Can't Miss Hand and Wrist Fractures in the ED


Written by: Justine Ko, MD (NUEM PGY-3) Edited by: Spenser Lang MD (NUEM Alum ‘18 ) Expert commentary by: Matt Levine, MD

“Can’t Miss” Hand and Wrist Injuries in the ED

In the emergency department, orthopedic complaints make up a large percentage of presentations, up to 50% in the pediatric population and close to 33% in the adolescent and young adult population. Many of these injuries are uncomplicated, but an astute clinician can diagnose subtle and uncommon injury patterns. Three less common injuries are reviewed here. If found, these injuries can alter the management and disposition of the patient. Each of these injuries should be carefully assessed for on physical exam and imaging. 


What exactly is the distal radioulnar joint and why is it important?

The distal radioulnar joint (DRUJ) consists of both the bony radioulnar articulation as well as the soft tissue components, including ligaments. It has significant contributions to the axial load-bearing capabilities of the forearm. The injury can be an isolated injury or associated with forearm fractures and should be tested for with every forearm injury as its presence can alter the disposition and even functionality of the patient. 


When does it occur?

A DRUJ injury may occur, although rarely, in isolation. This is usually related to a fall on outstretched hand (FOOSH). A DRUJ injury is more often associated with a fracture. Common associations include: 

  • Distal radial fracture (DRF)

    • DRF + DRUJ = Galeazzi fracture (pictured to the right)

  • Ulnar styloid fracture 

How should I assess for a possible DRUJ injury?

  • Routine AP and lateral views are poor for determining a DRUJ injury. This is largely a CLINICAL DIAGNOSIS.

  • Piano Key Sign: with the patient’s hand in pronation, push on the dorsal aspect of the ulnar head. Depression and rebound of the ulnar head suggest DRUJ instability

  • Table Top Test: have patient place hands on a table and apply force. A DRUJ injury will show dorsal depression of the ulna

  • Grind Test: hyperextend the wrist and axial load the forearm. A positive sign elicits pain over the joint 

How does this alter management?

When associated with a fracture, operative management is often indicated and consultation with our orthopedist is warranted. When missed, a DRUJ injury will result in instability of the joint and arthrosis. 



It has been reported that these injuries are missed in up to 25% of ED presentations.

How do these injuries occur?

In perilunate and lunate dislocations, the mechanism is usually hyperextension in the setting of trauma. Patients presents with hand and wrist pain/swelling.

How do I distinguish perilunate from lunate dislocations?


Lunate and perilunate dislocations can be easily confused or mistaken for each other. The key to distinguishing these injuries on imaging is the alignment between the metacarpal, carpal, and the radius/ulna bones.

In a normal lateral x-ray, these bones should all align (Figure 1, far left). In a lunate dislocation, the lunate itself is physically removed or out of line with the rest of these bones (Figure 1, far right), resulting in the classic “spilled teacup” appearance on x-ray. In a perilunate dislocation, the lunate sits in line with the radius/ulna, however the capitate/metatarsal bones are dislocated dorsally. 

On an AP film, a break in Gilula’s arc/lines may be used to assess for a perilunate or lunate dislocation (Figure 2).

How Are These Injuries Treated?

In the ED, closed reduction can be attempted. If successful, definitive treatment can occur up to 7 days later. If unsuccessful, operative management is indicated. Definitive treatment involves open reduction and internal fixation. 

How Would I Reduce These Injuries in the ED?

Usually, the assistance of our orthopaedic colleagues is warranted. Finger traps can be used for traction. The wrist should be extended while placing palmar pressure on the lunate. Then, with continued traction, the wrist should be gradually flexed so that the capitate falls back into place within the concavity of the lunate. Once the lunocapitate joint is reduced, the wrist can be extended in traction again for full reduction.


What is a scapholunate dissociation?

Scapholunate dissociation is caused by injury to the scapholunate ligament. Injury to this ligament can occur with acute FOOSH injury or be caused by degenerative rupture of the ligament. 


How do I diagnosis it?

These patients present with radial wrist pain. On imaging, the following signs can aid in diagnosis. 

  • Terry Thomas sign: This is seen on an AP wrist film and is indicated by a gap >3mm between the scaphoid and lunate bones 

  • Cortical Ring sign: occurs when the scaphoid is in a flexed position, making the scaphoid tubercle more prominent. A measure distance less than 7mm between the end of the cortical ring and the proximal end of the scaphoid suggests scapholunate dissociation and instability.  

How do I manage it?

In the ED, patients should be placed in a thumb spica cast for stabilization and referred to orthopaedics for follow up. Operative indication includes injury within 3 weeks and associated imaging and physical exam findings. During this time frame, the SL ligament is still viable for repair. 

Expert Commentary

Great choice by Dr. Ko to highlight these injuries that are often subtle, yet important because of the comorbidities associated with missing the diagnosis. 

The Galeazzi fracture is a classic EM boards question, because it is important!  It was termed by Campbell as the “fracture of necessity” (modern day translation = “this needs surgery!”) in 1942 because nonoperative management was observed to be associated with recurrent ulna styloid dislocations.  Hughston confirmed this is 1957, reporting that 35/38 cases treated nonoperatively had unsatisfactory outcomes.

There’s a saying in orthopedics that “the most commonly missed injury is the second injury”.  The radial shaft fracture is usually obvious and can distract the clinician from the less dramatic DRUJ injury.  DRUJ injury is radiographically diagnosed by:

  • Fracture at the BASE of the ulna styloid process (not the tip)

  • A widened DRUJ (a comparison x ray may be necessary), or

  • >5mm of shortening of the radius relative to the distal ulna.

A subtle clinical finding often associated with the Galeazzi fracture is anterior interosseus nerve injury.  It is a branch of the median nerve and is purely motor, so there will be no sensory deficit or paresthesia!  It manifests as loss of pinch strength between the thumb and index finger.  So have the patient make the OK sign and resist as you try to open it!

Mayfield, Johnson and Kilcoyne described a pattern of carpal injury caused by wrist hyperextension, ulnar deviation and intercarpal supination in 1980. In their original research on cadavers, progressive hyperextension force was applied and resulted in a consistent, sequential, progressively more unstable intercarpal injury pattern known as the four stages of carpal instability:

  1. Scapholunate dissociation

  2. Perilunate dislocation

  3. Perilunate and triquetral dislocation

  4. Lunate dislocation

Acute scapholunate dissociation is the most common pattern of carpal instability. It occurs secondary to a tear of the scapholunate interosseus ligament.  Scapholunate dissociation can also be chronic secondary to arthritic changes when there is no history of recent trauma.

