative J Thromb Thrombolysis. 2006; 21:211–220

  10. Oler A, et al. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis. JAMA. 1996; 276(10):811-5.

  11. Andrade-Castellanos CA, et al. Heparin versus placebo for non-ST elevation acute coronary syndromes. Cochrane Database. 2014; (6):CD003462.

  12. Antman EM, et al.The TIMI risk score for unstable angina/non-ST elevation MI: A method for prognostication and therapeutic decision making. JAMA. 2000; 284(7):835-42.

Posted on March 18, 2019 and filed under Cardiovascular.

Optic Neuritis

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Written by: Steve Chukwulebe, MD (NUEM PGY-4) Edited by: Victor Gappmaier, MD (NUEM Alum ‘18) Expert commentary by: Shira Simon, MD, MBA


31-year-old female, with no significant past medical history, presents to the emergency department with a mild headache and blurry, decreased vision in the right eye for the past 2 days. Other historical elements include that the patient has been experiencing pain with eye movement.  However, she denies difference in color perception. She also denies any trauma to the eye, recent fevers, chills, malaise, exposures, or travel. The left eye is unaffected.



Normal vitals and a well appearing female of stated age

Ocular exam reveals normal appearing eyes without chemosis, proptosis, conjunctival injection, scleritis, icterus, or foreign bodies

Non-dilated funduscopic exam is unremarkable

Visual acuities are OD: 20/40 and OS: 20/20 

Tonometry reveals right and left eye pressures are < 20 mmHg 

Slit lamp exam is without cells or flare 

Fluorescein stain is without any corneal uptake

CN 3-12 are intact, and no focal neurologic deficits on exam


Differential Diagnosis [1,2]: 

Painless Vision Loss

  • Central retinal artery occlusion

  • Central retinal vein occlusion

  • Retinal detachment

  • Vitreous detachment/vitreous hemorrhage

  • Tumor/Mass

  • Stroke 

Painful Vision Loss

  • Acute angle closure glaucoma

  • Scleritis

  • Anterior uveitis (iritis)

  • Optic neuritis

  • Keratitis

  • Corneal abrasion/trauma

  • Temporal arteritis

The challenge in diagnosing optic neuritis is to exclude other causes of acute monocular vision loss.  Therefore, a normal appearing eye, slit lamp exam, fluorescence stain, and intraocular pressures eliminates scleritis, uveitis, keratitis/abrasion, and glaucoma respectively [5].  Additionally, the history is less suggestive of other urgent and emergent ocular pathologies such as retinal detachment and central retinal artery occlusion.

Some physical exam findings more specific to optic neuritis include:

  • Afferent pupillary defect

  • Optic disk swelling and papilledema, which can be seen by ultrasound [6]

  • Decreased perception in the saturation of deep red colors

  • Decreased visual acuities ranging from 20/25 to 20/190, and even no light perception[4]

  • Eye pain, especially with eye motion, is seen in 92 percent of patients

  • Loss of color vision out of proportion to the decrease in visual acuity

  • Retro-orbital headache

Further diagnostics may include an MRI of the brain and orbits, but is not necessary for the diagnosis of optic neuritis [5].  MRI can help characterize the disease burden and assess the risk for the development of multiple sclerosis [7].

Given the patient’s age and constellation of symptoms, both neurology and ophthalmology consultation were performed with the leading concerning diagnosis being optic neuritis. The patient was admitted for further evaluation with a dilated ocular exam, MRs of the brain, and treatment.


Pathophysiology and Clinical Disease:

Optic neuritis is an inflammatory and demyelinating process that usually presents with monocular vision loss [3-4].  While there are many causes for optic neuritis, the demyelinating lesions seen in optic neuritis are similar to those that have been associated with multiple sclerosis.  Patients are typically women between the ages of 20-40.  Patients often develop progressive symptoms over a period of a few hours to several days.


Treatment and Timing:

Typical treatment is high dose intravenous steroids for three days. Another treatment regimen that has been described is intravenous methylprednisolone (250 mg four times per day) for three days, followed by oral prednisone (1 mg/kg per day) for 11 days, and then a four-day taper [8, 9]. 

If the diagnosis is uncertain, then is it acceptable to delay treatment for an MRI or specialist consultation the following morning?

The Optic Neuritis Treatment Trial described treatment of optic neuritis with high dose intravenous methylprednisolone.  The initial multicenter trial enrolled 457 patients from July 1, 1988, through June 30, 1991.  They ultimately randomized 389 patients with acute optic neuritis (and without known multiple sclerosis) to receive intravenous methylprednisolone (250 mg every six hours) for 3 days followed by oral prednisone (1 mg per kilogram of body weight) for 11 days, oral prednisone (1 mg per kilogram) alone for 14 days, or placebo for 14 days.  They then assessed the neurologic status of the subjects for a period of two to four years and published their results in 1993.  Also by following the subjects longitudinally, the authors were able to reanalyze the data and publish again in 2003. From the initial study, it was learned that high the steroids hastened the recovery of visual function, but did not affect long term visual outcomes when compared to both placebo and oral prednisone [10, 11, 12] after six months, and ten-year follow-up.  It was found that a 3-day course of methylprednisolone reduced the rate of development of multiple sclerosis over a 2-year period [12]. Multiple sclerosis developed within the first two years in 7.5 percent of the IV methylprednisolone group vs. 14.7 percent of the oral prednisone group vs. 16.7 percent of the placebo group.  The adjusted rate ratio for the development of definite multiple sclerosis within two years in the intravenous methylprednisolone group was 0.34 as compared with the placebo group and 0.38 as compared with the oral-prednisone group.  However, after a 5-year period the treatment effect was no longer significant for the same group of patients.

Therefore, in a scenario when a provider may delay high dose steroids for a neurology and ophthalmology consultation, or for an MRI, it can be inferred that this delay will not affect long term outcomes for the patient. However, given that early treatment hastens symptom recovery and delays progression to multiple sclerosis, it may be beneficial to start high dose IV steroids in the emergency department in patients if optic neuritis is the suspected diagnosis.

Expert Commentary

This is a very good review of optic neuritis. There are just a few, additional nuanced points I’d like to mention, as well as some tips on counseling the patient.

  • Visual field changes: A central visual field deficit is commonly seen with this entity. It is most easily detected on formal visual field testing in the ophthalmology clinic (Humphrey or Goldmann visual fields), though some patients may report this on their own in the acute care setting.

  • Optic nerve swelling: In the ONTT, only 35% of patients had disc swelling (65% had normal appearing optic nerve heads on fundoscopy), so evaluating with ultrasound would not be revealing in most cases.

  • MRI for diagnosis: MRI is actually very important for the diagnosis of optic neuritis, as inflammation of a different part of the optic nerve (other than the nerve head) can only be visualized radiographically. MRI of the orbits and brain should be obtained with thin slices through the orbits, with fat suppression, and gadolinium (in addition to FLAIR sequences to look for demyelination).

  • Differential diagnosis: While this article talks about optic neuritis from demyelination related to possible MS, it’s important to bear in mind that there are other causes of optic neuritis: autoimmune disease (e.g., lupus), infections (e.g., syphilis or Lyme), other inflammatory conditions (e.g., sarcoidosis), other demyelinating processes (like neuromyelitis optica), or it can be idiopathic.

When counseling the patient about prognosis, it may be helpful to remember the “10-20-40-60” rule. I had been taught this, and it helps quickly summarize the ONTT prognostic statistics (that are outlined very nicely in this article). The “10-20-40-60 rule” mnemonic reminds us that at 10 years: there is a 20% chance of developing MS after an episode of idiopathic optic neuritis if there were no white matter lesions found on MRI; a 40% chance regardless of MRI findings; and, a 60% chance if 1+ white matter lesions are found on MRI.

It is also helpful to let the patient know that visual recovery is often excellent. Most patients return fairly close to their baseline vision within 3-5 weeks, although they may note some lingering difficulties with contrast sensitivity and color vision. An afferent pupillary defect may also persist.


Shira Simon, MD, MBA

Assistant Professor of Ophthalmology and Neurology

Northwestern Medicine

How to Cite This Post

[Peer-Reviewed, Web Publication] Chukwulebe S, Gappmaier V. (2019, March 11). Optic Neuritis. [NUEM Blog. Expert Commentary by Simon S]. Retrieved from

Other Posts You May Enjoy


  1. Dargin JM, Lowenstein RA. The painful eye. Emerg Med Clin North Am. 2008;26(1):199-216, viii.

  2. Vortmann M, Schneider JI. Acute monocular visual loss. Emerg Med Clin North Am. 2008;26(1):73-96, vi.

  3. The clinical profile of optic neuritis. Experience of the Optic Neuritis Treatment Trial. Optic Neuritis Study Group. Arch Ophthalmol. 1991;109(12):1673-8.

  4. UpToDate

  5. Germann CA, Baumann MR, Hamzavi S. Ophthalmic diagnoses in the ED: optic neuritis. Am J Emerg Med. 2007;25(7):834-7.

  6. Teismann N, Lenaghan P, Nolan R, Stein J, Green A. Point-of-care ocular ultrasound to detect optic disc swelling. Acad Emerg Med. 2013;20(9):920-5.

  7. Beck RW, Arrington J, Murtagh FR, Cleary PA, Kaufman DI. Brain magnetic resonance imaging in acute optic neuritis. Experience of the Optic Neuritis Study Group. Arch Neurol. 1993;50(8):841-6.

  8. Beck RW, Cleary PA, Anderson MM, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med. 1992;326(9):581-8.

  9. Sellebjerg F, Nielsen HS, Frederiksen JL, Olesen J. A randomized, controlled trial of oral high-dose methylprednisolone in acute optic neuritis. Neurology. 1999;52(7):1479-84.

  10. Beck RW, Gal RL, Bhatti MT, et al. Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial. Am J Ophthalmol. 2004;137(1):77-83.

  11. Beck RW, Trobe JD, Moke PS, et al. High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial. Arch Ophthalmol. 2003;121(7):944-9.

  12. Beck RW, Cleary PA, Trobe JD, et al. The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group. N Engl J Med. 1993;329(24):1764-9.

Posted on March 11, 2019 and filed under Ophthalmology.

Verbal De-escalation in the ED

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Written by: Vidya Eswaran, MD (NUEM PGY-3), Zach Schmitz, MD (NUEM PGY-2), Abiye Ibiebele, MD (NUEM PGY-2) Edited by: Michael Macias, MD and Arthur Moore, MD (NUEM Alum ‘17) Expert commentary by: John Bailitz, MD


I’ve been suffering in that waiting room for hours!

That worthless tech stabbed me with a needle ten times!! 

If you don’t give what I want right now, I am going to hurt someone!!!

Every emergency physician can recall a time when they hear these words or similar phrases echoing throughout the Emergency Department (ED). As a patient becomes increasingly agitated, nearby staff and visitors become distracted, and ultimately concerned about everyone’s safety. Emergency Physicians can help restore the calm amidst the chaos by recognizing subtle clues and intervening early.

According to the Bureau of Labor Statistics, those who work in the healthcare sector had three times the rate of illness and injury from violence compared to all private industries [1]. In a survey of emergency medicine residents, 65.6% reported an experience of physical violence by a patient, 96.6% reported verbal harassment from a patient, and 52.1% reported sexual harassment by a patient. Often these patients were under the influence of drugs or alcohol, had a psychiatric disease, or an organic cause of their agitation, such as dementia [2]. In Australian emergency departments, 3 of every 1000 ED visits are associated with an episode of violence or acute behavioral disturbance [3].

When violence by a patient is imminent or has already occurred, the patient requires immediate restraint by either chemical or physical means [4]. ACEP guidelines for patient restraints supports the careful and appropriate use of restraints or seclusion if “careful assessment establishes that the patient is a danger to self or others by virtue of a medical or psychiatric condition and when verbal de-escalation is not successful [5].” Verbal “de-escalation techniques aim to stop the ascension of aggression to violence, and the use of physically restrictive practices, via a range of psychosocial techniques [6],” and should be tried before one simply grabs “5 and 2.”


Clinical Approach to Agitation 

How do you determine which patients would benefit from verbal de-escalation?

Look for the agitated patient, the one who has an angry demeanor, using loud and aggressive speech, seems tense and is grasping their bed rails or clenching their fists, the one who is pacing or fidgeting [4]. These patients are in the pre-violent stage, and may have the potential to be successfully talked down. If a patient has already engaged in violent acts, it is too late to intervene with verbal de-escalation methods.


What principles should be used to assist with verbal de-escalation of the agitated patient?

In 2012 the American Association for Emergency Psychiatry offered a consensus statement on verbal de-escalation and created ten key domains to guide care of agitated patients. These domains offer a great framework for how to approach the agitated patient before the situation escalates [7].


Domain 1: Respect the patient’s and your personal space. First and foremost in any patient encounter, especially one with an agitated patient, is your safety. Aim to keep at least 2 arms lengths distance between you and the patient. This offers you room for your own personal safety, and is seen as non-confrontational and non-threatening in the eyes of the patient. Ensure that both you and the patient have an unobstructed pathway to the exits and that you do not stand in the way of the patient’s path to leaving the room.


Domain 2: Do not be provocative. The majority of our interpersonal interactions is communicated not by the words we say, but how we say them. Our body language is crucial and we must be mindful of it when attempting to calm a patient. Keep your hands visible and at ease, bend your knees slightly, avoid excessive direct eye contact and approach your patient from an angle instead of head-on. These positions convey a non-threatening demeanor.


Domain 3: Establish verbal contact. The first person to interact with the patient should be the one who leads the verbal de-escalation. Introduce yourself and tell the patient your role and orient them to their surroundings. Then, ask the patient what they would like to be called. This gives the patient the impression that you believe he or she is important and has some control over the situation.


Domain 4: Be concise and caring. Use short sentences and simple vocabulary to get your point across. Give your patients time to process what you have said and to respond before continuing. You should be prepared to repeat your message multiple times until your patient understands.


Domain 5: Identify wants and feelings. In order to provide empathetic care, you must understand your patient’s perspective. Listen carefully to what your patient says to pick up clues and respond to their desires. One tactic is to say “I really need to know what you expected when you came to the ED today. Even if I can’t provide it, I would like to know so that we can work on it together.”


Domain 6: Listen closely to what the patient is saying. This is closely related to Domain 5. Practice closed loop communication, repeat what the patient has told you to ensure you have understood them correctly.


Domain 7: Agree, or agree to disagree. Look for something that you can agree with in what the patient is saying. “I agree, waiting can be frustrating” or “Yes, I understand that the nurse has stuck you three times.” However, if you can’t find something to agree with the patient about, do not lie - agree to disagree.


Domain 8: Lay down the law and set clear limits. Draw a line which the patient must not cross. Let him or her know that harming himself or others is unacceptable and will result in specific consequences (seclusion, arrest, prosecution). This should not be portrayed as a threat, but rather be conveyed in a respectful manner. You can preface it with “Your behavior is making our staff uncomfortable and that makes it difficult for us to help you.”


Domain 9: Coach the patient on how to stay in control. Give the patient tactics they can use to help de-escalate the situation. “If you sit down we can discuss why you are here.”


Domain 10: Be optimistic and provide hope that the patient will be able to get to a favorable outcome. “I don’t want you to stay here longer than you need to. Let’s work together to help you get out of here feeling better.” Be sure to debrief with the patient and staff after the de-escalation, so that there is a strategy in place if this were to happen again.


Other strategies include recruiting the patient’s friends and family to help and to employ the three Fs technique - feel, felt, found [8]. “I understand that you feel X. Others in the same situation have felt that way to. Most have found that doing Y can help [4].”


Think of verbal de-escalation as a procedure just like intubations or central lines - with practice, comes mastery. Rehearse what you plan to say, and do mental run-throughs of de-escalations. Watch and learn from others who do this well. The English Modified De-Escalating Aggressive Behaviour Scale (EMDABS) is a validated tool you can use to assess your performance during de-escalations [9].



Unfortunately, physical and chemical restraint of the severely agitated patient is sometimes needed to protect ED staff, visitors, and the patient themselves. [10,11]. But by recognizing subtle signs of agitation early, we can often utilize effective verbal-de-escalation techniques to create safety for everyone!

Check out our infographic for an easy to use mnemonic which summaries key points.

Expert Commentary

Thank you for this outstanding review of an incredibly important topic topic with tragically little supporting evidence to guide best practice. Colleagues and patients in multiple different practice settings throughout Chicago have repeatedly taught me several key pearls and pitfalls when dealing with the agitated patient.


For the mildly agitated patient, always open with an apology that empathically validates the patient or visitor emotions. “I am very sorry that you have been suffering in the waiting room for so long. That must have been very frustrating. My sincere apologies.” Never reply with a sharp justification or any explanation. Just acknowledge their frustration, own it, and the patient will quickly move past the emotion. Often times, this first connection forms the foundation of a healthy patient physician relationship and even a thank you letter to your ED Director.


For the patient whose agitation is escalating despite appropriate efforts by trained ED staff, call security or hit the duress button for back up before stepping into any potentially risky situation. If you are single covered at 3 AM, you cannot become another patient. When help arrives, ask security to simply stand in the hallway as you begin your DEFUSE techniques. Politely but purposefully excuse inexperienced staff members who have themselves become agitated and entered into a shouting match with patients or visitors. Always keep your own emotions in check and debrief with everyone involved after each learning opportunity.


Finally, when the sedation is needed for patient and staff safety, assemble your team, and proceed with the utmost professionalism. As a physician, you have no role in the physical restraint process unless absolutely necessary. Your security staff has been trained in proper physical restraints while chemical sedation catches up with the dangerous patient. If the patient is acutely agitated without concerns for respiratory depression, utilize 5 mg of Haldol + 5 mg of versed instead of the traditional 2 mg of Ativan. Everyone in the ED will become safer more quickly and the patient will wake up more rapidly for reassessment.


Just remember, “Patients First” always starts with everyone’s safety first!


John Bailitz, MD

Program Director, Northwestern Emergency Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Eswaran V, Schmitz Z, Ibiebele A, Macias M, Moore A. (2019, March 4). Verbal De-escalation in the ED. [NUEM Blog. Expert Commentary by Bailitz J]. Retrieved from

Other Posts You May Enjoy


  1. Nonfatal Occupational Injuries and Illnesses Requiring Days Away From Work, 2014.Bureau of Labor and Statistics News Release. 2015.

  2. Schnapp et al. Workplace Violence and Harassment Against Emergency Medicine Residents, WJEM 2016: 17(5) 567-573.

  3. Downes et al. Structured team approach to the agitated patient in the emergency department. Emergency Medicine Australasia (2009) 21, 196-202

  4. Moore, G and Pfaff, J. Assessment and emergency management of the acutely agitated or violent adult.Up to Date.

  5. ACEP Policy on Patient Restraints

  6. Price et al. Learning and performance outcomes of mental health staff training in de-escalation techniques for the management of violence and aggression. The British Journal of Psychiatry (2015) 206, 447-455

  7. JS Richmond et al. Verbal De-escalation of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project BETA De-escalation Workgroup. Western Journal of Emergency Medicine: Integrating Emergency Care with Population Health 2012: 13(1) 17-25.