X rays in lunate and perilunate dislocations are often not as clear and obvious as the diagrams used to teach these injuries.  The key to realizing that there is a carpal bone dislocation is recognizing that the carpal arcs are disrupted on the AP view. The distal and proximal carpal rows should never overlap on this view.  If you recognize this, you will heighten your suspicion and won’t miss these injuries, even if you cannot immediately tell the exact diagnosis.  

The name perilunate dislocation has always been a pet peeve of mine. There is no perilunate bone, so this nomenclature just introduces confusion.  It should simply be called a capitate dislocation, because that it what it really is.

All of these injuries, and more, are further detailed in our Ortho Teaching Files!


Matthew R. Levine, MD

Assistant Professor

Department of Emergency Medicine

Northwestern University

How to Cite this Post

[Peer-Reviewed, Web Publication] Ko J, Lang S. (2019, Aug 19). Can't Miss Hand and Wrist Fractures in the ED. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from

Other Posts You Might Enjoy

To learn more about the diagnosis and management of orthopedic injuries from head to toe, check out our Ortho Teaching Files!


  1. Bowen WT, Slaven EM. 2014. “Evidence-based management of acute hand injuries in the emergency department.” Emergency Medicine Practice 16 (12):1-28. 

  2. “Distal Radial Ulnar Joint (DRUJ) Injuries - Trauma - Orthobullets.” n.d. Accessed March 7, 2018.

  3. Kardashian G, CHristoforou DC, Lee SK. 2011. “Perilunate dislocations.” Bulletin of the NYU Hospital for Joint Diseases 69 (1):87-96.

  4. “Lunate Dislocation (Perilunate Dissociation) - Hand - Orthobullets.” n.d. Accessed March 2, 2018.

  5. Pappou, Ioannis P., Jennifer Basel, and D. Nicole Deal. 2013. “Scapholunate Ligament Injuries: A Review of Current Concepts.” Hand (New York, N.Y.) 8 (2): 146–56.

  6. Reisler T, Therattil PJ, Lee ES. 2015 “Perilunate Dislocation.” Eplasty

  7. Rodner CM, Weiss APC. “Acute scapholunate and lunotriquetral dissociation.” American Society for Surgery of the Hand. 155-171.

  8. Scalcione LR, Gimber LH, Ho AM, Johnston SS, Sheppard JE, Taijanovic MS. 2014. “Spectrum of carpal dislocations and fracture-dislocations: imaging and management.” AJR 203: 541-550.

  9. Thomas, Binu P, and Raveendran Sreekanth. 2012. “Distal Radioulnar Joint Injuries.” Indian Journal of Orthopaedics 46 (5): 493–504.

Posted on August 19, 2019 and filed under Orthopedics.

Don't Forget aVL!

Don't forget aVL.png

Written by: Laurie Aluce, MD (NUEM PGY-3) Edited by: Kimberly Iwaki MD (NUEM Alum ‘18 ) Expert commentary by: Daniel Schimmel, MD

The Case: 

Patient: 57 year old male

Chief Complaint: Chest Pain 

PMH: Hypertension

Pain: Mid-sternal, non-radiating, 6/10, constant pressure

Onset:  45 minutes ago while watching TV

Associated symptoms: No diaphoresis, light-headedness, nausea, vomiting, or back pain 

Vitals: T 98.8, HR 70, BP 110/68, RR 14, Sat 100% on room air

Physical Exam:

General: Alert, no apparent distress, sitting comfortably in cart 

Cardiac: Regular rate and rhythm, no murmurs/rubs/gallops

Pulmonary: Clear to auscultation bilaterally, no crackles/wheezes

Extremities: Warm and well perfused, 2+ distal pulses, cap refill < 2s 

Labs: In process 

Triage EKG: 

Image from Stephen Smith, MD.

Image from Stephen Smith, MD.

What abnormalities do you see in this EKG? 

  • Prolonged PR interval

  • Slightly widened QRS

  • Hyperacute T waves in II, III, aVF

  • T wave inversion (TWI) in aVL

  • < 1mm ST depression in I, avL

What are you concerned about? What elements of this EKG raise your concern?   

  • Inferior myocardial infarction (MI) due to hyperacute T waves in II, III, aVF

  • Inferior MI or significant mid left anterior descending (LAD) lesion due to TWI in aVL [3] 

How will you differentiate an inferior MI from a chronic mid LAD lesion? 

Clinical picture and a repeat EKG. If the TWI is due to a chronic mid LAD lesion, it should not change on serial EKGs. If the TWI is due to an inferior MI, you may see it evolve to ST depression in aVL and/or ST elevation in II, III, aVF. [3]

You obtain a repeat EKG with one right-sided lead, V4R:

Image from Edward Burns, MD.

Image from Edward Burns, MD.

What abnormalities do you see in the repeat EKG?

  • Hyperacute T waves and ST elevation in II, III, aVF

  • ST depression and TWI in aVL

  • ST depression in V2

  • <1mm ST depression in I

  • <1mm ST elevation in V4R

What are you concerned about? What elements of this EKG raise your concern?

  • Concern for inferior MI

    • ST elevation in II, III, aVF

    • ST depression and T wave inversion in aVL

      • EKG sensitivity for inferior MI increases from 60% to 77% when criteria includes ≥ 1mm reciprocal ST depression in aVL in addition to ≥ 1mm ST elevation in II, III, aVF [1]

  • Concern for right ventricle (RV) involvement

    • 25% – 53% of inferior MIs have RV involvement [5]

    • ST elevation in III > II

    • Isoelectric ST segment in V1 with ST depression in V2

    • ST depression and T wave inversion in aVL

      • >1mm ST depression in aVL has sensitivity of 87% and positive predictive value of 90% for RV involvement with acute inferior MI [5]

  • Other findings suggestive of RV involvement not pictured in this EKG

    • ST elevation in V2 > 50% the magnitude of ST depression in aVF [4]

    • Right bundle branch block, 2nd and 3rd degree AV block

    • ST elevation in V1

How can your further evaluate for RV involvement?  

You ask for a right-sided EKG to check for ST elevation in V3R-V6R, but your EKG tech doesn’t remember where to place the leads. The tech looks to you for help. Where do you put the leads? 

                 Full Right-Sided EKG                                                         Standard EKG with V4R

Images from Tom Bouthillet.

Images from Tom Bouthillet.

If you don't have the time to perform a full right-sided EKG, you can perform a standard EKG but switch V4 to V4R as shown with the prior EKG. V4R is considered the best single lead for diagnosing a right ventricular MI.[2] ST elevation ≥ 1 mm in V4R has a sensitivity of 88% and a specificity of 78% for RV infarction. [6]

EKG with V4R-V6R:

Image from Ary Goldberger, MD. UpToDate: Electrocardiogram in the diagnosis of myocardial ischemia and infarction

Image from Ary Goldberger, MD. UpToDate: Electrocardiogram in the diagnosis of myocardial ischemia and infarction

What abnormality do you see in the right-sided leads?

  • ST elevation in V4R-V6R  

What is your diagnosis?

  • Inferior MI with RV infarction  

Take Home Points:

  1. Don’t forget aVL. T wave inversion and ST depression in aVL can be a marker of serious cardiac pathology:

    1. Significant mid-LAD lesion

    2. Evolving inferior MI and possible RV involvement

  2. If you are concerned for inferior ischemia, obtain a right-sided EKG to evaluate for right ventricular involvement

Expert Commentary

This is an excellent review of aVL, an important lead for diagnosis and prognosis.  Because it can be a modifier, or is used in conjunction with other criteria for diagnosis, it often gets overlooked.

In the acute setting, aVL can be used to help identify ST elevation myocardial infarction (STEMI) in various locations.  In addition to the aforementioned use in identifying RV involvement in inferior STEMI and mid LAD lesions, aVL is considered a high lateral lead which is fed by diagonal vessels.  As such, acute blockages that affect the proximal LAD with anterior STEMI in V3, V4, anteroseptal involvement in V1, V2 and may also have high lateral involvement in aVL. While I am always watching for shock and unstable arrhythmias taking patients to the cardiac catheterization lab, if I see this distribution with an anterior STEMI, I am even more concerned due to the amount of myocardium subtended by the lesion.  I often preemptively get access for cardiac mechanical support in case cardiogenic shock develops. In this way, the prognostic information from aVL may change practice in the cardiac catheterization lab.

Not to be overlooked, leads I and aVL may be the only leads with ST elevation in an isolated high lateral STEMI in a diagonal vessel.  Diagonal 1 or diagonal 2 may be large vessels and be the only vessel with acute thrombosis. aVL is the reciprocal lead to the inferior leads in inferior STEMI.  Similarly, lead III may move reciprocally, showing ST segment depression in the high lateral STEMI with elevation in aVL.

As nice as it can be to have aVL to prognosticate inferior STEMI, prognosticate anterior STEMI and identify isolated high lateral STEMI, aVL ST segments and T waves can be abnormal for non-acute reasons leading to a lack of specificity.  The most common reason for an abnormal repolarization in aVL is strain in the setting of LVH. So how do we differentiate acute reciprocal changes from strain pattern? 

A frequently overlooked bit of information on the EKG is the QRS-T angle.  Luckily this is reported for us on the EKG at the top. In the setting of T wave inversion, if the angle is greater than 100 degrees, this is more consistent with strain.  Furthermore, if the ST segment leading to the T wave is downwardly concave (think downward parabolic curve) with asymmetry of the T wave, this also is more consistent with strain.  If we look at the presented case’s EKGs, we can dissect them a bit further. In the triage EKG, there isn’t ST segment depression at all. In fact there is elevation with a T wave inversion.  This is concerning. The ST segment may be isoelectric with an inverted T wave, but there should not be ST elevation with a T wave inverted in the opposite direction. This morphology is often used in Sgarbossa criteria to identify STEMI in left bundle branch block.  So in addition to the hyperacute T waves of this triage EKG, aVL is very concerning. In the follow-up EKG, we can see dynamic changes that have occurred in the inferior leads solidifying the diagnosis. But aVL also suggests RV involvement. The ST segment is downsloping, depressed without concavity (more linearly pointing down to the right).  To clinch the diagnosis of RV involvement, we also see the right sided leads with elevation.

It is definitely possible to have a patient with LVH/strain findings and also have an acute inferior STEMI.  As demonstrated successfully in this case, the statement about serial EKGs is a critical one. Even in the setting of a normal EKG, a good story for myocardial infarction should prompt a serial EKG and often a posterior EKG to identify a supposedly electrocardiographically silent STEMI.  Remember STEMI is an EKG diagnosis that is supposed to correlate with the physiologic condition of an acute 100% occlusion of a vessel. In the early period, there can be stuttering pain with opening and closing of the vessel and the EKG may not capture it in that moment or may miss the posterior STEMI if the posterior EKG is not obtained.

To sum up the importance of aVL:

  1. Inferior STEMI: Improved diagnosis when aVL has a depressed ST segment with an inverted T wave

  2. Inferior STEMI: Considered worse prognosis when aVL has a depressed ST segment with an inverted T wave as it suggests a more proximal RCA occlusion with RV involvement.  ST elevation in V1 or right sided V4 may also be helpful in identifying proximal RCA occlusion with RV branch involvement.

  3. Anterior STEMI: aVL STEMI confers a worse prognosis, suggesting more proximal LAD involvement.

  4. Isolated high lateral STEMI: ST elevation in leads I and aVL may identify an acute 100% blockage in a diagonal vessel.  Lead III may have reciprocal ST segment depression.

To differentiate strain from ischemic changes in aVL:

  1. QRS-T angle:  If greater than 100, may be consistent with strain.

  2. ST segment slope:  If concave, consider strain.  If downsloping but the ST segment is more straight as it aims downward, consider an acute event.

  3. T Wave inversion:  If there is asymmetry to the inverted T wave, it may be more consistent with strain.

In summary, the EKG has so much data in it.  Pattern recognition can be a wonderful tool for quick diagnosis of clear problems.   But a methodical evaluation of the EKG can still be done quickly and identify what others may miss.


Dr. Daniel R. Schimmel

Assistant Professor of Medicine

Bluhm Cardiovascular Institute

Northwestern University


1. Birnbaum Y, et al. ST segment depression in aVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart J 1993;14(1):4-7.

2. Carley SD. Beyond the 12 lead: Review of the use of additional leads for the early electrocardiographic diagnosis of acute myocardial infarction. Emergency Medicine 2003;15: 143-54.