  8. Nickson, C. De-Escalation. Life in the Fast Lane. 2014.

  9. Mavandadi et al. Effective ingredients of verbal de-escalation: validating an English modified version of the ‘De-Escalating Aggressive Behaviour Scale’. Journal of Psychiatric and Mental Health Nursing, 2016, 23, 357-368.

  10. Weingart, S. Podcast 060 – On Human Bondage and the Art of the Chemical Takedown. EMCrit. 2011.

  11. Nickson, C. Chemical Restraint. Life in the Fast Lane. 2014.

Posted on March 4, 2019 and filed under Psychiatry.

Intraosseous Lines

Written by: Dana Loke, MD (NUEM PGY-3) Edited by: Victor Gappmaier, MD (NUEM Alum ‘18) Expert commentary by: John Sarwark, MD

Since its development in the 1940s, intraosseous (IO) access has been a mainstay of resuscitation in both pediatric and adult patients[1]. IO access has been used in medical emergencies requiring immediate access when peripheral IV access is either not possible or time-prohibiting, such as cardiac arrest, status epilepticus, shock, trauma, and burns[2]. There is mounting evidence supporting the continued use of IO lines both in-hospital and pre-hospital. Studies have demonstrated similar outcomes between IO and IV access with return of spontaneous circulation, further supporting their use during cardiac arrest3. In fact, the International Liaison Committee on Resuscitation (ILCOR) stated in 2010 that “Delivery of drugs via an endotracheal tube is no longer recommended – if IV access cannot be achieved, drugs should be given by the IO route”[4]. Currently, IO access is achievable in two ways: manually or with commercially-available drill-inserted devices (such as the EZ-IO).


Why use an IO instead of a central line during a resuscitation?

Besides the obvious advantage that IO insertion is quicker, it is also cheaper than central line insertion. On average IO lines cost about $100 compared to $300 for central lines[4]. Additionally, there are far fewer complications associated with IO lines compared to central lines. All medications that can be given via central line can also be given via IO line. Blood can be drawn and sent for lab analysis just as with IV access. Although an IO line only has one lumen, there are multiple possible insertion sites, and multiple IO lines can be placed in the same patient simultaneously. Furthermore, IO lines are easy to remove when more definitive vascular access has been obtained. 

But perhaps one of the biggest advantages of an IO is that it requires less training and experience to insert than a central line. Their ease of use allows trained RNs, techs, and novice providers to obtain vascular access without interrupting assessment by senior providers. In fact, a recent study showed that IO access can effectively be taught as a four-step approach to medical students[5].



There are a few important contraindications to IO access for the EM physician to be aware of. The first is any fracture at or proximal to the insertion site, as this can cause extravasation of fluids or medication and increases the risk of compartment syndrome[2]. The second is cellulitis or evidence of other infection such as abscess at the insertion site, similar to other procedures like central lines and PIV access[2]. Sites of prior attempts should not be used for a second attempt. Lastly, patients at risk for fracture (for instance, osteogenesis imperfecta or osteopetrosis) should not be given an IO line[4].


Although manual insertion of an IO line is possible using a Cook or Jamshidi needle, commercial devices such as the EZ-IO are widely available and should always be used for IO insertion if available. The EZ-IO kit includes the IO needle set (with 45 mm, 25 mm, and 15 mm needles), power driver, IO tubing, and adhesive dressing as shown in the image below[6]. The 25 mm needle is the standard needled used for adults. If the humerus is used or there is excessive tissue (i.e. muscular or obese patients), then the 45 mm needle should be used. The 15 mm is generally used in children or any adults <40 kg.


There are multiple sites in which IO access can be obtained as shown in the image below [4,5]:

  • Proximal humerus – insert about 1 cm above the surgical neck (which can be found by sliding a finger up the anterior humeral shaft until the greater tubercle is felt)

    • Of note, this is the preferred insertion site during resuscitation, especially those involving abdominal trauma, as medications and fluids enter the circulation faster as they reach the central circulation via the SVC and bypass the pelvic and abdominal vessels.

  • Proximal tibia – insert 2 finger breadths below the patella and 1-2 cm medial to the tibial tuberosity in adults

  • Distal tibia – insert 3 cm proximal to the most prominent aspect of the medial malleolus

  • Femur, iliac crest, sternum – not routinely used and may require a special device


After choosing the correct needle and site, clean the site with alcohol swabs or chlorhexidine, and connect the needle set to the power driver (i.e. the drill). Remove the needle cap and insert the needle by drilling with a consistent downward pressure perpendicular to the bone surface. It is customary to feel a sudden loss of resistance, as the needle “gives” when entering the medullary space. Remove the power driver from the needle and secure the site with the adhesive dressing. At this point, you can aspirate blood for lab analysis and then connect primed IO tubing to flush the IO line. Now the line is ready for use to primed IV tubing. Make sure to document the time of insertion as IO lines should not be left in for more than 24 hours.


Any medication that can be given intravenously can also be given intraosseously[2]. This includes contrast media and blood transfusions[7]. Some amount of hemolysis of transfused blood has been documented when given intraosseously, although this is of unclear clinical significance[4]. According to multiple studies, the IO route is pharmacokinetically equivalent to the IV route and therefore there is no need to change medication doses when administering via IO8.


While any lab can be sent from an IO blood sample, it is important to be cognizant of the correlation between certain labs when obtained via IO vs IV. Labs that have good correlation include hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin[4]. However, other labs including WBC, platelets, serum CO2, sodium, potassium, calcium do not correlate well or in any predictable way with venous samples4.


All IO lines should be removed within 24 hours of the insertion time or earlier if there is any sign of extravasation (i.e. progressive pain or swelling at the insertion site). After disconnecting all infusions, the EZ-IO needle and hub can be removed by attaching a 10 cc luer-locked syringe to the hub and rotating clockwise while pulling back[4]. As with all potential sharps, the device should be disposed of in a biohazard sharps container.


Although rare, there are several complications of IO access to be aware of. These include osteomyelitis, fracture, extravasation, compartment syndrome, and necrosis of the epiphyseal plate[4]. However, perhaps the most common complication is injury to self or others while obtaining access. To avoid injury, warn conscious patients about the procedure and in unconscious patients make sure to stabilize the site.

Key Points

  • IO lines are a mainstay of resuscitation and used when peripheral IV access is either not possible or time-intensive.

  • Compared to central access in resuscitations, IO access is cheaper, quicker, safer, and easier to obtain.

  • Contraindications to IO insertion include fracture at or proximal to the insertion site, cellulitis or other infection overlying the insertion site, prior attempt at the insertion site, or bone disease such as osteogenesis imperfecta or osteopetrosis.

  • Make sure to choose the appropriate needle and insertion site prior to obtaining IO access.

  • All medications that can be given intravenously can be given intraosseously at the same doses.

  • Remember that not all lab values from an IO sample correlate with IV samples. Accurate IO labs include: hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin.

  • IO lines should be removed within 24 hours of insertion.

  • Complications are rare but include osteomyelitis, fracture, extravasation, compartment syndrome, and necrosis of the epiphyseal plate.

Expert Commentary

Intraosseous lines in the emergency department have always made perfect sense to me so I appreciate the scrappy enthusiasm for them in this article.  In my opinion, they are an incredibly logical alternative to “crash” central lines.  I mean, seriously, in a scenario where a patient is coding or about to code, why in god’s name should we be farting around with a femoral line?  People get stuck with needles.  Arteries are inadvertently punctured.  There’s a huge mess and it’s often not sterile.  An IO goes in clean and easy within seconds and boom, you’ve got yourself access, and essentially central access at that.  You can put pretty much anything in it, although I did hear in my time around the ICU circuit in residency that the exception to this is TPN.  That’s largely a piece of meaningless chin stroking trivia but, hey, maybe it will make you sound smarter on MICU rounds tomorrow AM.

The needle sizes can be a bit confusing in a tense situation.  To avoid any issues, just remember this to keep it simple: USE THE BLUE NEEDLE.  I have yet to have a patient who was so obese they needed the yellow needle in their tibia, and the pink one is exclusively just for kids.  The best route is indeed via the humerus as the flow rate is reportedly as good as a subclavian line.  Folks tend to jump for the tibia as their go-to site, and that’s perfectly fine but if you’re doing this out of uncertainty with the landmarks of the humerus it’s easier than you think.  One way I was taught was to place your hands in an inverted “V” over the proximal humerus, and where your thumbs meet over the bone there is your target for your drill. 

Not to be a Robert Downer Junior but I should remind everyone that there was an article in Annals this year entitled “Intraosseous Vascular Access Is Associated With Lower Survival and Neurologic Recovery Among Patients With Out-of-Hospital Arrest.”  The title really states it all, showing a lower rate of “favorable” modified Rankin score in the patients that got IO over IV.   Another study from Resuscitation last year titled “Intraosseous compared to intravenous drug resuscitation in out-of-hospital cardiac arrest” also showed decreased rates of ROSC and survival to hospitalization (but not to discharge) in the IO group.  Bear in mind the IO’s in these articles are placed in the field and not in the hospital, although I can’t think there’s too much difference in technique between us and our friends out in the rigs.  

I’m not going to get into the nitty gritty of each of these papers and I certainly don’t think we are actively making moves to remove them from our practice in our specialty but keep your eyes open for more discussion and research on this in the coming months to years.  I still like the IO and it’s still a part of my practice and I encourage you to use it as well.  Drill, baby, drill!

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John P Sarwark, MD

NUEM Alumnus 2016

How to Cite This Post

[Peer-Reviewed, Web Publication] Loke D, Gappmaier V (2019, February 25). Intraosseous Lines [NUEM Blog. Expert Commentary by Sarwark J]. Retrieved from


  1. Foëx, B.A. (2000). Discovery of the intraosseous route for fluid administration. J Accid Emerg Med, 17(2) 136-137.

  2. Faga, M., & Wolfe, B. (2016). Vascular access in hospitalized patients. Hospital Medicine Clinics, 5(1), 1-16.

  3. Clemency, B., Tanaka, K., May, P., Innes, J., Zagroba, S., Blaszak, J., Hostler, D., Cooney, D., McGee, K., & Lindstrom, H. (2017). Intravenous vs. intraosseous access and return of spontaneous circulation during out of hospital cardiac arrest. Am J Emerg Med , 35(2), 222-226.

  4. Nickson, C. (2015, June 10). Intraosseous access. Retrieved February 26, 2018, from

  5. Afzali, M., Kvisselgaard, A.D., Lyngeraa, T.S., & Viggers, S. (2017). Intraosseous access can be taught to medical students using the four-step approach. BMC Med Educ, 17(1), 50.

  6. Teleflex. (2018). Intraosseous access. Retrieved February 26, 2018, from

  7. Winkler, M., Talley, C., Woodward, C., Kingsbury, A., Appiah, F., Elbelasi, H., Landwher, K., Li, X., & Fleischmann, D. (2017). The use of intraosseous needles for injection of contrast media for computed tomographic angiography of the thoracic aorta. J Cardiovasc Comput Tomogr, 11(3), 203-207.

  8. Von Hoff, D.D., Kuhn, J.G., Burris, H.A. 3rd, & Miller, L.J. (2008). Does intraosseous equal intravenous? A pharmacokinetic study. Am J Emerg Med, 26, 31–38

Posted on February 25, 2019 and filed under Procedures.

Diagnose on Sight: Rhabdomyolysis

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Written by: David Kaltman, MD (NUEM PGY-3) Edited by: Charles Caffrey, MD (NUEM Alum ‘18) Expert commentary by: Josh Waitzman, MD

Case: A 25 year-old man with no significant past medical history presents to the ED with discolored urine. He states that he does not exercise regularly, but two days ago he went to a spinning class with several co-workers. He endorses increasingly severe bilateral lower extremity soreness over the past 24 hours that has not improved with ibuprofen. Overnight, he began to note discoloration of his urine, prompting his presentation. Vital signs are unremarkable. Physical exam is notable for diffuse and equivalent tenderness to palpation of his thighs; his lower extremities are neurovascularly intact distally.



Clinical Questions: What should be the disposition of this patient: home vs. medical floor vs. ICU? Is the initial CK useful in this risk stratification? 

This patient has a classic case of exercise-induced rhabdomyolysis. Rhabdomyolysis is a clinical syndrome and is variously defined; most criteria use CK > 5x upper limit of normal as a cutoff. The most common etiologies in adults are:

  1. Trauma, often crush injury or prolonged downtime

  2. Prolonged exertion, particularly in hot weather and in those who are not well conditioned

  3. Toxicologic, including alcohol, sympathomimetics, PCP, carbon monoxide, statins, envenomations

  4. Viral infection

Patients often present with myalgias, weakness, and dark urine. In severe cases, nausea and mental status changes (secondary to uremia or other metabolic catastrophe) may be present. Muscle necrosis leads to the release of intracellular contents into the systemic circulation, making hyperkalemia and hypocalcemia the most immediately life-threatening problems.

Workup should include:

  1. Serial physical exams for compartment syndrome

  2. ECG, given the likelihood of electrolyte derangements

  3. Labs: Chemistry panel (including Mg and Phos), CBC, urinalysis, total creatine kinase (CK) *note: urine myoglobin is specific but not sensitive; its half-life is only 1-3 hours

  4. If very ill-appearing, consider adding DIC panel, LDH, and hepatic chemistries

Does the total initial CK level in the ED correlate with risk of acute renal failure? Not really. The risk of renal failure depends more on concurrent conditions such as sepsis, acidosis, hypovolemia, and comorbidities. However, multiple reviews have shown that the risk is higher when the total level approaches 15,000. One 2013 retrospective review of 2,000 patients did not find any significant correlation until CK levels exceeded 40,000. On the other end, one prospective study showed that no patients with CK levels <5,000 went on to develop renal failure.



Initial management should include identifying and treating the underlying cause (detoxification, removing offending agent, cooling, etc.), and then treating to prevent renal failure and other long term complications. Prompt IV fluid resuscitation can generally begin with a bolus of 1-2L. Much like DKA, do not give more than this until the patient is able to urinate. Once urination is proven, titrate fluid resuscitation to achieve about 250mL/hr of UOP (3mL/kg/hr). Urinary alkalinization with a bicarbonate drip is a controversial treatment that may have a renal protective effect; no randomized controlled trials to date have demonstrated benefit. This may be a reasonable option in severe cases if the urine is very acidic (pH<6.5) and if your hospital has an ICU experienced with a urinary alkalinization protocol. Signs of renal failure should merit nephrology consultation and consideration of dialysis.




  1. Discharge with close follow up for patients who are generally healthy, have normal creatinine, downtrending CK, and can reliably consume lots of fluids at home

  2. Medical admission for patients with AKI, co-morbidities (pre-existing or trauma, heat injury)

  3. ICU admission for impending renal failure (unable to void, highly elevated creatinine, severe metabolic acidosis), arrhythmia, DIC, concern for early compartment syndrome


Case Conclusion

The patient is able to urinate after receiving 2L of NS. His initial CK is 45,000 but serum creatinine and potassium are within normal limits. He is admitted to the general medicine service where he receives aggressive IV fluid resuscitation. Fortunately, he does not develop acute kidney injury and is later discharged in his usual state of health with only a newfound aversion to bicycles.

Expert Commentary

The above is a really nice presentation of a mild-to-moderately severe case of rhabdomyolysis. A few additional points of emphasis:

Although we like to think about rhabdo as a disease of excess Cross Fit, the history often includes a broad variety of causes.


 I think the most common rhabdomyolysis history in a patient on whom nephrology is consulted is “found down after a fall.” Patients can spend hours or days with prolonged muscle compression and resulting muscle breakdown. Individuals who have this presentation tend to be older and more frail, and often have more medical comorbidities like CKD, DM and HTN that predispose them to acute kidney injury.

In addition to the nice list of causes that Dr. Kaltman provides, I’d add a few other rarer, but can’t miss conditions, including

- seizure and electrocution injuries (which break down muscle from prolonged activation)

- compartment syndrome (from burns or vascular occlusion, including ECMO cannulation)

- eating quail (called “coturnism”). I’ve never actually seen this, but please call nephrology if you do! It makes for great cocktail party chatter. 

I agree with the statements re: CK levels for diagnosis of rhabdomyolysis. There is no CK level that perfectly excludes rhabdomyolysis, but it is hard to attribute an AKI to rhabdomyolysis without a CK in the tens of thousands. CK can be added onto a mint green tube in our laboratory, which makes it an easy test to add on after you see hyperkalemia or AKI.

A very useful and rapid screening test for rhabdomyolysis is the urinalysis, which will often show large blood but few or no RBCs on microscopy. Both myoglobin and hemoglobin contain heme, which is recognized by the urine dipstick as “blood”; however free myoglobin (from rhabdomyolysis) or free hemoglobin (from hemolysis) do not appear in the urine as RBCs. The test can be done in under 30 minutes and allow for rapid diagnosis and initiation of therapy. Urine myoglobin can also be checked, but has a longer turnaround time.

Prompt treatment of the patient with aggressive (1-2L per hour to start) IV crystalloid resuscitation is critical to the management of rhabdomyolysis. I can’t overstate enough how important volume is. If a patient is failing medical management, it is often from under-resuscitation. I don’t necessarily buy into the “proving they can make urine” before giving more volume—keep giving volume and trial high dose diuresis or dialysis if the patient is showing clinical signs of volume overload.

In terms of which fluid to use, classically the recommendation has been for saline because balanced crystalloids contain potassium. However, the amount of potassium in LR is quite low, and LR has never been shown to cause hyperkalemia in patients.

If patients are acidemic and have a normal/high calcium, isotonic bicarbonate is probably the crystalloid of choice. However, if the patient is hypocalcemic prior to receiving bicarbonate, treating their acidosis with bicarbonate can in further calcium binding to albumin, lower serum ionized calcium and symptomatic hypocalcemia.


  • Don’t forget about rhabdomyolysis in older people who are found down.

  • In true rhabdomyolysis CK should be 10,000+ to explain a severe kidney injury.

  • The UA is a fast test that can suggest rhabdomyolysis with large blood and few RBCs.

  • Be aggressive with early isotonic fluid resuscitation. We can always take fluid off later with dialysis if we need to.

  • LR or NS are reasonable fluid choices. Isotonic bicarbonate is great as long as the patient is both acidemic and does not have a low calcium.

  • Call nephrology if you are worried about your patient or if they say that they ate quail.


Josh Waitzman, MD

Nephrology Fellow

Northwestern Medicine

How to Cite This Post

[Peer-Reviewed, Web Publication] Kaltman D, Caffrey C (2019, February 18). Diagnose on Sight: Rhabdomyolysis [NUEM Blog. Expert Commentary by Waitzman J]. Retrieved from

Other Posts You May Enjoy


  1. Bosch, X., et al. (2009). "Rhabdomyolysis and acute kidney injury." N Engl J Med 361(1): 62-72.

  2. Brown, C. V., et al. (2004). "Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference?" J Trauma 56(6): 1191-1196.

  3. Chatzizisis, Y. S., et al. (2008). "The syndrome of rhabdomyolysis: complications and treatment." Eur J Intern Med 19(8): 568-574.

  4. Chavez, L. O., et al. (2016). "Beyond muscle destruction: a systematic review of rhabdomyolysis for clinical practice." Crit Care 20(1): 135.

  5. McMahon, G. M., et al. (2013). "A risk prediction score for kidney failure or mortality in rhabdomyolysis." JAMA Intern Med 173(19): 1821-1828.

  6. Parekh, R. (2014). Chapter 127: Rhabdomyolysis. Rosen's Emergency Medicine. R. H. John Marx, Ron Walls, Saunders: 1667-1675.


Posted on February 18, 2019 and filed under Renal.

Post-Intubation Checklist

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Written by: Andra Farcas, MD (NUEM PGY-2) Edited by: Paul Trinquero, MD (NUEM PGY-4) Expert commentary by: Andrew Pirotte, MD

Developing a Post-Intubation Checklist

Multiple studies have shown checklists in medicine can be beneficial. They have been used to reduce rates of catheter-related blood stream infections and ventilator associated pneumonias and to improve team performance in various settings.  

In the ED setting, a peri-intubation checklist for trauma patients resulted in more use of rapid sequence intubation and a trend towards improvement in post-intubation sedation rates.[1] This checklist included meds for pre-intubation (pre-treatment, induction, paralytics) and information about which intubation device was used but had only one line for post-intubation medications and did not include other post-intubation safety measures.  

One of the few studies that we could find specifically focused on a post-intubation checklist was a MICU study by McConnell, et al. They looked at the proportion of patients who had an ABG drawn within 60 minutes of mechanical ventilation initiation, as well as rates of respiratory acidosis and acidemia. They found that after initiating a post-intubation checklist and timeout, the rates of ABGs increased, which led to earlier recognition of inappropriate ventilation settings.  

There are a lot of pre-intubation checklists available for public use. For example, a great podcast/blogpost by Scott Weingart on the topic was developed into a checklist by Jeffrey Siegler and Christ Huntley. Their versions can be found at

Our goal was to design a checklist specifically for the post-intubation setting that could potentially be implemented in our emergency department. We took ideas from aforementioned studies and existing checklists, as well as personal experience. In addition to covering a broad array of post-intubation tasks, we wanted to focus especially on post-intubation sedation and initial vent settings. In regards to these important tasks, what we do in the ED matters. Not only are the first few hours a critical period in the course of illness, but there is significant downstream momentum associated with choices made in the Emergency Department.  

The SPICE trial showed a link between deep early sedation and prolonged ventilation and increased mortality.[6] Conversely, an analgesia only, no-sedation approach has been shown to reduce time on the ventilator.[7] Consequently, we advocate for an analgesia-first approach. Fentanyl is a commonly used opioid for this purpose because of its rapid onset and short half-life. An easy starting point is a 0.5 - 1mcg/kg fentanyl push, followed by a drip starting at 25mcg/hr and uptitrated by 25mcg every 15-30 minutes (concurrent with another bolus as needed to control pain).

If pain is under control and additional sedation is needed, there are many options. Propofol is commonly used and is easily titratable. Start with a bolus of 5 mcg/kg/min (for 5 min) and start the drip at 5 to 10 mcg/kg/min, increasing by 5-10mcg/kg/min intervals every 5 min as needed (usual range 5-50mcg/kg/min). In the case of hypotension precluding the use of propofol, consider ketamine. Try to avoid benzodiazepines as these have been shown to increase risk of delirium.

Similarly, the initial vent settings that we chose in the ED matter and they can affect duration of ventilation, ICU length of stay, hospital length of stay, and other patient-oriented outcomes.[2] Not all illnesses requiring intubation and mechanical ventilation are the same and consequently vent-settings are not a one size fits all selection. Try to tailor settings to the individual patient and illness and choose one of the following broad strategies[9]:

  1. Lung Protective Strategy (ARDS, lung injury, default for most patients): goal is to minimize additional injury via volutrauma or barotrauma. Set the tidal volume at 6-8cc per kg (of ideal body weight). Soon after intubation, drop Fio2 to 30% and PEEP to 5cm then titrate according to ARDSNet strategy for goal oxygen saturation 88-95%.

  2. Obstructive Strategy (asthma or COPD): goal is to minimize air trapping by maximizing expiration time. Hence, set a low rate (perhaps 10) which will minimize I:E ratio (perhaps 1:4). Tidal volume can be standard 8cc/kg. This strategy may require permissive hypercapnea.

  3. Severe acidosis (DKA, severe sepsis, etc.): Goal is to mimic the pre-intubation minute ventilation. Set the respiratory rate to match pre-intubation rate (usually at least 25-30).

Below is our designed post-intubation checklist:


Expert Commentary

This column highlights the need for optimized post-intubation management.  This process requires attention to detail and patient needs.  Effective management not only involves delivery of adequate analgesia and sedation, but also efficient titration of the ventilator.  Each of these aspects of post-intubation management can be multi-faceted and challenging.  To assist with these processes and to simplify tasks, a checklist can be of great value.

Checklists can help create a stepwise clinical approach and trigger timely delivery of individual tasks.  Checklists can also help prevent omission of vital steps.  A task as simple as a chest X-ray to confirm endotracheal tube placement and positioning can be overlooked in an emergent situation.  The checklist provided in the review provides a simple, direct pathway to assist with post-intubation management, and avoid task omission.  In addition, this checklist can help emphasize strategies in the post-intubation period.  For example, the use of an “analgesic first” pathway for patient comfort following intubation.

As stated in the blog post, evidence now suggests “analgesic first” pathways improve patient outcomes.  The clinician should strive to enhance analgesia prior to escalating sedation.  Sedation has its role in post-intubation management, but should be employed only if escalated analgesic efforts fail.  “Analgesic first” pathways decrease ICU length of stay, decrease complications, and improve outcomes.  In addition to managing patient comfort, the clinician must also focus on optimizing ventilation and oxygenation.

Successful ventilator management requires attention to detail and the clinical scenario.  Every patient has different ventilation and oxygenation needs.  In addition to frequently reevaluating the patient clinically, a common and effective strategy for optimizing a ventilated patient is use of frequent blood gas measurement.  Titration of ventilation and oxygenation can be aided greatly with serial blood gas monitoring.  The use of blood gas data can also guide the provider utilizing a specific ventilation strategy (eg Lung-protective strategy).  Common problems in early post-intubation management include excessive oxygen delivery and hypoventilation.  Both of these can be identified by blood gas sampling.  Once optimal ventilation and oxygenation is achieved, the clinician can proceed with further diagnostic and stabilization pathways.

 Within the airway community, much focus is placed on optimized laryngoscopy and endotracheal tube delivery, no desaturation during intubation, interesting new equipment, etc.  However, managing an airway does not conclude with delivery of the endotracheal tube.  All clinicians managing airways would benefit greatly from accompanying this enthusiasm for intubation with focused and detailed care (often supplemented by checklists) in the post-intubation period. 

Special thanks to Dr. Jordan Kaylor and Dr. Matthew Pirotte


Andrew Pirotte, MD

Department of Emergency Medicine, University of Kansas Hospital

Clinical Assistant Professor, University of Kansas Medical Center

How To Cite This Post

[Peer-Reviewed, Web Publication] Farcas A, Trinquero P (2019, February 11). Post-Intubation Checklist [NUEM Blog. Expert Commentary by Pirotte A]. Retrieved from

Other Posts You Might Enjoy


  1. Conroy, M.J., Weingart, G.S., Carlson, J.N. Impact of checklists on peri-intubation care in ED trauma patients. American Journal of Emergency Medicine, 2014; 32:541-544.

  2. Fuller, B.M., Ferguson, I.T., Mohr, N.M., Drewery, A.M., Palmer, C., Wessman, B.T. et al. Lung-Protective Ventilation Initiated in the Emergency Department (LOV-ED): A Quasi-Experimental, Before-After Trial. Annals of Emergency Medicine, 2017; 70(3):406-418.  

  3. Guthrie, K., Rippey, J. Emergency Department Post-Intubation Checklist. Agency for Clinical Innovation, 2013. Accessed May 26, 2018.

  4. McConnell, R.A., Kerlin, M.P., Schweickert, W.D., Ahmad, F., Patel, M.S., Fuchs, B.D. Using a Post-Intubation Checklist and Time Out to Expedite Mechanical Ventilation Monitoring: Observational study of a Quality Improvement Intervention. Respiratory Care, 2016; 61(7):902-912.

  5. Nickson, C. Post-intubation care. Life In The Fast Lane, Jan 5 2013. Accessed May 26, 2018.

  6. Shehabi, Y., Bellomo, R., Reade, M., Bailey, M., Bass, F., Howe, B. et al. Early Intensive Care Sedation Predicts Long-Term Mortality in Ventilated Critically Ill Patients. American Journal of Respiratory and Critical Care Medicine, 2012; 186(8):724-731.

  7. Strøm, T., Martinussen, T., Toft, P. A protocol of no sedation for critically ill patients receiving mechanical ventilation: a randomised trial. The Lancet, 2010; 375:475-480

  8. Weingart, S. Podcast 84 – The Post-Intubation Package. EMCrit RACC, Oct 16 2012. Accessed May 26, 2018.

  9. Weingart, S. Managing Initial Mechanical Ventilation in the Emergency Department. Annals Of Emergency Medicine, 2016; 68(5):614-61

Posted on February 11, 2019 and filed under Pulmonary.

Intubation Positioning: Beyond Sniffing

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Written by: Katie Colton, MD (NUEM PGY-4) Edited by: Charles Caffrey, MD (NUEM Alum ‘18) Expert commentary by: Andrew Pirotte, MD

The patient

On a recent Thursday night in a single-attending ED, we received a call that a patient was several minutes out with respiratory distress.  He had been enjoying his routine post-dinner cocaine insufflation and became dyspneic, per bystanders. We could hear yelling in the back of the ambulance and EMS reported that they were only able to get an oxygen saturation, which was about 70%. 


The scene

Two minutes later, EMS rushed in with a patient who looked to be in his mid-50s who was clearly struggling to breathe; it required 6 people to transfer him to our cart.  He was altered, hypoxic, approximately 500 pounds, and needing an airway in the near future.  While there are many considerations for the difficult airway, what are particular positioning options that may increase the chances of success in this patient?

“Positioning is 90% of the battle”

Beyond the technical difficulties posed by the morbidly obese patient, there are physiologic differences that complicate their oxygenation and ventilation.  Due to the weight of the chest and larger abdomen they will have a decreased functional residual capacity and total lung capacity.  Supine position can complicate pre-oxygenation, endotracheal intubation (ETI), and cause hypotension in these patients.  

Many providers are still trained almost entirely in ETI with a supine patient, but there is growing evidence that a head-up position can improve pre-oxygenation and facilitate ETI.

Some authors advocate for an aggressive ramped position, using either a pre-formed foam ramp or a stack of pillows or blankets, like in the pictures below.  I would argue that unless you have a stack of pillows at the ready and a number of spare hands this technique may be difficult in the less-controlled setting.

(Simoni 2005)

(Simoni 2005)


So then what?

Newer studies – and anecdotal experience - are showing good results with upright intubation through simple manipulation of the head of the bed.  One example of this is the back-up head-elevated position as seen below[2]. First, by brief placement of the patient into Trendelenburg, the patient is brought all the way to the top of the bed (1 in image), and then the back of the bed is ramped up to at least 30 degrees above the horizontal (2 in image), with the head placed into the “sniffing” position with a towel roll (3 in image).[2] In their retrospective analysis, Khandelwal et al. found a lower rate of intubation-related complications as compared to a supine cohort, 9.3% vs 22.6%.[2]

(Khandewal 2016)  How to place the patient in the advised back-up, head-elevated position.

(Khandewal 2016)

How to place the patient in the advised back-up, head-elevated position.

A team from IU showed improved intubation success with head of bed elevation in both a simulated [4] and ED setting [3].  This approach allows the patient to be positioned during preoxygenation.  Redundant tissue falls away from the face and chest, improving the patients ability to breathe for themselves and the ease of BVM, if needed.  Khandelwal et al found lower risk of aspiration and esophageal tube placement. For every 5 degree increase in head of bed angulation above the horizontal, Turner et al found increased likelihood of first pass success with ETI.

(Turner 2017)

(Turner 2017)

In short, consider using the bed to your advantage in these difficult patients.  It takes time to overcome habits but there is good evidence for changing up your positioning plan.


Case Conclusion

The patient’s head of the bed was ramped up to 45 degrees. Utilizing rapid sequence intubation, the resident took one look with a size 4 Macintosh acquiring a Grade II view, and was able to place an 8-0 tube. A follow-up chest x-ray showed appropriate placement and frank pulmonary edema.  The patient was treated for pulmonary edema and admitted to the ICU.

Expert Commentary

As with all clinical excellence, the devil is in the details.  Skillful airway management requires attention to detail, notably patient positioning.  This case and review serve as a reminder that close attention to setup and positioning can help enhance successful airway management.

Positioning is critical to airway success.  Particularly in the setting of higher body-mass index patients, optimized positioning is a critical step to safe and successful airway management.  As suggested by the review, simply placing the patient in supine positioning is not optimal and should be avoided if possible.  Improved positioning can be achieved in several ways, but often the most straight-forward is by raising the head of the bed, or stacking towels and pillows.  This position is often referred to as the “sniffing” position. 

The sniffing position refers to bringing the sternal notch and the ear into the same plain (see blog post image).  This positioning not only improves ergonomics for the clinician, but provides enhanced laryngoscopy and endotracheal tube delivery success.  In addition, sniffing positioning compliments and enhances other airway optimization strategies. 

One significant benefit of the sniffing position is preventing collapse of soft tissue and occlusion of the airway.  The relief of redundant tissue with the sniffing position likely improves high-quality mask ventilation, as the tissue collapse into the posterior oropharynx is less prominent.  Physiological benefits of sniffing position also include decreased lung atelectasis and improved delivery of oxygen during airway preparation. Considering these points, utilization of the sniffing position (rather than supine positioning), vitally strengthens the airway management pathway.

Positioning remains crucial to optimized airway delivery. The sniffing position does not require expensive equipment or great skill; it is a straight-forward, useful, and impactful strategy to enhance airway management.  As emergency airway management continues to evolve, much focus has been on enhancing laryngoscopy.  In addition, there have been great strides in technology and monitoring equipment.  But even with the best equipment and technology, simple strategies such as optimizing positioning can lead to high-yield results. 

Special thanks to Dr. Jordan Kaylor and Dr. Matthew Pirotte


Andrew Pirotte, MD

Department of Emergency Medicine, University of Kansas Hospital

Clinical Assistant Professor, University of Kansas Medical Center

How to Cite This Post

[Peer-Reviewed, Web Publication] Colton K, Caffrey C (2019, February 4). Intubation Positioning: Beyond Sniffing [NUEM Blog. Expert Commentary by Pirotte A]. Retrieved from

Other Posts You May Enjoy


  1. RF Simoni et al. Tracheal Intubation of Morbidly Obese Patients: A Useful Device. Brazilian Journal of Anesthesiology, 2005; 55: 2: 256-260

  2. N Khandelwal et al. Head-Elevated Patient Positioning Decreases Complications of Emergent Tracheal Intubation in the Ward and Intensive Care Unit. Anesth Analg. 2016 Apr;122(4):1101-7.

  3. Turner JS et al.  Feasibility of upright patient positioning and intubation success rates at two academic emergency departments. Am J Emerg Med. 2017 Feb 5. pii: S0735-6757(17)30100-6.

  4. Turner JS et al. Cross-over study of novice intubators performing endotracheal intubation in an upright versus supine position. Intern Emerg Med. 2016 Jun 14.





Posted on February 4, 2019 and filed under Airway.

Flexor Tenosynovitis

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Written by: Kevin Dyer, MD (NUEM PGY-3) Edited by: Adnan Hussain (NUEM Alum ‘17) Expert commentary by: Aviram Giladi, MD

Case Presentation

A 29 year old right-handed male with no significant past medical history presents to the ED with left hand pain for the past 4 days. He reports that the pain started in the MCP joint of his left 2nd digit and was just “achy” at first, a mild 3/10. He noted associated swelling and erythema over the joint as well. Symptoms slowly became worse and he went to an urgent care facility yesterday where he was diagnosed with gout and sent home with NSAIDs and Norco. Overnight the pain became markedly worse, 8/10, and he began having subjective fevers. He denied any trauma to the area, no history of gout, no immune compromising diseases or medications, and no IV drug use.  In the ED his vitals were stable and he was afebrile. He appeared uncomfortable. His left 2nd digit had fusiform swelling, pain with passive extension, tenderness to percussion along the flexor sheath, and was held in slight flexion at rest. The MCP was noted to be erythematous with the erythema extending to the palmar surface of the hand.


This patient’s exam was concerning for flexor tenosynovitis (FTS), an infection of the flexor tendon and its synovial sheath that can result in deformity, tendon necrosis and adhesions leading to loss of function, or loss of limb, especially if treatment is delayed [1]. The flexor tendon sheath consists of visceral and parietal layers and functions to provide a gliding surface and nutrition to the extrinsic tendons of the digits. Once bacteria are inoculated into the space between the two layers, the synovial fluid becomes a medium for bacterial growth and the closed nature of the sheath limits the host’s immune response to fight infection [2].

Most patients with FTS will endorse a traumatic injury occurring 2-5 days prior to ED presentation [2]. Pang et al noted that 57 of their 75 patients (76%) with flexor tenosynovitis were caused by a traumatic event [4]. Of these, 81% were caused by a puncture wound. Often times, the inciting injury may have been trivial and patients may not endorse an event. Therefore, it is incredibly important to still consider the diagnosis of FTS even if a traumatic component is missing from the patient’s history.

Patients should be asked about associated symptoms such as fever, chills, anorexia, and malaise. Additionally, questions assessing the patient’s handedness, immune status, proximal extent of the pain, and other sites of pain should also be asked.



The most likely causative bacteria for FTS are skin flora. A review of four studies published within the past 10 years showed that out of 201 cases, 92 (46%) were caused by Staphylococcus with 20 (10%) being methicillin-resistant Staphylococcus aureus(MRSA). Streptococcus species were the cause of 30 cases (15%), gram negative bacteria were the cause of 28 cases (14%), and 18 (9%) were olymicrobial. Interestingly, 49 (24%) cases of confirmed FTS were culture negative, which has been attributed to early use of intravenous antibiotics or an aggressive immune response [4].