3. Hassen GW, et al. Lead aVL on electrocardiogram: emerging as important lead in early diagnosis of myocardial infarction. Am J Emerg Med 2014;32(7)785-88.

4. Somers MP, et al. Additional electrocardiographic leads in the ED chest pain patient: right ventricular and posterior leads. Am J Emerg Med 2003;21(7):563-73.

5. Turhan H, et al. Diagnostic value of aVL derivation for right ventricular involvement in patients with acute inferior myocardial infarction. Ann Noninvasive Electrocardiol 2003;8:185-88.

6. Zehender M, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993; 328:981-88.

How to Cite this Post

[Peer-Reviewed, Web Publication] Aluce L, Iwaki K. (2019, Aug 12). Don’t Forget aVL. [NUEM Blog. Expert Commentary by Schimmel D]. Retrieved from

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Posted on August 12, 2019 and filed under Cardiovascular.

Fluid Responsiveness

Fluid responsiveness.png

Written by: Brett Cohen, MD (NUEM PGY-3) Edited by: Duncan Wilson, MD (NUEM Alum ‘18) Expert commentary by: Luisa Morales-Nebreda, MD


Expert Commentary

I’ll start by saying that the assessment of a patient’s intravascular volume status and fluid responsiveness is one of the most difficult tasks in clinical medicine, yet it remains a crucial one to adequately manage acute circulatory failure.

After decades of dedicated research to the critically ill, we’ve learned that rigid protocols lead to large amounts of fluid administration, and that fluid overload is associated with increased morbidity and mortality in septic shock and ARDS patients. As you mentioned, only half of hemodynamically unstable patients are fluid responsive, prompting clinicians to describe novel tools/methods to better evaluate fluid responsiveness.

How do we define fluid responsiveness? What are the determinants of fluid responsiveness?

Fluid responsiveness has been defined as a 10-15% increase in cardiac output after a 500 cc bolus fluid challenge. I find this arbitrary definition unhelpful, but I do think that understanding what determines a fluid bolus leading to a preload-responsive state is important. 

Figure 1: Frank Starling curve

Figure 1: Frank Starling curve

When giving a fluid bolus, the expectation is that it will increase cardiac preload (by increasing both the stressed volume and mean circulatory filling pressure). Once this condition has been met, the next assumption is that the increase in venous return will lead to a change in stroke volume/cardiac output (venous return = cardiac output). This is the ideal situation! Both ventricles working on the ascending limb of the Frank-Starling curve without any major changes in other determinants of cardiac output (contractility, afterload, diastolic function) Figure 1. Unfortunately, our critically ill patients are not that simple and most times display significant changes in cardiac contractility (e.g., due to acidosis) and afterload (e.g., due to vasoactive agents) that could place them on the flat portion of this curve.

Cardiac Output = Heart Rate x Stroke Volume

Stroke Volume is determined by: contractility, preload, afterload

How do we measure fluid responsiveness?

Despite a great amount of evidence showing that “static” measurements, such as central venous pressure (CVP) are poor predictors of fluid responsiveness, they continue to be widely used. I don’t mean to say that measuring CVPs is useless. After all, perfusion is determined by the pressure gradient between MAP (mean arterial pressure) and CVP, and CVP is a good marker of preload (just NOT of preload responsiveness). 

To circumvent this limitation, we can use “dynamic” measurements of heart-lung interactions during mechanical ventilation. Specifically, if changes in intrathoracic pressure under positive pressure ventilation lead to cyclic changes in stroke volume (stroke volume variation or SVV), pulse pressure (pulse pressure variation PVV), or vena cava diameter it indicates that both ventricles are preload-dependent and the patient is fluid responsive. Limitations to these 3 methods include: a) patients need to be mechanically ventilated and without spontaneous breaths (during which changes in intrathoracic pressure become unreliable) b) tidal volume of at least 8 cc/Kg and normal respiratory system compliance (in order to generate significant swings in intrathoracic pressure, tidal volume needs to be on the high end and your lungs/chest wall can’t be stiff). 

So you can think about how limited these maneuvers are in the ICU setting. Most intubated patients take spontaneous breaths (unless paralyzed or deeply sedated). If paralyzed for ARDS, they need to be on low-tidal volume ventilation and their lungs are generally pretty stiff.

As you mentioned a maneuver that is unaffected by these limitations is the passive leg raise test (PLR). Importantly, PLR raises preload by shifting venous blood not only from your lower extremities, but mainly from your splanchnic compartment (where ~70% of unstressed volume reservoir lies). This is why in order to adequately perform the maneuver, patients are placed in a semi-recumbent position (rather than horizontal) and the bed is adjusted to 45֯, followed by assessment of cardiac output changes within 60 seconds (NOT blood pressure changes).

PLR is one of the most validated maneuvers for assessment of fluid responsiveness, and as you described, many downstream methods to measure cardiac output have been used, including: a) velocity time integral of the left ventricular outflow tract b) peak velocity of the carotid artery c) changes in end-tidal CO2. 

Given the widespread use of critical care echocardiography and their inherent practicality, I think echocardiographic indices are the most useful dynamic parameters to predict fluid responsiveness.

What to expect and my two cents on fluid responsiveness

Given the pace of technology, innovation in hemodynamic monitoring methods will likely improve in the not too distant future. Pocket echo probes and non-invasive wearable sensors measuring cardiac output will make assessment of fluid responsiveness much easier and reliable. Check out:

Michard et al. Intensive Care Medicine (2017) 43:440-442

Vincent et al. Intensive Care Medicine (2018) 44:922-924

For now, I go to the bedside and after a physical exam perform a basic point-of-care ultrasound to assess heart function, look for interstitial lung edema (B lines) and IVC collapsibility before and after a PLR maneuver (if tolerated). Combining information from these maneuvers not only allows you to better assess a patient’s current volume status and likelihood to be fluid responsive (hyperdynamic LV, absent B lines, collapsible IVC), but can also help you identify what type of shock your patient has and if giving fluid could make things worse (RV failure). 

When a patient is likely fluid responsive, I give a small/moderate fluid bolus (250-500 cc) then come back to the bedside to repeat my assessment with the tools I feel most comfortable. Then I ask myself: are things getting better? (Improved mental status/blood pressure, increased in urine output and decreased vasoactive agent requirement). And then do it all over again!