Screen Shot 2019-01-12 at 6.14.05 PM.png


The clinical diagnosis of FTS is based on the work of Dr. Allen B. Kanavel who described the four cardinal signs as:

  1. Fusiform swelling.

  2. Pain with passive extension of the digit.

  3. Tenderness over the flexor sheath.

  4. The digit held in slight flexion at rest.

No published study has validated the sensitivity and specificity of Kanavel’s signs, nor has there been a study validating inter-observer reliability. However, several studies have looked at the presence of the individual signs in patients diagnosed with the condition. Studies published by Pang et al and Nikkah et al had a combined 91 patients [3,6]. The most common sign was fusiform swelling and was present in 89 of 91 patients (98%). The second most common was pain on passive extension (73%), followed by tenderness over the flexor sheath (67%), and finger held in slight flexion (67%). Dailiana et al reported that only 54% of their 41 patients exhibited all four of Kanavel’s signs [5]. However, all of their patients displayed tenderness over the flexor sheath, which has been described by several authors as the most important sign when distinguishing FTS from other infections of the hand [4,5,8,9].

Image from EM in 5, used with permission from Anna Pickens, MD (10).

Image from EM in 5, used with permission from Anna Pickens, MD (10).

Work up for patients with suspected FTS should include plain films to rule out a retained foreign body and fractures [2]. Laboratory studies should include white blood count (WBC), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR). Bishop et al studied 71 patients with clinically diagnosed FTS, 69 of which were confirmed by operative findings or positive intraoperative cultures [7]. All 69 patients had elevation of at least one of the three inflammatory markers, a positive predictive value of 100%. They reported negative predictive values for WBC, ESR and CRP as 4%, 3%, and 13%, respectively. The two patients without FTS were diagnosed with calcific tendinitis, both patients had normal inflammatory markers. These results suggest that a positive inflammatory marker when FTS is suspected makes the likelihood of infection extremely high. However, normal inflammatory markers cannot reliably rule out an infection.



The two cornerstones for treating FTS are prompt administration of IV antibiotics and emergent hand surgery consultation. Antibiotic treatment should be guided by local antibiotic susceptibilities as well as the mechanism of infection. As discussed above, Staphylococcus, including MRSA, and Streptococcus species account for 61% of FTS cases whereas an additional 23% of cases are caused by gram negatives or are polymicrobial.  Therefore, broad spectrum antibiotics are required. A common approach is to use vancomycin with piperacillin/tazobactam [2]. Consultation with an infectious disease specialist or a clinical pharmacist should be considered for patients with antibiotic allergies, immunocompromise, or chronic infections.


Learning Points

  • FTS can cause a loss of hand function or a loss of limb if treatment is delayed.

  • Patients may not endorse a traumatic event and the diagnosis must still be considered despite this.

  • The clinical diagnosis of FTS is made using Kanavel’s Signs:

    • Fusiform swelling.

    • Pain with passive extension of the digit.

    • Tenderness over the flexor sheath.

    • The digit held in slight flexion at rest.

  • Staphylococcus and Streptococcus species account for 61% of infections.

  • The two cornerstones of treatment are:

    • Broad antibiotics – Vancomycin and Zosyn is sufficient

    • Emergent Hand Surgery Consultation

Expert Commentary

Thank you for putting together this nice case report.  Hand infections are common, and the challenge for the emergency provider is in deciding which patients are appropriate for a surgical consult (and for the surgery team, deciding which patients need surgery).  In the era of strong IV antibiotics, the timing and indications for intervention are shifting.  With early intervention using strict extremity elevation (hanging from the ceiling if possible) and IV antibiotics, we are avoiding surgery for some patients.  This includes some with early FTS, before all of the Kanaval ’cardinal signs’ are evident.  IV antibiotics have made it so that some patients with FTS, a condition traditionally considered to require surgery, are able to avoid surgery altogether.  Maintaining a high index of suspicion for these problems is important in seizing these opportunities. 

When specifically thinking about FTS, the notable challenge is that most patients (around 50% or more, as highlighted in the Dailiana article review) will present with only one or two ‘cardinal’ findings.  Identifying any potential inciting event – whether small puncture, cut, or even working in the garden – helps to increase your index of suspicion.  As the case highlights, many patients have a red joint, hand pain, or other presenting complaints that muddy the picture.  The obvious FTS patients are relatively easy to identify, but the other 50% or more can be very challenging to diagnose.

Many infection, gout, arthritis flare, “hand that’s swollen and red”, etc. patients have such pain that a good exam is difficult.  But, deciding on one of the four types of hand infection surgical emergencies – abscess, septic arthritis, purulent FTS, or necrotizing fasciitis – is critical.  If the patient will not tolerate passive extension of the finger, my preferred way to evaluate for FTS without being unnecessary cruel is by manually compressing the tendons in the distal 1/3 of the volar forearm.  You can try this on yourself – let your arm relax and then squeeze your forearm at the junction between the middle and distal 1/3 (where flexor tendons start to become distinct from muscles) and you can make your fingers flex; relax on the forearm and they will return to resting posture.  If that maneuver creates focal pain in the swollen finger, my concern for FTS goes up. 

Overall, high index of suspicion is critical.  Rule FTS out, not in – convince yourself the patient doesn’t have a potential surgical problem by doing whatever evaluation and early treatment you think is appropriate and following the course, rather than delaying intervention until the presentation is more obvious.  And, whenever in doubt, keep the patient NPO and consult a specialist so that a treatment plan can be put together without unnecessary delay or risk.   


Aviram Giladi, MD, MS

The Curtis National Hand Center, MedStar Union Memorial Hospital

How to Cite this Post

[Peer-Reviewed, Web Publication] Dyer K, Hussain A (2019, January 28). Flexor Tenosynovitis [NUEM Blog. Expert Commentary by Giladi A]. Retrieved from

Other Posts You May Enjoy


  1. Kennedy CD, Huang JI, Hanel DP. In brief: Kanavel’s signs and pyogenic flexor tenosynovitis.ClinOrthopRelat Res 2016;474:280–4.

  2. Hyatt MT, Bagg MR. Flexor Tenosynovitis.OrthopClin N Am 2017;48:217-27

  3. Pang HN, Teoh LC, Yam AK, et al. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am 2007; 89:1742.

  4. Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the hand. J Am AcadOrthopSurg 2012;20:373–82.

  5. Dailiana ZH, Rigopoulos N, Varitimidis S, et al. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand SurgEurVol 2008;33:280–5.

  6. Nikkhah D, Rodrigues J, Osman K, Dejager L. Pyogenic flexor tenosynovitis: one year’s experience at a UK hand unit and a review of the current literature. Hand Surg 2012; 17:199.

  7. Bishop GB, Born T, Kakar S, et al. The diagnostic accuracy of inflammatory blood markers for purulent flexor tenosynovitis. J Hand Surg Am 2013;38:2208–11.

  8. Boles SD, Schmidt CC. Pyogenic flexor tenosynovitis.Hand Clin 1998;14:567–78.

  9. Pollen AG. Acute infection of the tendon sheaths. Hand 1974;6:21–5.

  10. Pickens, Anna. "Flexor Tenosynovitis." EM in 5. N.p., 20 Apr. 2014. Web. 10 May 2017.


Posted on January 28, 2019 and filed under Orthopedics.

Unstable Cervical Spine Fractures

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Written by: Sarah Sanders, MD (NUEM PGY-4) Edited by: Alison Marshall, MD (NUEM Alum ‘17) Expert commentary by: Steve Hodges, MD

Fractures of the cervical spine are injuries that must be approached with caution. Some are stable, some are unstable, and mismanagement can lead to life-altering sequelae. Remembering which fractures fit into which category is imperative for optimum emergency department care.

A quick review of cervical spine anatomy is a helpful starting point:

All the cervical spine anatomy images are credited to Netter, FH Atlas of Human Anatomy, Sixth Edition.


All the cervical spine anatomy diagrams are credited to Agur, AMR & Dalley, AF of Grant’s Atlas of Anatomy: Twelfth Edition.

The common mnemonic “Jefferson Bit Off A Hangman’s Thumb,” is used to remember the unstable fractures, which will be reviewed in this post.

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Screen Shot 2019-01-05 at 11.10.04 PM.png
Screen Shot 2019-01-05 at 11.10.49 PM.png

Ultimately, understanding the mechanism of injury is crucial in identifying and accurately managing these injuries. The below PV cards are organized by mechanism and tailored down to be an on-shift reference.

In conclusion, cervical spine injuries required a high index of suspicion and caution by the emergency medicine physician as their variability and potential for neurological impairment is high. Hopefully this review can provide you with additional insight and ease of memory when the next Level 1 trauma rolls through the door.  

Expert Commentary

Thanks for this insightful post.  You've done a really nice job in laying out the most salient points.  It is important to have an understanding of the anatomy and this is a great review.  Knowing the factors that put people a high risk for injury is also paramount.   Certain chronic disease states and anatomic variances, as you note, do put select patient populations at risk for specific injury.  The mechanism of injury is something we always talk about, but when it comes to neck trauma we need to really pay attention to all available history including paramedic reports, or even cell phone video, to get the best possible picture or the mechanism of injury.   I can not stress enough the importance of a detailed neurological exam including sensation(s) and reflexes.  Any asymmetric finding should raise your level of suspicion for severe injury.   Moving to advanced imaging is especially important if there is a complaint of a focal neurological deficit; be that transient, subjective or blatantly obvious. 

Athletes or motorcyclist who have suspected cervical spine injury, who have protective shoulder pads and/or helmets pose a unique challenge.  Eventually the protective devices are going to need to be removed.   There are many opinions on how best to do this and whether an x-ray should be done before attempting the removal of protective gear.   From personal experience; it can be difficult to remove protective gear;  I recommend getting "all hands on deck" and using an methodical slow organized approach.  More recent thought is that cervical spine imaging should incorporate procedures for removal of equipment before initial radiographic evaluation.[1]  Once the gear is removed a c-collar should then be applied and you can proceed with imaging.

Recommendations for imaging the cervical spine for trauma has changed quit a lot over the last several years.  The National Emergency X-Radiography Utilization Study (NEXUS) and the Canadian C-Spine Rule (CCR) have been validated and have allowed our practice to advance such that we can effectively practice clinical medicine.  However, a word of caution on using these criteria with patients who could be impaired.  Sometimes the mild dementia, delirium or subtle drug, alcohol intoxication can lead us astray when we rely solely on these criteria.   The cross table lateral films and specifically flexion/extension views have fallen out of favor.  Most patients without focal neurological complaint or deficit are imaged with plain CT.  If your patient has a focal neurological complaint or deficit, a suspected ligamentous or disc injury an MRI should be done.  Depending on the exam and risk factors I would consider either a CTA or and MRA to evaluate for vascular injury.  

You asked about c-collars specifically.  What is available to you will be somewhat hospital - vendor specific.  I prefer the Aspen or the Miami collar, they are very similar in function overall and superior to the pre-hospital EMS ones.  When a patient has to be transported to another facility; make sure that the patient has full immobilization with back board and head-side blocks with the collar and head secured to the side blocks.    An immobilized patient that requires intubation can make an easy air way difficult and a difficult airway terrifying.  Make sure you have all your equipment prepared, including a surgical method, before you intubate.  The person holding c spine immobilization needs to knows their role.....don't let go and don't move.  This is the time when a video assisted intubation should be used.  Use either the intubating bronchoscope or a video laryngoscope.   This article talks a bit about managing airway in cervical spine injury and is a nice reference.[2]

Closing thoughts: maintain a high level of suspicion for injury in the setting of a focal neurological deficit, immobilize early immobilize often and don't be shy about intubating before transferring. 

  1.  Annals of Emergency Medicine; Baldwin et. al., "Football protective gear and cervical spine imaging" July 2001 Volume 38, Issue 1, Pages 26–30

  2. 10.4103/2229-5151.128013    International Journal of Critical Illness and Injury Science; Austin et. al., "Airway management in cervical spine injury" Jan-Mar; 4(1): 50–56


Steven W. Hodges, MD, FACEP

Assistant Medical Director

Northwestern Lake Forest Hospital

How To Cite This Post

[Peer-Reviewed, Web Publication] Sanders S, Marshall A (2019, January 21). Unstable Cervical Spine Fractures [NUEM Blog. Expert Commentary by Hodges S]. Retrieved from

Other Posts You May Enjoy


  1. Adams, J. Lin, M. Mahadevan, SV. “Spine Trauma and Spinal Cord Injury.” Section VIII, Chapter 75. Emergency Medicine: Clinical Essentials. Second Edition. P652 - 657.  

  2. Agur, AMR; Dalley AF. Grant’s Atlas of Anatomy. Twelfth Edition. Chapter 4: Back. 2009.

  3. Bergenheim, AT, Forssell, A. “Vertical Odontoid Fracture. Case Report.” Journal of Neurosurgery. Vol 74 (4) p665-667. 1991.

  4. Netter, F. Atlas of Human Anatomy. Section Head & Neck. Sixth Edition. 2014.

  5. Wheeless, CR. “Cervical Spine.” Wheeless Textbook of Orthopedics by Duke University. April 26 2016. 2 Jan 2017. 

Posted on January 21, 2019 and filed under Trauma.

PJP Pneumonia

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Written by: Julian Richardson, MD, MBA (NUEM PGY-2) Edited by: Sarah Sanders, MD (PGY-4) Expert commentary by: Michael Angarone, DO

Pneumocystis pneumonia (PCP) is one of the most common AIDS-defining opportunistic infections. It is a fungal disease that affects patients with an impaired immunity. Though it is most commonly associated with HIV and AIDS, the advent of HAART has been associated with a decreasing prevalence of PCP within the HIV population.[6] While the prevalence has been decreasing in the HIV population, it has been increasing in patients receiving immunosuppressive therapy.[2]

PCP in the non-HIV patient is becoming an important diagnosis but is less recognized in its early stages. PCP is now mostly diagnosed in the non-HIV population and is associated with higher mortality rates. When comparing PCP in the non-HIV versus HIV population at a single center, over nine years the ratio of non-HIV to HIV PCP patients increased from 1.7 to 5.6 and mortality at day fourteen was 25.9% v 1.4%, respectively.[1] Part of the explanation for the high mortality is that the non-HIV population frequently presents with less symptoms and diagnosis via microscopic examination, which is quicker, more often produces a false-negative compared to real-time polymerase-chain reaction (PCR). By lack of early recognition of PCP in the non-HIV patient and delay in diagnosis, there is a lag in treatment initiation which contributes to the higher mortality rate of the non-HIV patients with PCP.[4]

The clinical features and diagnostic work-up are non-specific and it takes a high-index of clinical suspicion to ensure these patients are treated appropriately. The symptoms of PCP are generally fever, non-productive cough, and progressive dyspnea. With regards to imaging, chest x-ray can be normal in ten percent of these patients or non-specific or inconclusive in thirty percent of these cases. The classic finding on chest x-ray is bilateral reticular infiltrates. Definitive diagnosis is identification of the Pneumocystis organism, which can be done by induced sputum, BAL or lung biopsy. Tests that can identify the organism include PJ DFA or PJ PCR. Induced sputum is just as good as BAL for those with AIDS, which may not be true for other populations. Both the induced sputum culture and BAL are time-consuming and thus PCR is becoming essential to assist with rapid diagnosis.[3,5]



Bactrim is the mainstay of treatment for both non-HIV and HIV PCP. In the non-HIV population, Bactrim has been shown to be highly effective and reduces PCP-related mortality by 83%.[7] The prophylactic dose is 80-160mg daily  while the treatment dose is 15-20mg/kg/day (both dosed based on the trimethoprim component) divided every six to eight hours for twenty-one days. Adverse reactions are commonly seen in HIV patients and can range from rash, fever, leukopenia, thrombocytopenia, azotemia, hepatitis, and hyperkalemia. Given the efficacy of bactrim compared to alternative regimens, it is suggested that supportive care be initiated prior to initiating alternative regimens which are listed below.[5]


Alternative regimens (for treatment) all twenty-one days [5]

  • Pentamidine (4mg/kg IV daily)

  • Primaquine (30mg PO daily) + Clindamycin (900mg IV every six hours or 600mg PO every eight hours)

  • Atovaquone: 750mg PO twice a day

When should steroids be utilized?

Steroids should be given for moderate to severe disease. Moderate to severe disease is defined as PO2 <70mmHg or A-a gradient >35mmHg on room air. The steroids are dosed on a twenty-one day prednisone taper, starting at 40mg PO twice a day. PO regimens taper from 40 mg BID for 5 days to 40 mg daily for 5 days to 20 mg daily for 11 days.  If the patient is unable to tolerate PO, IV methyprednisolone can be given at seventy-five percent of the prednisone dose. When considering steroids, early initiation is important and an ABG should be obtained in the emergency department.[5]


Managing Treatment Failure

Clinical failure is defined as lack of improvement or worsening respiratory function after four to eight days of PCP treatment. In patients with mild to moderate disease, this occurs in about ten percent of cases. It should be noted that in the absence of corticosteroids administration, clinical deterioration is not uncommon. ED providers must also consider co-infection with additional microbes, while the inpatient team may discuss bronchoscopy. Depending on disease severity, options for alternative therapies include atovaquone, clinidamycin, and primaquine, however these decisions should be held in conjunction with the patient’s primary physician and/or infectious disease doctor.[5]

Expert Commentary: 

Pneumocystis jerovecii pneumonia (PJP) is a life threatening and severe infection that traditionally affected individuals with AIDS. As described in the blog piece the epidemiology of affected patient populations has changed over the past 20 years with effective HIV therapy. It is currently more common to see PJP in persons that have had an organ transplant, stem cell transplant, those on glucocorticoid therapy and those receiving therapies that deplete their T-lymphocytes. A major risk factor for the development of PJP is the use of glucocorticoid medications. On average the median dose of steroids associated with the development of PJP is 30mg/day.[1] At Northwestern Medicine we recently published on our experience with PJP in the Solid Organ Transplant recipient population. We found 15 cases of PJP over a 15 year period. Among these 15 patients, six required intensive care unit management and three (20%) died from there infection. Low absolute lymphocyte count, especially <500 cells/mm3, had the strongest association with development of PJP.[2] This data demonstrates that the key immune cells that help defend against the development of PJP are the lymphocyte and in particular the CD4+ T-lymphocyte. The presentation of PJP in non-HIV infected individuals is similar to that in HIV-infected with fever, dry cough and progressive dyspnea, but many non-HIV infected individuals may present with fulminant respiratory failure.  Fortunately trimethoprim-sulfamethoxazole remains the treatment of choice for this infection, with adjunctive steroids used for those with severe respiratory compromise.  For the emergency room provider PJP should be on the list of potential causes of pneumonia or respiratory compromise not just in HIV-infected persons, but in those with compromised immune systems. Like all infections early recognition and early treatment result in better patient outcomes.

  1. Yale SH, Limper AH. Pneumocystis carinii pneumonia in patients without acquired immunodeficiency syndrome: associated illness and prior corticosteroid therapy. Mayo Clin Proc. 1996;71(1):5.