Luisa Morales-Nebreda, MD

Fellow, Pulmonary & Critical Care Medicine

Department of Medicine

Northwestern University


How to Cite this Post

[Peer-Reviewed, Web Publication] Cohen B, Wilson D. (2019, Aug 5). Fluid Responsiveness. [NUEM Blog. Expert Commentary by Morales-Nebreda L]. Retrieved from

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Posted on August 5, 2019 and filed under Pulmonary.

Spontaneous Bacterial Peritonitis


Written by: Kevin Dyer, MD (NUEM PGY-4) Edited by: Paul Trinquero, MD (NUEM Alum ‘19) Expert commentary by: Steven K. Herrine, MD


Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid without an evident intra-abdominal or surgically-treatable source [1]. The pathophysiology is poorly understood, but likely relates to bacterial translocation across an edematous bowel wall (due to portal hypertension) into the immunologically impaired ascitic fluid. SBP is common in patients with severe hepatic dysfunction (present in 20% of hospitalized patients with ascites) and carries a mortality rate of 10% [2,3]. The high incidence, grave mortality, and potential benefit of early treatment make SBP a can’t-miss diagnosis for the emergency physician.

Clinical Features

The classic triad of SBP is fever, abdominal pain, and increasing ascites [4]. However, like most other “classic triads” in medicine, patients rarely present with all three and instead are much more likely to have only 1 or 2 of these features. The most common signs and symptoms are fever (69%), abdominal pain (59%), altered mental status (54%), and abdominal tenderness (49%). Other less common signs and symptoms include diarrhea (32%), paralytic ileus (30%), hypotension (21%), and hypothermia (17%) [5]. In one study, 13% of patients with SBP were asymptomatic [6].

Importance of Paracentesis

As mentioned above, the clinical signs and symptoms of SBP are variable  and sometimes subtle, making it a difficult clinical diagnosis. Instead, diagnosis hinges on the results of an ascitic fluid sample obtained via a diagnostic paracentesis. Ascitic fluid findings indicative of SBP include an elevated absolute polymorphonuclear leukocyte (PMN) count ≥250 cells/mm3, a positive ascitic fluid bacterial culture, and exclusion of secondary causes of bacterial peritonitis (e.g. perforated viscous, intra-abdominal abscess). For the ED physician, a PMN level ≥250 cells/mm3 necessitates initiation of antibiotics as soon as possible, if they were not already started empirically [7].

Not only do patients at risk for SBP need a diagnostic paracentesis, but because treatment is time sensitive, it should be performed as quickly as is feasible. A study by Kim et al showed a 3.3 percent increase in in-hospital mortality for each hour paracentesis was delayed and revealed that delayed paracentesis for patients ultimately diagnosed with SBP led to a 2.7-fold increased risk of death [8-9].


Empiric therapy should be initiated in patients with ascites who have a temperature >100°F, abdominal pain and/or tenderness, altered mental status, or ascitic PMNs ≥250 cells/mm3. First line treatment is a third-generation cephalosporin such as Ceftriaxone 2g per day or Cefotaxime 2g q8hrs [10]. For those with a severe penicillin allergy, fluoroquinolones are a viable alternative provided the patient has not been on a prophylactic fluoroquinolone. Common choices are levofloxacin 750mg daily or ofloxacin 400mg BID [10-11].

An additional therapeutic consideration is albumin infusion. Current guidelines from the American Association for the Study of Liver Diseases (AASLD) recommend the administration of albumin at a dose of 1.5g/kg for patients with either a BUN >30mg/dL, a serum creatinine >1.30mg/dL, or a total bilirubin >4mg/dL. A meta-analysis of 4 studies demonstrated a significant reduction in renal impairment (8% vs 31%) and a decrease in mortality (16% vs 35%) in patients who received 1.5g/kg of albumin within 6 hours of diagnosis of SBP [12-13].

Take Home Points

  • Spontaneous bacterial peritonitis is an infection of ascitic fluid without an evident intra-abdominal or surgically-treatable source. 

  • Diagnosis is nearly impossible to make clinically due to variable, and sometimes subtle, presenting symptoms and therefore hinges on obtaining a fluid sample via a diagnostic paracentesis.

  • Early diagnostic paracentesis in the ED may improve mortality for hospitalized patients with ascites.

  • Polymorphonuclear leukocyte (PMN) count ≥250 cells/mm3 raises suspicion for SBP and should prompt initiation of empiric antibiotics - first line is 2g of Ceftriaxone and second line is a fluoroquinolone. 

  • In addition, AASLD guidelines recommend 1.5g/kg of albumin for patients with SBP who have BUN >30mg/dL, creatinine >1.3mg/dL, or bilirubin >4mg/dL as this may decrease mortality and reduce the incidence of renal impairment.

Expert Commentary

The blog authors make many excellent points about the recognition and management of SBP in the emergency department. From the standpoint of a hepatologists, several concepts and developments regarding this dangerous diagnosis are worth emphasizing. 

  • Clinical context is vital in making management decisions: a patient with advanced chronic liver disease, manifested by high MELD score, is more likely to have SBP than an individual with acute or less advanced disease. 

  • Prompt paracentesis is the key to proper management. It is considered safe to perform diagnostic paracentesis in all patients but those with evident hyperfibrinolysis or those in DIC. Some have advocated for midline paracentesis to avoid vascular structures, but LLQ has been demonstrated to be safer. (Sakai 2005)

  • Only a small amounts of fluid is required to make the diagnosis of PMN > 250 cells/mL. Even a drop in a hemocytometer can be sufficient

  • Patients on prophylactic antibiotics due to previous SBP or low-protein ascites should raise concern for resistant organisms. It is important to sample the ascites in these individuals before commencing antibiotic therapy. 

  • The use of dipstick (leukocyte esterase) diagnosis is supported by some literature but use has been limited mostly to developing nations (Mendler 2010)

  • There is a growing body of literature that supports initial intravenous therapy followed by transition to oral antibiotics in clinical scenarios meeting certain conditions. (Angeli 2006)


  1. Sakai H, Sheer TA, Mendler MH, Runyon BA. Choosing the location for non-image guided abdominal paracentesis. Liver International 2005;25:984-986. 

  2. Mendler MH, Agarwal A, Trimzi M, Magridal E, Tsushima M, Joo E, Santiago M, et al. A new highly sensitive point of care screen for spontaneous bacterial peritonitis using a leukocyte esterase method. J Hepatol 2010;53:477-483

  3. Angeli P, Guarda S, Fasolato S, Miola E, Craighhero R, Del Piccolo F, Antona C, et al. Switch therapy with ciprofloxacin vs intravenous ceftazidime in the treatment of spontaneous bacterial peritonitis in patients with cirrhosis: similar efficacy at lower cost. Aliment Pharmacol Ther 2006;23:75-84

Steven Herrine.png

Steven K. Herrine, MD

Professor of Medicine, Division of Gastroenterology and Hepatology

Vice Dean for Academic Affairs

Sidney Kimmel Medical College at Thomas Jefferson University

How to Cite this Post

[Peer-Reviewed, Web Publication] Dyer K, Trinquero P. (2019, July 29). Spontaneous Bacterial Peritonitis. [NUEM Blog. Expert Commentary by Herrine S]. Retrieved from

Other Posts You May Enjoy


  1. Such J, Runyon BA. Spontaneous bacterial peritonitis. Clin Infect Dis 1998; 27:669.

  2. Nickson, Chris. “Spontaneous Bacterial Peritonitis.” Life in the Fast Lane Medical Blog, 17 Dec. 2012,

  3. Guiney, Allan. “Should All Admitted Patients with Ascites Get a Paracentesis?” Core EM, 7 Dec. 2017,

  4. “Episode 123.0 – Paracentesis Journal Update.” Core EM, 27 Nov. 2017,

  5. McHutchison JG, Runyon BA. Spontaneous bacterial peritonitis. In Surawicz CM, Owen RL (Eds.), Gastrointestinal and Hepatic Infections, WB Saunders Company, Philadelphia 1995. P.455.

  6. Runyon BA. Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology 1990; 12:710Runyon BA. Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology 1990; 12:710.

  7. Runyon, B. (2018) Spontaneous bacterial peritonitis in adults: Clinical manifestations. In K.D. Lindor (Ed.), UpToDate. Retrieved April 2, 2018, from

  8. Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol 2014; 109:1436.

  9. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34:1589.

  10. Runyon, B. (2018) Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis. In K.D. Lindor (Ed.), UpToDate. Retrieved April 2, 2018, from

  11. Navasa M, Follo A, Llovet JM, et al. Randomized, comparative study of oral ofloxacin versus intravenous cefotaxime in spontaneous bacterial peritonitis. Gastroenterology 1996; 111:1011.

  12. Salerno F, Navickis RJ, Wilkes MM. Albumin infusion improves outcomes of patients with spontaneous bacterial peritonitis: a meta-analysis of randomized trials. Clin Gastroenterol Hepatol 2013; 11:123.

  13. Pescatore, Rick. “Should You Give Albumin in Spontaneous Bacterial Peritonitis (SBP)?” R.E.B.E.L. EM - Emergency Medicine Blog, 6 July 2017,

Posted on July 29, 2019 .

Pelvic Fractures

Written by: Justine Ko, MD (NUEM PGY-3) Edited by: Terese Whipple, MD (NUEM PGY-4) Expert commentary by: Matt Levine, MD

Pelvic Ring Fractures


Pelvic ring fractures make up about 3% of skeletal fractures [1]. In the emergency department, they are often seen with high-impact blunt trauma, such as MVCs, crush injuries, or falls.

The pelvis consists of the sacrum and the two innominate bones, which are made up of the ilium, ischium, and pubis [2]. The sacrum and the innominate bones together form a posterior arch and an anterior arch that join to make a ring, also known as the pelvic inlet. The stability of the pelvis is enforced by ligaments: the sacroiliac ligaments, the sacrospinous ligaments, and sacrotuberous ligaments [2]. The ligaments and bones together give the pelvis vertical and rotational stability. 

Pelvic ring fractures carry a significant mortality, ranging from 15-25% in closed fractures, and as much as 50% in open fractures [3]. They are often associated with other high-mortality injuries as well, such as chest injuries, spinal injuries.

What are the mechanisms associated with these injuries?

The Young-Burgess classification system categorizes injury patterns based on the mechanism of injury and the forces applied: anteroposterior compression (APC), lateral compression (LC), and vertical shear (VS) [1]. The most common mechanism is lateral compression, which occurs when lateral forces are applied to the pelvis (as the name would suggest). APC injuries result in the classic “open book” pelvic fractures (Figure 1). 

Figure 1

Figure 1

Figure 2

Figure 2

  • Anteroposterior compression: causes disruption of the pubic symphysis. A normal pubic symphysis should not exceed 5mm. Injuries where the symphysis widening is <2.5cm, with no significant posterior column injury or other fractures, are usually considered stable. APC injuries are often associated with significant blood loss, as the pelvic volume increases and can store more blood [4].

  • Lateral Compression: considered rotationally unstable. This mechanism causes the pelvic volume to decrease, and therefore, is associated with less blood loss [4].

  • Vertical shear: the most unstable, often associated with axial loading of the hemipelvis, such as with a fall or a jump from a height. 

table 1.png

What exam findings should I look for?

During a trauma workup, visual inspection for leg-length discrepancy or rotation of the pelvis may provide clues to a hip or pelvic injury. You may assess for stability of the pelvis by applying downward and medial pressure to the bilateral iliac crests. Apply pressure gently and slowly to avoid disruption of any possible clots that may have formed.

A digital rectal exam should also be performed to assess for spinal cord injury and frank blood. In males, the meatus should be assessed for possible bladder or urethral injury.

X-ray reading tips

  • Check the 3 circles! (Figure 3)

    • Pubic inlet

    • Two obturator foramina

    • Check for irregularities along the circles

    • In general, a vertical fracture pattern will be associated with APC or VS mechanisms. Horizontal fracture patterns will be associated with LC. [7]

Figure 3

Figure 3

  • Check the lines! 

    • ilioischial line (orange line in Figure 4)- disruption suggest posterior column fracture [5]. The posterior column involves the posterior half of the acetabulum and extends to the ischial tuberosity [4]. 

    • iliopectineal line (red line in Figure 4)- disruption suggests anterior column fracture [5]. The anterior column involves the anterior half of the acetabulum and extends to the lateral half of the superior pubic ramus [4].

    • It’s a circle! If it breaks in one location, it likely broke in another place. Be wary of isolated rami fractures in the setting of high-impact trauma!

Figure 4

Figure 4


  • As always, still stick to your ABCs!