  2. Werbel WA, Ison MG, Angarone MP, Yang A, Stosor V. Lymphopenia is associated with late onset Pneumocystis jirovecii pneumonia in solid organ transplantation. Transpl Infect Dis. 2018 Mar 7:e12876


Michael Angarone, DO

Assistant Professor of Medicine, Infectious Diseases

Northwestern Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication]  Richardson J, Sanders S (2019, January 14). PJP Pneumonia [NUEM Blog. Expert Commentary by Angarone M]. Retrieved from

Other Posts You May Enjoy


  1. Bienvenu, Anne-Lise, et al. “Pneumocystis Pneumonia Suspected Cases in 604 Non-HIV and HIV Patients.” International Journal of Infectious Diseases, vol. 46, 2016, pp. 11–17., doi:10.1016/j.ijid.2016.03.018.

  2. “DPDx - Pneumocystis.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 30 Dec. 2017,

  3. “Fungal Diseases.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 26 Apr. 2017,

  4. Liu, Yao, et al. “Risk Factors for Mortality from Pneumocystis Carinii Pneumonia (PCP) in Non-HIV Patients: a Meta-Analysis.” Oncotarget, Vol. 8, No. 35, Apr. 2017, doi:10.18632/oncotarget.19927.

  5. “PCP Adult and Adolescent Opportunistic Infection.” National Institutes of Health, U.S. Department of Health and Human Services, 25 July 2017,

  6. Rosen, Peter, et al. “HIV Infection and AIDS.” Rosen's Emergency Medicine: Concepts and Clinical Practice, Elsevier, 2018.

  7. Stern, Anat, et al. “Prophylaxis for Pneumocystis Pneumonia (PCP) in Non-HIV Immunocompromised Patients.” Cochrane Database of Systematic Reviews, Jan. 2014, doi:10.1002/14651858.cd005590.pub3.

Posted on January 14, 2019 and filed under Pulmonary.


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Written by: Andew Cunningham, MD (NUEM PGY-4) Edited by: Bill Burns, MD (NUEM Alum ‘17) Expert commentary by: Zaffer Qasim, MBBS, FRCEM, FRCPC(EM), EDIC

REBOA: Ready for Prime Time?

 For years, the resuscitative thoracotomy has been the sole weapon in the physician’s arsenal against a loss of a perfusing pressure in the crashing trauma patient. With the advent of new endovascular technologies, novel methods to control hemorrhage are being refined, among them Resuscitative Endovascular Balloon Occlusion of the Aorta or REBOA. With this newer method getting a lot of attention in the emergency and trauma communities, it’s time to take a look at what it is, how successful it is, and where we are going with it.


What Is It?

  • Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a possible alternative to resuscitative thoracotomy in cases of non-compressible torso hemorrhage (NCTH) that present to the Emergency Department in extremis.1

  • REBOA works via the insertion of a catheter through the femoral artery to allow an endovascular balloon to be deployed within the aorta, allowing for bleeding control and augmentation of afterload in hemorrhagic shock.2

  • REBOA can be deployed in Zone III of the Aorta, as depicted in the image below, for pelvic hemorrhage, or in Zone I of the Aorta for abdominal hemorrhage.3

Borrowed from Reference 3

Borrowed from Reference 3

  • The primary indications for REBOA include:

    • PEA arrest secondary to abdominal or pelvic hemorrhage within 10 minutes of the onset of arrest

    • Severe hypovolemic shock secondary to abdominal or pelvic hemorrhage

    • Unstable hemodynamics refractory to volume resuscitation in patients with abdominal or pelvic hemorrhage2

  • The major contraindications include age older than 70, significant comorbidities, prolonged PEA arrest (lasting longer than 10 minutes),  or high suspicion for proximal aortic injury (REBOA may exacerbate bleeding from thoracic sources).2

Does It Work?

  •  A study at U of Arizona showed that 45% of patients who received thoracotomy may have benefited from REBOA based on autopsy results, but only 32% of the patients receiving a thoracotomy did not have a contraindication for it, and of those who did not have a contraindication, only roughly half would have potentially benefited. Compared to prior literature, this may suggest that REBOA is not as useful in patients in extremis.1

  • Although the literature does suggest that REBOA reduces the amount of overall hemorrhage, there is still no definitive evidence in humans of a decrease in mortality.4

  • There are still risks of complications in humans, including arterial injury and limb ischemia.3 In animal models, REBOA has also resulted in renal failure, liver failure, intestinal ischemia, and multiple other injuries which result from occlusion of the aorta.5

  • Given that REBOA still obstructs distal flow, just like cross-clamping the aorta in a resuscitative thoracotomy, it is still reserved as a last resort maneuver. The effects of aortic occlusion can be reviewed below6:

Borrowed from Reference 6

Borrowed from Reference 6

Where Is It Going?                      

  •  An alternative to REBOA may be Selective Aortic Arch Perfusion (SAAP); in this similar yet separate endovascular approach, a catheter that has two ports is utilized instead of the single-port REBOA catheter. This allows for both occlusion of the aorta and selective administration of blood, pressors, or other medications directly to the heart and brain. Where REBOA may be useful for exclusively shock, SAAP may have advantages in cardiac arrest secondary to trauma.7

  • A new, smaller REBOA catheter, the 7 French ER-REBOA, may cause fewer injuries and also allows for simultaneous blood pressure monitoring.8

  • Partial REBOA, or P-REBOA, allows for controlled blood flow to the body distal to the area of occlusion, in efforts to limit ischemia.5 

Is It Feasible for ER Docs to Perform?

  •  Yes! Some of the larger studies performed in Japan required placement by either a surgical or emergency medicine-trained attending.9

  • In England, there are case of REBOA being deployed in the pre-hospital setting to act as a bridging method for resuscitation during transport.7 As the relay between the hospital and Emergency Medical Services, it is an EM physician’s responsibility to be aware of this method and its utility in her area.

Take-Home Points

  • REBOA is a newer up-and-coming method of controlling hemorrhage secondary to abdominopelvic trauma that may act as an alternative to resuscitative thoracotomy.

  • Although more data still needs to be collected, REBOA has not yet shown to clearly improve mortality, and does come with certain risks and complications.

  • There are more novel methods of REBOA undergoing research and development, including SAAP, ER-REBOA, and P-REBOA, which may strengthen the utility of REBOA and reduce some of the complication risks.

  • REBOA is within an EM physician’s scope of practice, and may play a role in EMS in the future. As such, it is our duty to be aware of it and follow along with its developments.

Expert Commentary

Thanks for a great post on an evolving temporary hemorrhage control concept.  Hemorrhage, and torso hemorrhage in particular, remains the largest cause of death in trauma in the first 24 hours.  In the right patient, REBOA can be another effective procedure in the emergency physician’s toolbox.  Some additional points to consider:

1.     Access is key!  The rate limiting step is early common femoral artery (CFA) access.  It’s important to emphasize accessing the common as placing the sheath in one of the smaller branch vessels could increase the risk of iatrogenic injury.  I advocate using ultrasound to define the anatomy and routinely placing a CFA arterial line in your “big sick” patients to maintain skills.  As you state, this step is well within the wheelhouse of the Emergency Physician, and the foundation to build on to train in placing REBOA

2.     Patient selection is critical! The available data generally has the inclusion/exclusion criteria listed, but definitions on who is “unstable” vary. In my opinion, an arbitrary blood pressure cutoff of <90mmHg in someone with torso hemorrhage should not automatically trigger REBOA. I think these patients should get a CFA line, and then proceed to REBOA only if not responding to initial resuscitative measures or rapidly deteriorating to imminent arrest.

3.     Placement before arrest will likely lead to better outcomes.  The evolving data shows that the group that benefits most in terms of mortality are the nonresponders who will imminently arrest unless they have a lifesaving procedure.  In the arrested patient, as mentioned, determining the time of arrest is crucial. This can certainly be challenging with prehospital arrest.

4.     While the data does not show improved mortality compared to thoracotomy, there does seem to be a trend to improved neurologically intact survival – this is our ultimate goal and speaks to the ability to use REBOA proactively, before traumatic arrest happens

5.     It is absolutely critical that REBOA is used in a system that can rapidly deliver these patients to definitive care (OR/IR). The consequences of prolonged balloon occlusion as listed are dire.  Based on collective clinical experience and translational animal data, I would not recommend occluding beyond 45 minutes to 1 hour in Zone 1.

6.     REBOA in the US is currently used only at level 1 and 2 trauma centers. I think (as the British have shown), the biggest benefit is likely at smaller centers and ultimately prehospital.  Success here will be based on procedural considerations (like p-REBOA to prolong safe inflation times), appropriate training, and systems issues (expedited transfer to definitive care). 



Assistant Professor of Clinical Emergency Medicine

UPenn Medicine

How to Cite This Post

[Peer-Reviewed, Web Publication]  Cunningham A, Burns W (2019, January 7). REBOA [NUEM Blog. Expert Commentary by Qasim Z]. Retrieved from

Other Posts You May Enjoy


  1. Joseph B, Ibraheem K, Haider AA, et al. Identifying potential utility of resuscitative endovascular balloon occlusion of the aorta: An autopsy study. J Trauma Acute Care Surg. 2016;81:S128-S132.

  2. Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA). Vol 2016. LIFTL.

  3. Napolitano LM. Resuscitative Endovascular Balloon Occlusion of the Aorta: Indications, Outcomes, and Training. Crit Care Clin. 2017;33:55-70.

  4. Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemorrhagic shock. J Trauma Acute Care Surg. 2016;80:324-334.

  5. Perkins ZB, Lendrum RA, Brohi K. Resuscitative endovascular balloon occlusion of the aorta: promise, practice, and progress? Curr Opin Crit Care. 2016;22:563-571.

  6. Russo RM, Neff LP, Johnson MA, Williams TK. Emerging Endovascular Therapies for Non-Compressible Torso Hemorrhage. Shock. 2016;46:12-19.

  7. Bebarta V. REBOA - Ready for Prime Time? ACEP EM Education.

  8. Weingart S. Podcast 170 - the ER REBOA Catheter with Joe DuBose. Vol 2016. EMCrit Blog.:Available at [].

  9. Saito N, Matsumoto H, Yagi T, et al. Evaluation of the safety and feasibility of resuscitative endovascular balloon occlusion of the aorta. J Trauma Acute Care Surg. 2015;78:897-903; discussion 904.


Posted on January 7, 2019 and filed under Trauma.

Herpes Zoster

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Written by: Kevin Dyer, MD (NUEM PGY-3) Edited by: Simiao Li-Sauerwine, MD (NUEM Alum ‘18) Expert commentary by: David Zull, MD

The Patient

A 76-year-old man with a history of metastatic colon cancer (on Bevacizumab), HTN, and DM2 presents with a skin rash on his back wrapping around to his groin. He went on to say that 4 days ago he began having a dull, aching pain in this region and about 18 hours ago this rash appeared. He denied having a rash in any other location, and also denied oral sores, vision changes, confusion, neck pain, fevers, cough, or shortness of breath. His last infusion of bevacizumab was 9 days prior to ED presentation and he did not receive the shingles vaccine.

Upon examination he had a unilateral erythematous vesicular rash in the distribution of his T12 and L1 dermatomes that was classic for Herpes Zoster (HZ) along with erythema at the base that was concerning for an underlying cellulitis. His labs were remarkable for a white count of 2,200 and an absolute neutrophil count of 1,200.

Given his immunocompromised status, he was given Acyclovir 750mg (10mg/kg) IV and Ancef 2g IV in the ED and admitted for continued IV anti-viral therapy.



To me, this case was much more interesting than the average case of HZ given the patient’s immunocompromised status and it served as an important reminder that there are several pitfalls and complications surrounding HZ that the ED physician must be aware of and constantly on the lookout for.


Post-Herpetic Neuralgia (PHN)

PHN is defined as pain that persists more than 30 days after the onset of rash. Both the incidence (8-70%) and duration are directly correlated with the patient’s age.[1-3] Symptoms of PHN include pain, numbness, dysesthesias, and allodynia. While PHN is not applicable to the patient with an acute attack of HZ, it is included here because it is the most common complication of HZ and should be included in the counseling given to patients who are discharged from the ED.


Herpes Zoster Ophthalmicus

Herpes Zoster Ophthalmicus (HZO) is an ocular and peri-ocular disease that is the result of virus reactivation in the trigeminal ganglion.

Patients with HZO may present with a vesicular eruption along the trigeminal dermatome, conjunctivitis, episcleritis, and lid droop. Clinicians should also pay particular attention the nose and be on the lookout for vesicular lesions at the base, side, or tip of the nose. Commonly known as Hutchison’s sign, lesions on the nose indicate involvement of the nasociliary branch and are strong predictors of ocular involvement, which occurs in 50-72% of HZO cases.[4,5]

Corneal involvement can lead to significant vision loss and should be evaluated for via fluoroscein staining in all patients with suspected HZO. Keratitis may present as punctate or dendriform lesions that are easily mistaken for Herpes Simplex Keratitis.[5]



Herpes Zoster Oticus

Often referred to as Ramsay Hunt Syndrome (RHS), Herpes Zoster Oticus manifests as a triad of ipsilateral facial paralysis, ear pain, and vesicles in both the auditory canal and auricle. RHS is considered a polyneuropathy affecting cranial nerves V, VII, VIII, IX, and X.7 Involvement of these nerves leads to tinnitus, hearing loss, hyperacusis, dysgeusia, and vertigo. It is worth noting that when compared to those with Bell’s Palsy, patient’s with RHS were found to have more severe palsy and a less favorable recovery.[8]

Panel A displaying a crusted lesion in the ear of a patient with RHS. Panel B highlights the CN VII palsy that can be seen in RHS.[9]

Panel A displaying a crusted lesion in the ear of a patient with RHS. Panel B highlights the CN VII palsy that can be seen in RHS.[9]

Disseminated Zoster

Disseminated cutaneous HZ is a complication that is often accompanied by visceral organ involvement.[10] Though it is more common in immunocompromised hosts, it can also be seen in immunocompetent patients, as well. As the name implies, patients with disseminated zoster will have midline-crossing vesicular skin lesions in multiple dermatomes. Visceral involvement can be life threatening and may present as fulminant pneumonia, hepatitis, or encephalitis.11



Skin Infection

Patients with HZ lesions are at an increased risk for skin superinfection regardless of immune status. The most likely causative agents are Staphylococcus and Streptococcus species. When encountering a patient with HZ, the clinician should be sure to look for signs of bacterial infection and treat with antibiotics in addition to antivirals.



In immunocompetent patients, antiviral therapy should be started within 72 hours of rash occurrence or if new lesions continue to occur as this is a sign of ongoing virus replication.[13] For immunocompromised patients, antiviral therapy should be started regardless of when the lesions appeared.

The three antivirals currently recommended for use are acyclovir, valacyclovir, and famciclovir, with dosing regimens as follows:

                  Acyclovir – 800mg, 5 times per day for 7 days

                  Valacyclovir – 1000mg, 3 times per day for 7 days

                  Famciclovir – 500mg 3 times per day for 7 days


A meta-analysis of placebo-controlled trials have shown that patients who received acyclovir within 72 hours of rash onset are more likely to have resolution of neuritis and PHN.[14] A commonly used alternative option is valacyclovir which, when compared to acyclovir, has equal efficacy in the resolution of cutaneous lesions, and the added benefit of accelerated resolution of neuritis.[15] The TID dosing is also thought by many clinicians to lead to better patient compliance. The caveat to this, however, is valacyclovir is much more expensive than acyclovir and can be cost prohibitive depending on the patient’s insurance status.

Patients should be treated with intravenous acyclovir 10 mg/kg if they are immunocompromised,  have disseminated zoster, are found to have sight threatening disease on exam, or if they have symptomatic meningitis, encephalitis, or myelitis.[12]



The overwhelming majority of patients with HZ can be treated as outpatients with an oral agent as discussed above. Admission is indicated for patients who meet the criteria for IV acyclovir as outlined in the previous section.


Take Home Points

When caring for a patient with herpes zoster, be on the lookout for herpes zoster ophthalmicus, herpes zoster oticus, signs of disseminated zoster, and underlying cellulitis.

Initiate antivirals if the onset of rash is within 72 hours of presentation or if the patient is immunocompromised.

Oral antivirals are acceptable for the majority of patients with herpes zoster, but those who are immunocompromised, have disseminated zoster, sight threatening involvement, or signs of CNS involvement should be treated with IV acyclovir.

Expert Commentary

It is estimated that up to one third of the population will develop Herpes Zoster virus infection (shingles) sometime during our lifetime, such that it is a very common ED presentation.    Emergency physicians should be keenly aware of the complications of HZV and be able to recognize it early.  Antiviral treatment within the first 72 hours of the skin eruption can limit progression of lesions, halt development of new lesions, minimize infectious risk to household contacts, decrease the risk of complications of HZV infection, and in particular ameliorate the severity of post herpetic neuralgia.

Ramsay Hunt syndrome is typically limited to a triad of Bell’s palsy (7th Nerve palsy), ear pain and vesicles in the auditory canal and external ear.  The skin lesions are often subtle and frequently limited to just a few papules such that the syndrome is often missed.  Other cranial nerves (5,8,9,10) can also be involved in Ramsay Hunt syndrome, most notably 8th nerve involvement with tinnitus, hearing loss or hyperacusis, and vertigo. 

Herpes Zoster ophthalmicus is usually limited to punctate keratitis and is not vision threatening.  Dendritic lesions can occur in HZV but they are referred to as pseudodendrites because they are composed of heaped up epithelial cells with no epithelial defects. These pseudodendrites do not take up fluorescein since the epithelium remains intact but fluorescein often collects at the edges thereby outlining the dendrites.  In contrast, the dendrites of HSV are comprised of denuded epithelium which do take up fluorescein.  The HSV dendrite can lead to corneal erosion, scarring, and even perforation.  HZV can also affect the corneal stroma and not the corneal epithelium leading to white rounded opacities with no overlying fluorescein uptake.  Pink eye can result from conjunctivitis or iritis but is often overlooked.   The most feared ocular complication of V-1 Zoster is acute retinal necrosis which leads to rapidly progressive vision loss often complicated further by retinal detachment.

Disseminated herpes zoster is defined as the presence of more than 20 lesions outside the involved dermatome. This unusual presentation is more common in immunosuppressed patients.  Lesions in an ipsilateral adjacent dermatome are usually not of concern.  Disseminated zoster can resemble acute varicella or smallpox, as well as acute vesiculating drug eruptions like erythema multiforme and toxic epidermal necrolysis.   Disseminated HZV is distinguished by the onset primarily in one dermatome before dissemination of lesions.  Systemic organ involvement can occur with dissemination of HZV including pneumonia, hepatitis, aseptic meningitis, encephalitis, motor neuropathy, myelitis, GBS, and CNS vasculitis with stroke.

Post herpetic neuralgia, a common complication of HZV infection, is best prevented by prompt antiviral therapy in the acute phase.  Although steroids may have some benefit in ameliorating the severity of pain in the acute setting, they have not been shown to decrease the development of PHN.  Pain management of PHD frequently requires use of TCA’s, gabapentin or pregabalin. 