    • Initiate blood transfusion early for patients in shock 

    • Hemodynamic instability occurs in about 10% of these injuries [1]

  • Try to obtain IV access above the pelvis if a pelvic fracture is suspected.

  • Stabilize the pelvis with a TPOD or a sheet for patients with open book pelvic fractures

    • Apply over the GREATER TROCHANTERS

    • Do not apply a compressive device for isolated lateral compression pelvic fractures as the device can cause further compression and worsen the displacement [4].

  • If the hemorrhage or hypotension is suspected to be from pelvic hemorrhage, activate IR early.

  • If stable, obtain a CTA of the pelvis to assess for vascular injury

What other injuries should I look for?

  • Urologic Injury: incidence in pelvic fractures is ~5%. Patient with blood at the meatus will need a retrograde urethrogram and then a cystogram [4].

  • Neurologic Injury:  pelvic fractures can be associated with plexus injuries and even cauda equina syndrome. Check for rectal tone and saddle anesthesia [4].

  • Gynecologic injury:  blood a the introitus can represent urethral injury or an open pelvic fracture [4].

Expert Commentary

Dr Ko has provided a high yield concise guide of the key cognitive and clinical features of pelvic fractures.  A few points worthy of further emphasis:

When examining for pelvic instability, do not rock on the pelvis to further open it.  Instead, compress medially to feel instability while closing, rather than opening, the pelvis.

For most studies we order, we have the luxury of waiting for a formal report. Pelvis x rays are one of the few radiographic studies that the Emergency Physician must be able to rapidly interpret independently at the bedside for patient management!  Do not just eyeball the film.  It is impossible to find multiple pelvic fractures that way. Go over every arc, curve, and ring visually.  If something appears possibly abnormal, compare to the other side for (a)symmetry.  And if you find one break in the pelvic ring, scrutinize for more, there almost always are.  Many of these are in the posterior ring, the part of the pelvis for which plain films are least sensitive. CT will help evaluate the posterior elements if feasible.

Understanding the classic LC, APC, VS mechanism classifications lend insight into when a binder will help.  Realize, however, that in vehicular trauma, often the forces are multidirectional, so there will be mixed injury patterns.  Ask yourself what you are trying to achieve by placing the binder.  If it is closing the open book to tamponade hemorrhage, then go for it!  If it is to provide some stability to a VS injury so you can move the patient without their pelvis flopping around than OK but it won't be therapeutic.  If it is an LC injury where the femoral head has crushed through the acetabulum, avoid using a binder, you will only further intrude bony fragments into the pelvis!  

Call IR the instant you realize there is a bleeding pelvic fracture.  It takes time to prepare the suite, especially overnight!


Matt Levine, MD

Assistant Professor of Emergency Medicine

Northwestern Feinberg School of Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Ko J, Whipple T. (2019, July 22). Pelvic Fractures. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from

Other Posts You May Enjoy


Halawi MJ. Pelvic ring injuries: Emergency assessment and management. Journal of Clinical Orthopaedics and Trauma. 2015;6(4):252-258. 

  1. Khurana B, Sheehan SE, Sodickson AD, Weaver MJ. Pelvic ring fractures: What the orthopedic surgeon wants to know. RadioGraphics. 2014;34:1317-1333

  2. Weatherford B. Pelvic ring fractures. Orthobullets website. Accessed October 14, 2018.

  3. Walls RM, Hockberger RS, Gauche-Hill M. (2018). Rosen's emergency medicine: Concepts and clinical practice (9th ed.). Philadelphia, PA: Elsevier/Saunders.

  4. Murphy A, Jones J. Pelvic radiograph (an approach). Radiopaedia website. Updated August 2018. Accessed October 14, 2018. 

  5. Tile M. Pelvic ring fractures: should they be fixed? J Bone Joint Surg Br Vol. 1988;70(1):1–12.

  6. Singh, AP. Pelvic fractures: Presentation and treatment.


Case courtesy of Dr Jeremy Jones, From the case" rID: 28928

Posted on July 22, 2019 .

Clostridium Difficile

Written by: Luke Neill, MD (NUEM PGY-4) Edited by: Keith Hemmert, MD (NUEM ‘18) Expert commentary by: Michael Angarone, DO

Expert Commentary

Dr. Neill has provided an excellent overview of the important points from the latest iteration of the IDSA/SHEA guidelines for the diagnosis and management of Clostridioides difficile (formerly Clostridium difficile) infection (CDI). There are a few important changes to this current update to the guidelines. For the diagnosis of C. difficile infection the guidelines recommend hospitals to not test persons on laxatives, that have formed stools or another diagnosis for the patient’s diarrhea. This is an important change in the way that most practitioners think of testing for C difficile and will result in less tests being performed.  Hospitals that do not adopt pretesting criteria for testing stool for C diffiicile should develop a multi-step testing algorithm, such as glutamate dehydrogenase test followed by toxin test, arbitrated by C difficile PCR. The guidelines do not recommend probiotics for primary prevention of CDI stating that there is insufficient data to recommend the use of these agents. This is contrary to a recent Cochrane review from 2017 that analyzed 31 studies and found that in individuals at high risk for CDI may benefit from probiotics, with a number needed to benefit of 12.  The biggest change in this version of the guidelines is that metronidazole is no longer recommended for therapy. Patients should be treated with either oral vancomycin or fidaxomicin. For multiple recurrent CDI (>2 episodes), patients should be considered for fecal microbiota transplantation. This is the first time that FMT has been recommended as a treatment option in the IDSA/SHEA guidelines. The changes in this guideline should not change the way that most practitioners approach CDI, with the exception of the above important changes.


1.       McDonald LC, Gerding DN, Johnson S, et al. Clinical practice guidelines for Clostridium difficile infection in adults and children: 2017 update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA) [published online February 15, 2018]. Clin Infect Dis.doi: 10.1093/cid/cix1085

2.       Cochrane Database Syst Rev. 2017 Dec 19;12:CD006095.  Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. PMID 29257353


Michael P. Angarone, DO

Assistant Professor

Department of Medicine (Division of Infectious Diseases) and Medical Education

Northwestern University, Feinberg School of Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Neill L,  Hemmert K. (2019, July 15). Clostridium Difficile. [NUEM Blog. Expert Commentary by Angarone M]. Retrieved from

Other Posts You May Enjoy

Posted on July 15, 2019 and filed under Infectious Disease.