A common complication of HZV dermatomal lesions is secondary bacterial infections with staph aureus, usually with an impetiginous superficial purulent discharge with or without local cellulitis.   Staph septicemia and toxic shock syndrome is a rare complication in dermatomal zoster but is well described in primary varicella infections in neonates and immunocompromised children.

The emergency physician should have a low threshold for initiating antiviral therapy acute shingle, typically Valcyclovir 1gm TID or Acyclovir 800mg five times per day, for 7 days in immunocompetent hosts with uncomplicated disease, or 14 days in compromised hosts and those experiencing complications of HZV.


David N. Zull, MD, FACEP, FACP

Professor of Emergency Medicine & Internal Medicine

Northwestern University

How to Cite This Post

[Peer-Reviewed, Web Publication]  Dyer K, Li-Sauerwine S (2018, December 17). Herpes Zoster [NUEM Blog. Expert Commentary by Zull D]. Retrieved from

Other Posts You May Enjoy


  1. Choo PW, Galil K, Donahue JG, Walker AM, Spiegelman D, Platt R. Risk factors for postherpetic neuralgia. Archives of internal medicine 1997;157:1217-24.

  2. Gnann JW, Jr., Whitley RJ. Clinical practice. Herpes zoster. The New England journal of medicine 2002;347:340-6.

  3. Ragozzino MW, Melton LJ, 3rd, Kurland LT, Chu CP, Perry HO. Population-based study of herpes zoster and its sequelae. Medicine 1982;61:310-6.

  4. Zaal MJ, Volker-Dieben HJ, D'Amaro J. Prognostic value of Hutchinson's sign in acute herpes zoster ophthalmicus. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 2003;241:187-91.

  5. Pavan-Langston D. Herpes zoster ophthalmicus. Neurology 1995;45:S50-1.

  6. Shaikh S, Ta CN. Evaluation and management of herpes zoster ophthalmicus. American family physician 2002;66:1723-30.

  7. Adour KK. Otological complications of herpes zoster. Annals of neurology 1994;35 Suppl:S62-4.

  8. Robillard RB, Hilsinger RL, Jr., Adour KK. Ramsay Hunt facial paralysis: clinical analyses of 185 patients. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery 1986;95:292-7.

  9. Espay AJ, Bull RJ. Petrositis in Ramsay Hunt Syndrome with multiple cranial neuropathies. Arch Neurol 2005;62(11):1774-5.

  10. Locksley RM, Flournoy N, Sullivan KM, Meyers JD. Infection with varicella-zoster virus after marrow transplantation. The Journal of infectious diseases 1985;152:1172-81.

  11. Jantsch J, Schmidt B, Bardutzky J, Bogdan C, Eckardt KU, Raff U. Lethal varicella-zoster virus reactivation without skin lesions following renal transplantation. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2011;26:365-8.

  12. Dworkin RH, Johnson RW, Breuer J, et al. Recommendations for the management of herpes zoster. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2007;44 Suppl 1:S1-26.

  13. Cohen JI, Brunell PA, Straus SE, Krause PR. Recent advances in varicella-zoster virus infection. Annals of internal medicine 1999;130:922-32.

  14. Jackson JL, Gibbons R, Meyer G, Inouye L. The effect of treating herpes zoster with oral acyclovir in preventing postherpetic neuralgia. A meta-analysis. Archives of internal medicine 1997;157:909-12.

  15. Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrobial agents and chemotherapy 1995;39:1546-53.


Posted on December 17, 2018 and filed under Dermatology.

Topical Hemostatics

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Written by: Alex Ireland, MD (NUEM PGY-3) Edited by: Andrew Moore, MD (NUEM Alum ‘18) Expert commentary by: Joseph Posluszny, MD

Ireland (1).png

Expert Commentary

The above summary of the mechanism of actions, indications for and limitations of topical hemostatic agents is comprehensive and thorough.

As with most summaries of hemostatic agents, we focus on the mechanism of action or aspect of coagulation by which the agent works.  Clinically, it may be easier to take a different approach.

Sometimes, the most difficult aspect of applying a topical hemostatic agent is determining the appropriate agent given the clinical scenario- all work in some fashion, but which will work best?

To help approach this, an initial question to help frame what to do in the trauma bay or ED would be: does this wound require just a hemostatic agent as a covering/dressing to promote hemostasis or are both assisted hemostasis and pressure needed to control the bleeding?  For superficial, low volume, but persistently bleeding wounds, topical agents like Dermabond, thrombin (with gelfoam) and Surgicel are ideal.  For deep, complex wounds that require hemostatic agents and pressure, QuikClot Gauze, Ativene and Combat Guaze are more effective.

Hospitals and EMS systems purchase a variety of topical hemostatic agents.  It is imperative to become familiar with these agents and be prepared for their indications before you are presented with bleeding uncontrolled by conventional dressings or pressure.


Joseph Posluszny, MD

Assistant Professor of Surgery

Trauma and Critical Care, McGaw Medical Center of Northwestern University

How to Cite this Post

[Peer-Reviewed, Web Publication]  Ireland A, Moore A (2018, December 10). Topical Hemostatics  [NUEM Blog. Expert Commentary by Posluszny J]. Retrieved from

Posted on December 10, 2018 and filed under Trauma.

Implicit Bias

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Written by: Vidya Eswaran, MD (NUEM PGY-3) Edited by: Meghan Quigley, MD (NUEM Alum ‘17) Expert commentary by: Bernard L. Lopez, MD, MS, CPE, FACEP, FAAEM

First, do no harm, it’s an oath we take when we are given the title of physician.  On the surface it sounds easy enough - nobody practices medicine intending to harm patients. Yet as we all know, mistakes are easy to make, especially in the emergency department. We work in a fast-paced, high acuity environment with limited information and time to make decisions. We depend on pattern recognition, heuristics and, often, generalizations to aid in our decision-making. Accordingly, we open ourselves to inadvertent errors, especially if our decision aids are based on stereotyping. Implicit biases are defined as unconscious beliefs that affect our understanding, actions and decisions. These biases can be both favorable and unfavorable, and are activated involuntarily - without the individual’s knowledge.[1] Implicit biases are ubiquitous - we all have them. Our biases are learned at a young age and are based on our cultural backgrounds and upbringing.[2] Biases do not make us racist, sexist, ageist, or any other -ist, however it is imperative that we understand that these biases exist and that they can affect our patient care.


Studies show that race contributes to differences in ESI scoring for triaging patients in ED waiting rooms,[3] to analgesic administration, and even to the therapeutic options offered to patients with coronary artery disease.[4] These disparities are presumably multifactorial, but implicit biases likely have a role to play. When using the Implicit Association Test, the current gold standard in implicit bias assessment, physicians routinely express an implicit pro-white/anti-black bias.[2] Just because we have these biases, however, does not mean we have to act upon them. In one study, Johnson et al. found that emergency physicians expressed more pro-white/anti-black bias when their EDs were overcrowded and they were personally caring for over 10 patients.[5] Such stressful environments may cause us to fall back onto our implicit biases. So what can we do to prevent biases from affecting our clinical care? Here are ten easy strategies that physicians and hospitals can implement to create a safer environment for our minority patients:


1.         Take an Implicit Association Test online (and take them often!). Our biases are not immutable, and data over time is more valuable than a single result. With the results of your IAT in hand, take a minute at the end of your shift to evaluate your patient interactions. Do you think your biases affected your patient care? What could you do in the future to prevent this from happening? Simple awareness that biases exist can make a significant impact.

2.         We utilize our stereotypes when we do not know our patients. Healthcare disparities have been shown to decrease when providers take a minute to learn a personal, not necessarily medically relevant, fact about their patients.[6] Where are they from? Do they have kids? What do they do for work? When we think about patients as individuals we are much less likely to generalize or stereotype.

3.         Do you live in the same community as your patients? If not, get to know where your patients come from. Ask a community organizer to arrange for a tour of neighborhoods where your patients live or invite patients to speak at your hospital about their experiences both inside and out of the healthcare system.

4.         Recognize situations when you are susceptible to unconscious biases, and take steps to prevent those situations from arising. This may require buy-in from hospital administrators to help ease the cognitive burden or additional tasks (reading triage EKGs, accepting interhospital transfers, etc) during busy shifts. This will likely help boost physician wellness as well!

5.         In some cases it is impossible to ease cognitive load from an administrative standpoint. It’s up to us then to develop coping strategies during these times. Being well fed and hydrated are important first steps. Make sure to go to the bathroom. Take two minutes out of your shift for breathing or meditation exercises. These steps can go a long way to improve your physical and mental wellbeing and prevent mistakes.

6.         Promote racial diversity at all levels of your hospital/departmental organization. Increased exposure to people of diverse backgrounds has been shown to decrease prejudices and racial anxiety.

7.         Encourage administrators to consider surveying patients on their ED experience and how biases may have impacted their patient-physician interaction.

8.         Support projects that encourage positive images of persons of color, LGBT and women. Distribute stories and pictures widely that portray stereotype-busting images. Biases can be mitigated just by seeing these positive images on a regular basis.

9.         Encourage and participate in research regarding biases and health disparities and test interventions to combat them. Without data, we are nothing.

10.   Consider professional training sessions on implicit bias and diversity and inclusion for your physician group. Encourage discussion - you’ll learn that you are not the only one with biases and can learn how your colleagues deal with similar struggles.

Expert Commentary

This is a great post on the topic of unconscious bias and how it affects us as physicians (and as human beings).  Unconscious biases are simply part of how we are wired as human beings.  We have them and cannot help but have them. They affect almost every human interaction and are especially important in healthcare as poor interpersonal communications may lead to mistreatment and misdiagnosis. However, while we cannot help but have them, we can work with them. 

Stereotypes, while often thought of in a negative way, are simply patterns of the mind developed by our conscious and unconscious experiences and are examples of our unconscious biases.  These unconscious patterns help us to function in a speedy and efficient manner. Pattern recognition can help but can also have negative consequences.  We use and rely on our pattern recognition (stereotypes) to move quickly in times of stress (such as a busy ED).  This makes us more "efficient" in completing tasks.  However, we may erroneously complete these tasks if we have biases that take us down the wrong pathways. 

Awareness that these unconscious cognitive biases exist and can have both positive and negative consequences in our dealings with people is the key take-home from this post. Recognizing that they come into play the busier and more stressful things get might help us to slow down a little to make better decisions.   The suggestion in the ten-item list of getting to know the members of the community, encouraging positive images of those with whom you may be unfamiliar, participating in research and promoting racial diversity all help to change our unconscious biases and potentially lessen its negative effects.

If you take the IAT, recognize that it is not a measure of racism, sexism, or any other -ism - it is a measure of association only.  If you can reduce the cognitive load (much easier said than done in a busy ED), take whatever steps one can (this typically requires systems changes) to lessen the urgency to make too quick of a decision based on unconscious biases.

Working with your unconscious bias is possible.  It is necessary for providing the best care possible to our patients.


Bernard L. Lopez, MD, MS, CPE, FACEP, FAAEM

Associate Provost for Diversity and Inclusion, Thomas Jefferson University

How to Cite This Post

[Peer-Reviewed, Web Publication]  Eswaran V, Quigley M (2018, December 3). Implicit Bias [NUEM Blog. Expert Commentary by Lopez B]. Retrieved from

Other Posts You May Enjoy



  2. Chapman E, Kaatz A, and Carnes M. Physicians and Implicit Bias: How Doctors May Unwittingly Perpetuate Health Care Disparities. J Gen Intern Med. 2013 Nov, 28(11): 1504-1510.

  3. Vigil JM, Coulombe P, Alcock J, Kruger E, Stith SS, Parshall M, Chichowski SB. Patient Ethnicity Affects Triage Assessments and Patient Prioritization in U.S. Department of Veterans Affairs Emergency Departments. Medicine (Baltimore). 2016 Apr;95(14):e3191.

  4. Just Medicine

  5. Johnson T, Hickey RW, Switzer GE, Miller E, Winger DG, Nguyen M, and Hausmann LR. The Impact of Cognitive Stressors in the Emergency Department on Physician Implicit Racial Bias. Acad Emerg Med. 2016 Mar; 23(3): 297-305.

  6. Blair IV, Steiner JF, Havranek EP. Unconscious (Implicit) Bias and Health Disparities: Where do we go from here? Perm J. 2011 Spring; 15(2):71-78.

Posted on December 3, 2018 and filed under Ethics.

The UTI that isn’t: Why a common condition presents such a diagnostic challenge.

Written by:  Ashley Amick, MD (NUEM Alum ‘18)  Edited by:  Michael Macias, MD (NUEM Alum ‘17)  Expert commentary by : Alexander Lo, MD

Written by: Ashley Amick, MD (NUEM Alum ‘18) Edited by: Michael Macias, MD (NUEM Alum ‘17) Expert commentary by: Alexander Lo, MD

This is Part 2 of the blog post on the diagnosis of UTIs. Check out Part 1 here

Urinary tract infection (UTI) is the most common commonly diagnosed infection in the United States.  However, a high incidence of diagnoses does not render those diagnoses appropriate.  Increasing evidence suggests that this common condition poses a serious diagnostic challenge.  Erroneously identified UTIs frequently result in inappropriate treatment, as well as delays in management of the true underlying pathology.  In an era where ever more terrifying multi-drug resistant organisms continue to emerge, increasing emphasis is placed on evidence-based practice and antimicrobial stewardship.   In the acute care setting, where information is limited and time is scarce, guideline-based management can aid the Emergency Physician (EP) in improving both individual and community-level outcomes.

Despite increased awareness of UTI’s role in antimicrobial stewardship and cost-effective care, leading interest groups have failed to create a consensus definition of UTI.  (For an interesting experiment ask your colleagues what they consider diagnostic criteria for UTI, and prepare for wide variability).   Generally speaking, UTI is a diagnosis arrived at by two core features: 1) laboratory testing suggestive of infection, of which urine culture is considered gold standard; and 2) clinical symptomatology. 

Herein lies a major quandary for the Emergency Physician EP – culture data is not available in a timely fashion, and determining what defines a “symptom” of a UTI is, at best, elusive.  In the absence of culture data, the EP must rely upon a urinalysis (UA), with or without microscopy, as a surrogate.  Certain elements of the UA are thought to be particularly predictive of a true infection, including leukocyte esterase, nitrite, white blood cells, red blood cells, and bacteria.  However, when considered either alone or in combination, there is variable sensitivity and specificity of nearly all elements of a dipstick or UA.  Even when both leukocyte esterase and nitrite are present, the sensitivity and specificity is too poor to definitively diagnose or exclude a UTI.

Part of the poor predictive performance of UAs may be attributed to poor collection techniques and the presence of chronic bactiuria.  Obtaining a clean-catch sample in the emergency department setting can be a formidable challenge.  Studies suggest less than 10% of ED patients use proper midstream clean-catch techniques.  Concerningly, 50% of patients with a contaminated urine sample receive inappropriate intervention and antibiotics.  Proper education on sampling techniques as well as and in and out catheterization when appropriate, should be routinely employed. 

Despite adequate sample collection, UA interpretation is frequently confounded by the presence of asymptomatic bactiuria (ASB).  While definitions vary, the Infectious Disease Societies of America (IDSA) define ASB as isolation of a specified quantitative count of bacteria (105 cfu/ml from clean catch specimens) in a patient without symptoms or signs referable to urinary infection, such as frequency, urgency, dysuria, or suprapubic pain.  ASB is common in the geriatric population, and prevalence increase with age and in institutionalized patients.  ASB, like UTI, will frequently yield a UA positive for bacteria, LE, nitrate, and pyuria, therefore rending the UA of little use in differentiating between these two conditions. Given these considerations, the clinical symptoms become the most important factor in making the correct diagnosis.

When considering the diagnosis of UTI, beginning with an assessment of patient signs and symptoms seems not only rational, but intuitive. However, in the ever-increasing drive for efficiency, UAs are frequently drawn indiscriminately to expedite work-up.  In a recent study of patient treated for UTI in an ED population, 2/3 of patients diagnosed with a UTI had a UA collected as part of an order set, often before being evaluated by a clinician.  It was also found that antibiotics were administered inappropriately in 59% of those patients, due to lack of clinical signs or symptoms to substantiate a diagnosis of UTI.  Going about the diagnostic work-up in a backwards way invites not only anchoring bias when a UA is positive, but places pressure on the clinician to treat a UTI that isn’t.  Clinicians require discipline in looking beyond an abnormal UA, and work to objectively determine if the criteria for UTI are met based on symptomatology – or better yet – order UAs only when symptoms warrant further investigation.

Determining what constitutes a symptom – at least a symptom that should prompt a urinalysis – remains controversial.  According to the CDC and SHEA guidelines, symptoms consistent with a UTI include fever and lower genitourinary symptoms such as dysuria, urgency, frequency, suprapubic pain, and costovertebral angle discomfort.  Noteworthy is the omission of falls, altered mentation, and general malaise in the elderly in the absence of an indwelling catheter.  (See the related post: ‘delirium as a symptom of UTI, physiology or pseudoaxiom?’ for further discussion)

According to the most contemporary guidelines, these nonspecific symptoms without localizing symptoms or fever, are no longer sufficient to support the diagnosis of UTI.  This represents a shift in not only traditional clinical teaching, but a departure from prior guidelines.  This change results from a realization that both asymptomatic bactiuria and altered mentation are prevalent in the geriatric population, and there is a paucity of evidence supporting a causal link between these findings.  Despite these new recommendations, altered mentation, confusion, weakness, and falls are among the most frequent reasons for obtaining a UA in the geriatric population.  In a population where ASB is prevalent, and procuring a clean urine sample is challenging, geriatric patients are at high risk of morbidity from inappropriate antibiotic therapy and unnecessary testing.  Perhaps more concerning is that with a presumptive diagnosis of UTI, little thought may be devoted to other potential diagnoses – at least until the patient fails to improve.

Expert Commentary 

Over 50 million U.S. adults > 65 years of age (“older adults”), account for over 20 million Emergency Departments (ED) visits each year [1].  Many of these patients have unmet and complex underlying medical needs that are often understated by their chief complaints. The tempting application of traditional ‘one complaint; one algorithm’ approach taught to many emergency physicians, may often result in long-term, downstream, adverse outcomes.  One of those relevant to the accompanying blog, is the traditional “if grandma is delirious, look for and treat the UTI” doctrine.  A review of the literature proves that the evidence linking UTI’s to delirium in older adults is lacking [2]. Many older adults are bacteriuric; most do NOT have to be treated [3].  The delirium is not a reason to treat bacteriuria [4].  It is also just as likely that it is the other comorbid conditions causing the delirium, since 75% of older adults have two or more comorbid chronic conditions [5]. many of which have the potential to cause delirium at any time[6].   The patient may likely require admission for the delirium, but a more comprehensive investigation into its etiology is more helpful than treating the easy target of a contaminated urine sample

Alex_Lo (1).png

Alexander S Lo, MD, PhD

Assistant Professor of Emergency Medicine, Northwestern University 

How to Cite this Post

[Peer-Reviewed, Web Publication]  Amick A, Macias M (2018, November 26). The UTI that isn’t: Why a common condition presents such a diagnostic challenge [NUEM Blog. Expert Commentary by Lo A]. Retrieved from

Other Posts You May Enjoy


  1. Little, P., et al. "Dipsticks and diagnostic algorithms in urinary tract infection: development and validation, randomised trial, economic analysis, observational cohort and qualitative study." Health Technol Assess 13.19 (2009): 1-73.

  2. Van Nostrand, Joy D., Alan D. Junkins, and Roberta K. Bartholdi. "Poor predictive ability of urinalysis and microscopic examination to detect urinary tract infection." American journal of clinical pathology 113.5 (2000): 709-713.

  3. Schulz, Lucas, et al. "Top Ten Myths Regarding the Diagnosis and Treatment of Urinary Tract Infections." The Journal of emergency medicine (2016).

  4. Bent, Stephen, and Sanjay Saint. "The optimal use of diagnostic testing in women with acute uncomplicated cystitis." The American journal of medicine 113.1 (2002): 20-28.

  5. Klausing, Benjamin T., et al. "The influence of contaminated urine cultures in inpatient and emergency department settings." American Journal of Infection Control (2016).

  6. Gupta, Kalpana, et al. "International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: a 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases." Clinical infectious diseases 52.5 (2011): e103-e120.

  7. Nicolle, Lindsay E., et al. "Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults." Clinical Infectious Diseases (2005): 643-654.

  8. Detweiler, Keri, Daniel Mayers, and Sophie G. Fletcher. "Bacteruria and Urinary Tract Infections in the Elderly." Urologic Clinics of North America 42.4 (2015): 561-568.

  9. Kiyatkin, Dmitry, Edward Bessman, and Robin McKenzie. "Impact of antibiotic choices made in the emergency department on appropriateness of antibiotic treatment of urinary tract infections in hospitalized patients." Journal of hospital medicine (2015).

  10. Horan, Teresa C., Mary Andrus, and Margaret A. Dudeck. "CDC/NHSN surveillance definition of health care–associated infection and criteria for specific types of infections in the acute care setting." American journal of infection control 36.5 (2008): 309-332.

Posted on November 26, 2018 and filed under Infectious Disease.

Serotonin Syndrome

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Written by: Jason Chodakowski, MD (NUEM PGY-3) Edited by: Evan Davis, MD (NUEM Alum ‘18) Expert commentary by: Benjamin Schnapp, MD (NUEM Alum ‘16)


Serotonin syndrome is a condition characterized by increased serotonergic activity in the central nervous system. This can result from therapeutic use, inadvertent interactions, or intentional self-poisoning of any combination of drugs that have the net effect of increasing serotonergic neurotransmission. Serotonin syndrome most often causes mental status changes, autonomic and neuromuscular hyperactivity while severe cases may result in DIC, rhabdomyolysis, metabolic acidosis, renal failure, ARDS, and death.

Selective serotonin reuptake inhibitors (SSRIs) are the most commonly implicated group of medications, with other culprits including serotonin-norepinephrine reuptake inhibitors (SNRIs), monoamine oxidase inhibitors (MAOIs), and recreational drugs like cocaine, ecstacy, and amphetamines. The syndrome classically occurs after the initiation of a single drug, after increasing the dose of an existing medication, or simultaneous administration of two serotonergic agents. Serotonin syndrome involving a monoamine oxidase inhibitor may be especially severe and more likely to result in death. It’s important to keep in mind that antidepressants aren’t the only serotonergic agents, and that many commonly administered medications such as tramadol, meperidine, fentanyl, dextromethorphan, and linezolid among others have serotonergic activity.


Clinical Features

The majority of cases present within 24 hours, and most within 6 hours of a change or initiation of drug. The syndrome is characterized by the triad of mental status changes, autonomic hyperactivity, and neuromuscular abnormalities. The diagnosis, however, can be quite challenging as these three non-specific domains of symptomatology can present with very wide spectrum of severity.

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There is no confirmatory test for serotonin syndrome, the diagnosis is entirely clinical. The best validated diagnostic criteria for serotonin syndrome is the Hunter Toxicity Criteria. To fulfill the Hunter Criteria, a patient must have taken a serotonergic agent and meet one of the following conditions:

  • Spontaneous clonus

  • Inducible clonus plus agitation or diaphoresis

  • Ocular clonus plus agitation or diaphoresis

  • Tremor plus hyperreflexia

  • Hypertonia plus temperature above 38ºC plus ocular clonus or inducible clonus


Differential Diagnosis:

Multiple other entities can present with a general sympathomimetic picture and should be considered in the differential diagnosis. These include:

  • Neuroleptic malignant syndrome (NMS)

  • Anticholinergic toxicity

  • Malignant hyperthermia

  • Intoxication from other sympathomimetic agents

  • Opioid withdrawal

  • Sepsis

  • Meningitis/encephalitis

  • Heat stroke

  • Delirium tremens

  • Thyroid storm

Neuromuscular findings, particularly myoclonus is an important distinguishing feature of serotonin syndrome from the above etiologies.  

Serotonin syndrome can typically be differentiated from other similar conditions by its characteristic neuromuscular findings of hyperreflexia and clonus. For example, conditions such as NMS, malignant hyperthermia, and sympathomimetic toxicity all typically lack these features.



While serotonin syndrome is a clinical diagnosis labs and imaging can be useful for monitoring complications in severe cases and to help differentiate from other diagnoses in the differential above. The most severe complications of serotonin syndrome include DIC, rhabdomyolysis, metabolic acidosis, renal failure, and ARDS. Thus, you should consider checking the following to evaluate for these:

  • CBC

  • BMP

  • CK

  • LFTs

  • Lactic acid

  • DIC panel

  • UA

  • CXR

If the diagnosis is uncertain, you might also consider blood cultures, CT brain, lumbar puncture, urine toxicology screen and/or TSH to evaluate for other things on the differential.



The mainstay of therapy for serotonin syndrome is supportive care. The main hallmarks of management include:

  • Discontinue the offending agent.

  • IV fluids to correct hypovolemia

  • Sedation with benzodiazepines. Options include Lorazepam 2-4mg and Diazepam 5-10mg, which can be repeated every 10 minutes.

  • Aggressive control of hyperthermia with standard cooling techniques. Since hyperthermia is often due to increased muscle activity in serotonin syndrome, consider early intubation and paralysis in severe hyperthermia.

  • Management of autonomic instability. Consider esmolol and nitroprusside for hypertension and tachycardia, while avoiding long-acting agent like propranolol. MAOIs can sometimes cause hypotension, treat this with pressors such as phenylephrine, epinephrine, and norepinephrine as necessary.

If benzodiazepines and supportive care fail to improve agitation and correct vital signs, you can consider cyproheptadine, an antidote of sorts with anti-histaminergic and anti-serotonergic activity. Cyproheptadine is only dosed orally, with a recommended initial dose of 12mg, followed by 2 mg every two hours until clinical response is seen. Symptoms from serotonin syndrome typically resolve within 24 hours.

Expert Commentary

Gathering an accurate medication history is the key to making this diagnosis.  As mentioned above, this is a clinical entity that generally manifests quite quickly after medication initiation.  Checking the medication list in the computer isn’t going to help you here - ask the patient what kinds of new medication they might have been prescribed or they might be taking.  Remember - selective serotonin reuptake inhibitors (SSRIs) are not the only class of medications that can affect serotonin and it may be the interacting agent that you’re looking for.  Besides the above, other common medications that can be problematic include triptans, ondansetron, valproic acid, carbamazepine, lithium, cyclobenzaprine, and even herbal supplements like St. John’s wort (patients may not think supplements are worth mentioning!). 

One underappreciated aspect of serotonin syndrome is the extent to which it occurs on a spectrum.  Studying for the boards and looking at the Hunter Criteria can leave one with the impression that clonus is necessary to make the diagnosis of serotonin syndrome.  This is not the case, and it has been suggested that many milder cases, presenting with only symptoms such as tachycardia, diarrhea, and restlessness, may be going missed.  Again, medication history is essential here.


Benjamin Schnapp, MD

Assistant Residency Program Director, University of Wisconsin-Madison Emergency Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication]  Chodakowski J, Davis E (2018, November 19). Serotonin Syndrome  [NUEM Blog. Expert Commentary by Schnapp B]. Retrieved from

Other Posts You May Enjoy


  1. Boyer, Edward W., and Michael Shannon. "The serotonin syndrome." New England Journal of Medicine 352.11 (2005): 1112-1120.

  2. LoVecchio, Frank, and Erik Mattison.. "Atypical and Serotonergic Antidepressants." Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e Eds. Judith E. Tintinalli, et al. New York, NY: McGraw-Hill, 2016,

  3. Mason, Peter J., Victor A. Morris, and Thomas J. Balcezak. "Serotonin Syndrome Presentation of 2 Cases and Review of the Literature." Medicine 79.4 (2000): 201-209.


Posted on November 19, 2018 and filed under Toxicology.

ECMO Initiation in the ED

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Written by: Kaitlin Ray, MD (NUEM PGY-3) Edited by: Evan Davis, MD (NUEM Alum ‘18) Expert commentary by: Colin McCloskey, MD (NUEM Alum ‘16)

ECMO Initiation in the Emergency Department


Extracorporeal membrane oxygenation (ECMO) provides prolonged cardiopulmonary support in severe acute respiratory or cardiac failure. As the science behind ECMO continues to grow and with promising data regarding its use in acute hypoxemic respiratory failure, cardiac arrest, and cardiogenic shock, ECMO use in the United States has increased over 400% in the last ten years. This has stimulated an interest in earlier applications of ECMO both in the emergency department (ED) and even in the prehospital setting [1]. Initiation of ECMO in the ED is a relatively new development, with 65% of programs <5 years old and the majority of programs with <3 cases per year. However, this number continues to grow [2].

There two main types of ECMO: venoarterial (VA) and venovenous (VV). While VV ECMO provides respiratory support, only VA ECMO provides both respiratory and hemodynamic support. ECMO drains blood from the native vascular system, then circulates it outside of the body via a mechanical pump where it passes through an oxygenator and heat exchanger. Hemoglobin then becomes saturated with oxygen, CO2 is removed, and blood then reinfuses into the circulation [4]. Venoarterial ECMO is more commonly utilized in the emergency department as eligible ED patients often have concurrent hemodynamic and respiratory collapse.

Emergency medicine physicians have an increasing responsibility to initiate ECMO and/or make the decision to transfer to an ECMO capable facility. Knowing this, it is critical that we are familiar with the types of ECMO available, understand the indications, contraindications, risks, benefits, and logistics of initiating this form of extracorporeal life support.



The specific criteria and contraindications to ECMO vary from institution to institution, often making the decision and ability to initiate ECMO challenging. The Extracorporeal Life Support Organization (ELSO) provides specific guidelines for ECMO initiation. These indications include cardiogenic shock as defined as (1) hypotension and low cardiac output with inadequate tissue perfusion despite adequate intravascular volume and (2) persistent shock despite volume, inotropes, pressors, and possibly an intraaortic balloon pump. The ELSO also provides guidelines for ECMO in acute respiratory collapse, as well as contraindications for ECMO including: unrecoverable heart failure and not a candidate for transplant or LVAD, advanced age, chronic multi-system failure, compliance issues, terminal malignancy and prolonged CPR without adequate tissue perfusion. 

As emergency physicians, which patients should we consider as candidates for ECMO? Generally speaking, consider younger and healthier patients who experience an acute but reversible insult leading to rapid cardiopulmonary collapse.  Recall that ECMO should only be considered as a bridge to more definitive therapy. Examples of scenarios that fit this criterion include:

  • Massive pulmonary embolism

  • Myocardial infarction causing V-Tach/V-Fib or cardiogenic shock

  • Acute myocarditis or cardiomyopathy causing cardiogenic shock

  • Drowning

  • Hypothermia

  • Drug overdose causing cardiovascular collapse (such as beta-blocker or Ca-channel blocker)

  • Massive smoke inhalation, pulmonary contusion, or pulmonary hemorrhage causing refractory hypoxemia

As mentioned above, generally those with more chronic conditions such as end-stage heart failure, end-stage COPD, or those with chronic multi-organ failure, do not make good ECMO candidates. Other patient populations to consider in an ICU rather than ED setting include those with septic shock and/or ARDS. Note that patients with traumatic injury leading to hemorrhagic decompensation, although acute in nature, typically are not good candidates for ECMO as ECMO does not prevent further blood loss.

Additionally, we must consider what an ECMO-eligible patient clinically looks like. The majority of the patients who present with one of the above conditions will either be responsive to conventional therapies (intubation, fluids, inotropes), or they will be dead on arrival. However it is the rare, in-between patient that should be considered for ECMO. The condition of a good candidate would include things like: 

  • Persistent hypotension despite maximum conventional therapy

  • Persistent hypoxemia despite maximum ventilator therapy

  • Patients brought in in cardiac arrest but achieve periods of unsustained ROSC

  • Patients brought in with vitals but arrest in the ED

Unfortunately patients who arrest in the field, are brought to the ED already in cardiac arrest, or who do not achieve ROSC despite 30-45 minutes of well executed ACLS are unlikely to be appropriate ECMO candidates. The critical ECMO population is truly those who are flirting with life vs. death, especially the patients with intermittent periods of ROSC. Key exceptions to this include drowning and/or hypothermic patients. Generally these patients are better candidates for ECMO even if there has not been a recorded pulse, with the caveat that they should have been pulled out of the water or other environment quickly.



ECMO is unique in that it provides full cardiopulmonary support without the physical trauma of chest compressions, thereby decreasing trauma, stress, and number of interruptions. Additionally, it provides a higher flow state than would otherwise be provided by manual compressions [2]. VV ECMO also minimizes barotrauma, volutrauma, and oxidative stress. However ECMO is not without risks and complications. The risk of bleeding is significant in the context of continuous anticoagulation and platelet dysfunction. Thromboembolism may lead to stroke or limb ischemia [4]. Infection may also occur secondary to indwelling lines/tubes [1].



ECMO is a costly intervention that requires a multi-disciplinary approach and an organizational commitment in order to proceed. Consideration must be given to the required equipment, blood bank capabilities, cannulation, and personnel availability. In order for ECMO to be successfully initiated from the ED, coordination between EMS, emergency medicine physicians, the cath lab, nursing staff, neurocritical care, cardiothoracic surgery, and the ICU is required [3]. When cannulating for VV ECMO, one may use a two cannula approach (femoral vein and internal jugular/SVC), or a single dual-lumen cannula (right atrium/IVC via the IJ). VA ECMO typically involves cannulation through the femoral artery and femoral vein [1]. If CPR is ongoing during cannulation attempts, programs may use a modified ACLS algorithm with a continuous epinephrine infusion at 0.7 mg/kg/min and minimization of pulse checks by utilizing continuous TEE monitoring [3]. Aggressive anticoagulation is required with continuous infusion of either unfractionated heparin or direct thrombin inhibitor, and efforts should be made to maintain platelet counts >50K and hemoglobin >12 mg/dL6,7.



While initiation of ECMO from the emergency department is still a relatively new endeavor for many certified ECMO centers, the ED is in a unique position to bridge select patients in acute respiratory or cardiac failure to recovery using ECMO.  While institutional criteria for ECMO varies, the ELSO guidelines may be used as a reference to guide decision making in the absence of formal criteria. Generally speaking, pursue ECMO for younger, healthier patients with acute hemodynamic and/or respiratory collapse that is potentially reversible and unresponsive to conventional therapies. Typically patients with massive PE, MI, hypothermia, drowning, acute cardiomyopathy are the best candidates for ED ECMO. Contraindications generally include severe neurologic injury, end stage malignancy, advanced age, and irreversible multi-organ failure. Knowing that the emergency physicians are often the first to receive patients in acute cardiac and respiratory failure, it is critical that we are familiar with the types of ECMO available, understand the indications, contraindications, risks and benefits, and logistics of initiating this form of extracorporeal life support.

Expert Commentary 

This is a thoughtful and thorough overview of ECMO within the emergency department. I will limit my commentary to VA ECMO for cardiopulmonary failure (ECPR), given the enthusiasm for the topic in the FOAM world and my experience within a ED based ECMO program. Some broad themes I would like to highlight: Evidence, Patient selection and Systems of Care.

Evidence: There is a signal that ECPR is better than conventional CPR. A systematic review and metanalysis found that those with cardiac arrest who received VA ECMO had an association with increased neurologically intact survival, with a number needed to treat of 7 [1]. However, most of the data is retrospective and from single centers, making it subject to a number of confounders, as well as selection bias. Further, those who received ECPR were more likely to receive therapeutic hypothermia and percutaneous catheterization, both interventions known to improve outcome following cardiac arrest.  Another single center experience has been promising, with 9/18 patients surviving to hospital discharge with good neurological outcome [2]. This protocol involved EMS bypassing the ED and taking the patient to the cardiac catheterization lab where they were placed on ECMO and underwent catheterization. Those who had good outcome all had concomitant intervenable coronary artery disease. There are several centers that have similar experiences with published case series [3,4], but it depends thus far on quality patient selection and a viable system of care.

Patient Selection:  All the above trials had strict inclusion and exclusion criteria. Most established protocols include an age cutoff (65-75 depending on center), initial shockable rhythm, and a time from arrest to cannulation between 30-60 minutes. Pertinent exclusions include advanced comorbidities, initial asystole or prolonged downtime. This is done with the intent of cannulating patients with the best chance of surviving their ECMO run; namely young patients with likely coronary artery disease who need ECMO as a bridge to cardiac catheterization. VA ECMO’s other successful ED applications, namely pulmonary embolism [5], drug overdose [6], and acute myocarditis [7] all share the commonality that ECMO provides time for recovery or as a bridge to a viable intervention. A bridge to recovery must exist prior to any cannulation scenario; this cannot be understated.

Systems of care: Cannulation is just one step in a VA ECMO patients hospital course. When conceptualizing a successful ED ECMO program, the institutional commitment should be visualized: A patient requiring 5-7 days in the ICU, formal neuroprognostication and continuous goals of care discussions with family. You rightly include a logistics session in your review, but this system of care is paramount to a successful ECMO program. Prehospital EMS systems must be designed for quick recognition and transport of ECMO candidates.  Emergency physicians need to be trained, and maintain competency in ECMO cannulation; interventional cardiology must be willing to catheterize appropriate patients; ICU consultants must have a standardized protocol for post-arrest care and neurology/ICU must have an institutionally accepted neuroprognostication scheme. In parallel to this, the family discussions regarding prognosis and any transition of care should include social work, case management and palliative care professionals. Cannulation is as exciting a procedure an emergency physician can perform, but without a thoughtful, multidisciplinary system of care, these patients will do poorly.

In closing, VA ECMO in the emergency department is an exciting development to tertiary ED practice. More experience, and more data, will help define the niche of patients and the necessities of post-arrest care that provide these patients with the best outcome.

1. Ouweneel DM, Schotborgh JV, Limpens J, et al. Extracorporeal life support during cardiac arrest and cardiogenic shock: A systematic review and meta-analysis. Intensive Care Med. 2016;42(12):1922-1934.

2. Yannopoulos D, Bartos JA, Martin C, et al. Minnesota resuscitation consortium's advanced perfusion and reperfusion cardiac life support strategy for out-of-hospital refractory ventricular fibrillation. J Am Heart Assoc. 2016;5(6):10.1161/JAHA.116.003732.

3. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial). Resuscitation. 2015;86:88-94.

4. Bellezzo JM, Shinar Z, Davis DP, et al. Emergency physician-initiated extracorporeal cardiopulmonary resuscitation. Resuscitation. 2012;83(8):966-970.

5. Yusuff H, Zochios V, Vuylsteke A. Extracorporeal membrane oxygenation in acute massive pulmonary embolism: A systematic review. Perfusion. 2015;30(8):611-616.

6. Wang G, Levitan R, Wiegand T, et al. Extracorporeal membrane oxygenation (ecmo) for severe toxicological exposures: Review of the toxicology investigators consortium (toxic). Journal of Medical Toxicology. 2016;12(1):95-99.

7. Nakamura T, Ishida K, Taniguchi Y, et al. Prognosis of patients with fulminant myocarditis managed by peripheral venoarterial extracorporeal membranous oxygenation support: A retrospective single-center study. Journal of intensive care. 2015;3(1):5.


Colin McCloskey, MD
NUEM Alum ‘16, Critical Care Anesthesiology fellow - University of Michigan Medical Center/University of Michigan Health System

How To Cite This Post

[Peer-Reviewed, Web Publication]  Ray K, Davis E (2018, November 12). ECMO Initiation in the ED  [NUEM Blog. Expert Commentary by McCloskey C]. Retrieved from

Other Posts You May Enjoy


  1. Mosier, Jarrod M., et al. “Extracorporeal Membrane Oxygenation (ECMO) for Critically Ill Adults in the Emergency Department: History, Current Applications, and Future Directions.” Critical Care, BioMed Central, 17 Dec. 2015,

  2. Tonna, Joseph E., et al. “Practice Characteristics of Emergency Department Extracorporeal Cardiopulmonary Resuscitation (ECPR) Programs in the United States: The Current State of the Art of Emergency Department Extracorporeal Membrane Oxygenation (ED ECMO).” Resuscitation, Elsevier Ireland Ltd, 10 Sept. 2016,

  3. Tonna, Joseph E., et al. “Development and Implementation of a Comprehensive, Multidisciplinary Emergency Department Extracorporeal Membrane Oxygenation Program.” Annals of Emergency Medicine, Mosby Inc., 1 July 2017,

  4. Bartlett, Robert. Extracorporeal Membrane Oxygenation (ECMO) in Adults, 16 June 2017,

  5. Extracorporeal Life Support Organization - ECMO and ECLS. “Guidelines for Adult Respiratory and Cardiac Failure.” Extracorporeal Life Support Organization - ECMO and ECLS > Resources > Guidelines, ELSO (Extracorporeal Life Support Organization), Dec. 2013,

  6. Sklar MC, Sy E, Lequier L, et al. Anticoagulation Practices during Venovenous Extracorporeal Membrane Oxygenation for Respiratory Failure. A Systematic Review. Ann Am Thorac Soc 2016; 13:2242.

  7. Spinelli E, Bartlett RH. Anemia and Transfusion in Critical Care: Physiology and Management. J Intensive Care Med 2016; 31:295.


Posted on November 12, 2018 and filed under Cardiovascular.

Management of Myasthenia Crisis in the ED

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Written by: 
Kumar Ghandi, MD (NUEM PGY-3) Edited by: Arthur Moore, MD (NUEM Alum ‘18) Expert commentary by: Luke Rosiere, MD (NUEM Alum ‘12)

What do I need to know about myasthenia gravis?

Myasthenia gravis is the most common disorder of neuromuscular transmission. The disease can manifest as a combination of weakness in ocular, bulbar, and most importantly respiratory muscles. Myasthenia gravis is disease of the neuromuscular junction, in which autoantibodies are directed against nicotinic acetylcholine receptors (AChR) located on the postsynaptic end plate. These autoantibodies not only induce complement mediated destruction of receptors, but compete with acetylcholine for binding at the remaining receptors [1]. 


In over 50% of cases myasthenic patients present with ocular symptoms including blurred vision, ptosis, diplopia. 15% of patients present with bulbar symptoms including ptosis, dysarthria, dysphagia, and fatigue when chewing [2]. Isolated respiratory failure is a rare sign. It is important to remember that myasthenic patients will often present specific muscle complaints and not a generalized muscle fatigue [2].

What is myasthenic crisis?

Acute myasthenic Crisis is defined as acquired myasthenia gravis severe enough to require intubation and mechanical ventilation [3]. Typically, between 10-20% of myasthenia gravis patients will experience an episode of myasthenic crisis, most commonly within the first two years [4].


Myasthenic Crisis vs. Cholinergic Crisis

Though cholinergic crisis is a quite rare it is important to differentiate cholinergic crisis from myasthenic crisis in the early evaluation of these patients. Cholinergic crisis is precipitated by excess use of cholinesterase inhibitors. This can manifest as both nicotinic and muscarinic toxicity. Nicotinic symptoms include weakness and fasciculations, while muscarinic symptoms include diaphoresis, tearing, increased oral secretions, diarrhea, and bradycardia [4].


What can trigger myasthenic crisis?

Common triggers for myasthenic crisis include infection, surgical intervention (thymectomy), pregnancy, childbirth, or tapering of immunosuppressive medications [5]. Medications are another large source of triggers for myasthenic crisis [1] [3] [6]. 50% of patients who receive treatment with high dose corticosteroids develop an early exacerbation and 10% will go on to require mechanical ventilation [6].

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What are the priorities of management of myasthenic crisis in the ED?

The tried and true emergency medicine axiom of Airway, Airway, Airway is critical for the management of myasthenic patients. Recognition of impending respiratory arrest, early intubation, and placement of a definitive airway has reduced mortality from 40% in the 1960’s to less than 5% today [7]. Evaluation of respiratory function and airway management for patients in myasthenic crisis presents multiple unique challenges in the ED.


How do I best assess respiratory function in the emergency department?  

Signs and Symptoms

Patients may describe dyspnea when laying flat. This is thought to be secondary loss of diaphragmatic excursion due to increased dependence of gravity during a myasthenic crisis [4]. Patients may also demonstrate severe dysphagia, with weak cough and inability to clear secretions. Other signs respiratory weakness includes, pausing mid-sentence to take a breath, use of accessory muscles, and tachypnea with shallow breathing [3]. A simple bedside evaluation includes having a patient take a deep breath and count out loud to twenty-five. If they are unable to reach five without pausing for a breath the patient may be bordering on respiratory failure [7].

Forced Vital Capacity

  • Assesses function of both inspiratory and expiratory muscle function.

  • Assess in both supine and sitting position as respiratory function tends to decline when supine.

  • Elective intubation should be considered for FVC <15 [1]. 

Maximal Inspiratory Pressure/Negative Inspiratory Force

  • Patient maximally inhales against a closed valve and force at the mouth is recorded.

  • Inspiration is a negative generating force, thus the more negative the value the stronger the inspiratory effort.

  • NIF of 0 to -30 cm H20 indicates profound respiratory muscle weakness.

  • Elective intubation should be considered for those with a NIF in the range of 0 to -30 [3].

Use of these tools are best utilized both in combination and serially with repeat assessment every two hours to assess for progressive respiratory failure. This data allows for objective assessment of respiratory function and assessment for the necessity of a well-controlled elective intubation.

What do I need to consider before intubating?  

Neuromuscular Blockers in Myasthenia Gravis:

Due to the pathophysiology of the disease, myasthenic patients due to mechanism of disease are typically resistant to neuromuscular blockade with depolarizing neuromuscular blocking agents such as succinylcholine. Due to the decreased number of receptors myasthenic patients typically require 2.6 times the dose [8]. In addition, use of cholinesterase inhibitors typically used to treat myasthenia gravis can prolong the effect of succinylcholine.

Though succinylcholine is still considered a safe agent, higher doses and inhibition of metabolism can lead to an unpredictable and lengthy paralysis. Typically, a non-depolarizing agent such as rocuronium is the preferred paralytic drug of choice. Myasthenic patients can be sensitive to non-depolarizing agents, starting at 0.1 to 0.2 mg/kg can often provide sufficient neuromuscular blockade [8].

Ventilator Settings:

Initial setting on the ventilator include:

  • AC/VC mode

  • Tidal volumes of 8-10 cc/kg of ideal body weight

  • PEEP 8-15cm H20 to prevent atelectasis and minimize work of breathing [4].

Can I use NIPPV to prevent intubation in myasthenic crisis?

Noninvasive ventilation has previously been shown to prevent intubation in patients in myasthenic crisis. Up to 20% of patients with myasthenic crisis could potentially be managed with non-invasive ventilation. Given the propensity for difficulty swallowing, these patients must be able to protect their airway and manage their secretions in order for NPPV to be a safe alternative. Early NIV has been shown to be associated with reduction in days of ventilator support, length of stay in the ICU, and rate of reintubation [9].


Disposition and Post Emergency Department Care

It is critical to alert Neurology early in the course of a possible myasthenic crisis. Often, myasthenic patients are well known to the department of Neurology, as these patients often frequent the hospital for mild exacerbations of myasthenic symptoms. Myasthenic crisis patients often require close observation in an ICU given their high risk for respiratory failure or need for ventilator management. Treatment options once leaving the ED often include, plasma exchange (PLEX) or intravenous immunoglobulin (IVIG). The table below serves as an excellent comparison for PLEX vs IVIG, knowing the modality of choice from the Emergency Department can help determine the vascular access needed to perform each modality [4]. 

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Expert Commentary

Myasthenic crisis is such a great topic.  I can't think of another case that employs such a breadth of expertise.  

While it is most exciting to talk about how to manage a patient in crisis, it can't be understated how critical we are in preventing such a crisis.  Look closely at that list of precipitating medications.  At least half of those are on my Top 20 most common prescription list.  Myasthenia is like prolonged QT.  If you don't think twice about your therapies, you can put this patient in a heap of trouble and plant them in the ICU for 2 weeks.  So, first thing I can say is, if you ever see myasthenia gravis on a PMH, whether they're there for a UTI or a hang-nail, think twice and three times about every medication you write for (including IV contrast).

When it comes to the recognition and management of a crisis, the above description is great.  

As you would suspect by the word "crisis," this won't be subtle.   

I'll add the following bullets:

1)  Great patient to monitor with continous capnography.  It will be your quickest indicator of deteriorating ventilation.

2)  Keep myasthenia in your differential for any undifferentiated hypercarbic respiratory failure.  Before you paralyze and intubate, try and get a brief history and physical to assess for intermittent weakness, bulbar nerve palsies, etc.  Otherwise, this potential diagnosis may be missed for days until they can get this patient off the vent

3)  Non-invasive ventilation sounds great, but probably won't help that much.  These crises last for days, and you can't keep a mask on for that long.  These patients often have dysphagia, so will aspirate.  Many patients have excess secretions that are better managed through an endotracheal tube.  If they need positive pressure, you're best off securing the airway before it's full of vomit.

4)  Succinylcholine 2 mg/kg or rocuronium 0.6 mg/kg.  Anesthesia literature often recommends puny doses (if any at all) of NMBAs.  They're expecting to extubate that patient in 3 hours and fear prolonged paralysis.  We are expecting them to be on the vent for days.  You need to ensure you have adequate intubating conditions, and paralytics will help.  Don't forget to keep your patient well-sedated if you think they're still paralyzed.

5)  We're not expected to decide how to cure this crisis.  Call neurology and they'll tell you their preference.  You'll probably start steroids and they'll decide if they want IVIg or plasma exchange.  None are going to work in 5 minutes anyway, so they can deliberate a little.


Luke Rosiere, MD

Northwestern University Emergency Medicine Class of 2012; Attending Physician at Northwestern Medicine Central DuPage Hospital

How To Cite This Post

[Peer-Reviewed, Web Publication]  Ghandi K, Moore A (2018, November 5). Management of Myasthenia Crisis in the ED.  [NUEM Blog. Expert Commentary by Rosiere L]. Retrieved from

Other Posts You May Enjoy


  1. Adams, James, and Erik D. Barton. Emergency medicine: clinical essentials. Philadelphia: Elsevier Saunders, 2013. Print.

  2. Clinical Manifestations of Myasthenia Gravis . (n.d.). Retrieved April 19, 2017, from

  3. Myasthenic Crisis . (n.d.). Retrieved April 21, 2017, from

  4. Wendell LC, Levine JM. Myasthenic crisis. Neurohospitalist 2011; 1:16.

  5. Berrouschot J, Baumann I, Kalischewski P, et al. Therapy of myasthenic crisis. Crit Care Med 1997; 25:1228.

  6. EM:RAP. (2015, September). Retrieved April 20, 2017, from

  7. EM:RAP. (2006, January). Retrieved April 21, 2017, from

  8. Anesthesia for the patient with myasthenia gravis. (n.d.). Retrieved April 19, 2017, from

  9. Seneviratne J, Mandrekar J, Wijdicks EF, Rabinstein AA. Noninvasive ventilation in myasthenic crisis. Arch Neurol. 2008;65:54–58 


Posted on November 5, 2018 and filed under Neurology.

Bad Blood

Written by:  Ade Akhetuamhen ,  MD (NUEM PGY-2)  Edited by:  Spenser Lang, MD (NUEM Alum ‘18)  Expert commentary by : Matthew Levine, MD

Written by: Ade Akhetuamhen, MD (NUEM PGY-2) Edited by: Spenser Lang, MD (NUEM Alum ‘18) Expert commentary by: Matthew Levine, MD


Expert Commentary

Dr Akhetuamhen has provided a nice quick reference for topical hemostatic agents (THAs).  These agents have become more relevant in recent years, particularly in prehospital care, as the prehospital emphasis has shifted from resuscitating hemorrhage more towards hemorrhage control.  Much of our knowledge of these dressings come from battlefield studies of major hemorrhage.  Their use has been formally endorsed by the American College of Surgeons Committee on Trauma in 2014, particularly for junctional site hemorrhaging.  Dr Akhetuamhen has listed the properties of the ideal THA.  No current product fulfills all of these criteria.

Much of what we know about these agents comes from military studies.  There are limitations to these studies. There are fewer human studies, and these tend to be retrospective, observational, and based on questionnaires.  The possibility of reporting bias exists in these studies and study design made it impossible to control for the type of wound.  There are far more animal studies.  Animal studies allow for the ability to control for wound type, but are more difficult to simulate real life wounds from missiles or shrapnel.

Hemcon and Quickclot products were the earliest products studied by the military and became the early THA gold standards after they were determined to be more effective than standard gauze.  An earlier concern for Quickclot was exothermic reactions from the activated products that caused burns to patients.  As Quickclot transitioned its active ingredient from zeolite to kaolin, this concern diminished.  Quickclot is available in a roll called Combat Gauze that is favored by the military and available in our trauma bay.

Finally, there are some important practical tips for using these products.  THAs are not a substitute for proper wound packing and direct pressure.  Most topical hemostatic agent failures in studies were from user failure!  THAs must come into contact with the bleeding vessel to work.  Simply applying the THA over the bleeding areas does not mean it is contacting the bleeding vessel.  The product may need to be trimmed, packed, shaped or molded in order to achieve this.  Otherwise it is simply collecting blood.  After it is properly applied, pile gauze on top of it and give firm direct pressure for several minutes before checking for effectiveness. 

See what THA(s) you have available in your trauma bay, it is nice to know ahead of time before presented with a hemorrhaging patient what you have and in what form (a roll, sponge, wafer, etc).  Find out how the product is removed.  It may not be relevant to the patient’s ED stay but at some point the dressing needs to come off.   Some are left to fall off on their own.  The chitosan products are removed by soaking them.  When soaked, the chitosan turns slimy and can be slid off atraumatically.


Matthew Levine, MD

Assistant Professor of Emergency Medicine

Northwestern Medicine

How to Cite this Blog

[Peer-Reviewed, Web Publication]   Akhetuamhen A, Lang S (2018, October 29). Bad Blood.  [NUEM Blog. Expert Commentary by Levine M]. Retrieved from

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Posted on October 29, 2018 and filed under Hematology.

Anatomic Approach to Ocular Complaints

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Written by: Philip Jackson, MD (NUEM PGY-3) Edited by: Jesus Trevino, MD (NUEM PGY-4) Expert commentary by: Rehan Hussain, MD

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Expert Commentary

Thank you for this excellent diagram, which demonstrates a thorough and systematic approach to the most common ocular complaints one would encounter in the ED.  In assessing a painful red eye, there is so much value in determining whether the discomfort is relieved with topical anesthetics, as you can reliably confine the pathology to the cornea or conjunctiva in those cases. However, a red eye associated with deep achy pain that is not relieved with tetracaine could be caused by scleritis, which is highly associated with autoimmune disease.  If cells and flare are visible in the anterior chamber, uveitis is more likely.  Any history of a recent eye procedure should prompt you to consider endophthalmitis, which can be visually devastating, and warrants urgent ophthalmology referral. 

In diagnosing conjunctivitis, you did a great job of highlighting the importance of a good history in determining the etiology . I would add that asking about sexual history can be valuable, as gonorrhea can present with copious purulent discharge, and chlamydia can present with chronic follicular conjunctivitis. Both would warrant systemic antibiotics and treatment of partners, in addition to eyedrops. 

Acute angle closure glaucoma is a diagnosis that should be considered in almost all cases of unilateral headache. It can mimic migraine, since both may present with nausea, vomiting, and visual disturbances. Checking the eye pressure is the most important step to making the diagnosis. 

Finally, acute onset of floaters and/or flashes always warrants an ophthalmology consult to rule out retinal detachment. Ultrasound is a useful tool to differentiate retinal detachment from posterior vitreous detachment (PVD) and vitreous hemorrhage. PVD and vitreous hemorrhages tend to move freely when the eye moves, whereas retinal detachment is anchored to the nerve but still flaps with eye movement.   

Once again, this diagram serves as a very helpful flowchart to trouble-shoot eye complaints in the ED.


Rehan M. Hussain, MD
Vitreoretinal Surgery Fellow

Bascom Palmer Eye Institute

University of Miami Health System

How To Cite This Post

[Peer-Reviewed, Web Publication]   Jackson P, Trevino J (2018, October 22). Anatomic approach to ocular complaints.  [NUEM Blog. Expert Commentary by Hussain R]. Retrieved from

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