Ophthalmology-12 (1).png

Written by: Jonathan Hung, MD, (NUEM PGY-3) Edited by: Matt Klein, MD (NUEM ‘18) Expert commentary by: Dr. Glaucomflecken


Corneal abrasions are a commonly encountered eye-related presentation in the emergency department (ED) [1]. Patients will often have a significant amount of pain from even minor abrasions. Topical anesthetics such as tetracaine have been found to be effective in treating the pain and are now routinely used in the ED [2]. However, the use of topical anesthetics for corneal abrasions in the outpatient setting is controversial due to concerns over safety and delayed healing. These traditional concerns over the prolonged use of topical anesthetics are based on early animal studies and case reports in humans [3]. The current literature suggests that topical anesthetics are, in fact, safe and effective if given as a short course with appropriate follow up, but further studies with larger patient populations are needed to support these findings [4]. A recent study published in Annals of Emergency Medicine is one of the largest studies to date that examines the safety of discharging patients home from the ED with a short supply of tetracaine for corneal abrasions.


Waldman N, Winrow B, Densie I, et al. An Observational Study to Determine Whether Routinely Sending Patients Home With a 24-Hour Supply of Topical Tetracaine From the Emergency Department for Simple Corneal Abrasion Pain Is Potentially Safe. Ann Emerg Med. 2017. 

Study Design

The study design was a single-center, retrospective cohort study with ethics approval given by the Human Ethics Committee at the University of Otago. 


The study was performed at the ED of Southland Hospital, Invercargill, New Zealand. A computer search of the hospital’s ED information system was conducted looking for all eye-related diagnoses and charts were reviewed between February 1, 2014 to October 31, 2015. Patients were initially selected if they were seen in the ED with an injury or illness involving the cornea. 

Intervention protocol

Patients with simple corneal abrasions were discharged home with undiluted 1% tetracaine hydrochloride in addition to the standard treatment of acetaminophen and chloramphenicol eye ointment. Instructions were given to place tetracaine in the eye as often as every 30 minute over the first 24 hours.  

Outcome Measures

  • ED rechecks 

  • Persistent fluorescein uptake

  • Ophthalmology clinic referrals

  • Complications


There was a total of 1,576 ED presentations of corneal abrasions of which 532 were simple corneal abrasions (SCA) and 1,044 were defined as nonsimple corneal abrasions (NSCA). Tetracaine was given to 57% (303) of SCA patients and 14% (141) of NSCA patients. Overall, there were no serious complications or uncommon adverse events in either the SCA or NSCA group (0/459). The relative risk of patients with SCA receiving tetracaine and returning to the ED, having fluorescein uptake, or requiring a referral to ophthalmology was low compared to the standard treatment group. 


This study is one of the largest studies to examine the safety of outpatient tetracaine use in simple corneal abrasions. More importantly, it gives a robust conclusion similar to previous smaller studies in that there was no evidence that using topical tetracaine for a short duration caused harm. The strengths of this study include the large patient population and good patient follow-up. Furthermore, the physicians that administered tetracaine did not know that an observational study was planned, thus increasing the internal validity. However, the researchers were not blinded to the hypothesis which could have led to bias when collecting data. This was also a retrospective study and therefore due to the lack of randomization, those who received tetracaine may have differed from those who did not. Another limitation was that it was not known if all the patients administered the tetracaine as instructed after leaving the ED. Also, the diagnosis of simple corneal abrasion was limited to what the physician documented in the chart. The external validity is limited since this was a single-center study and about 71% of the patients were males. Overall, this study further strengthens the role of tetracaine in treating pain secondary to simple corneal abrasions and may gradually change practice patterns in the emergency department despite traditional teaching. 

Take Home Points

  • Topical tetracaine is effective in treating pain due to corneal abrasions

  • Patients with simple corneal abrasions can benefit from a short course of topical tetracaine to treat pain 

  • Topical tetracaine use over a 24-hour period is generally safe 

  • Emergency medicine physicians should consider incorporating topical tetracaine in their practice for treating SCAs 

Expert Commentary

This is an interesting observational study regarding the safety of prescribing a limited supply of topical tetracaine to patients who present to the emergency department with what the authors describe as “simple corneal abrasions.” It is well documented in the literature that long term use of topical anesthetics can lead to a variety of serious ophthalmic complications, including persistent epithelial defects, neurotrophic ulceration, secondary infectious keratitis, corneal scarring and perforation. However, many of these reports describe long term use of anesthetics ranging from 7 days to 6 months which have helped establish the long-held dogma that topical anesthetics are only appropriate for use during surgery or clinic examination. This study, as well as several smaller previous studies, has attempted to challenge that dogma in an effort to better treat the immense pain often associated with corneal abrasion.

The authors did a great job trying to distinguish between simple and non-simple corneal abrasions. This can be very difficult, even for an ophthalmologist. What may look like a simple corneal abrasion can easily turn out to be a different diagnosis altogether. Herpes simplex keratitis can present as a geographic ulcer, lighting up with fluorescein much like a corneal abrasion without the tell-tale sign of dendritic lesions to accompany it. Dry eye disease can result in confluent, punctate epithelial defects which can look like a corneal abrasion without the magnification afforded by a slit lamp. These conditions should not be treated with topical anesthetics and will only delay the patient in receiving appropriate care. Stating that topical anesthetics are safe for simple corneal abrasions assumes that the examiner is able to accurately diagnose a simple abrasion. In this study, several patients were misdiagnosed as simple abrasions and ultimately required follow up with ophthalmology. Patients who need to see ophthalmology for a non-simple abrasion may be less likely to follow up in a timely manner if they are given topical anesthetic that will effectively mask the pain. This can result in more extensive corneal scarring from a variety of diagnoses such as delayed rust ring removal or treatment of infectious keratitis.

The authors make a compelling point that a limited supply of tetracaine in a subset of corneal abrasions intended to last no more than 24 hours is safe with no significant difference in the number of ED rechecks, ophthalmology clinic referrals, persistent fluorescein uptake, or complications. If this is indeed true, is treating with topical anesthetic worth it? At best, you are providing a minimally-painful healing process which will be complete in 48-72 hours regardless of topical anesthetic use. At worst, you are masking pain of a potentially vision-threatening process that may have been misdiagnosed as a simple abrasion. I contend that setting patient expectations regarding pain (very severe for first 24 hours, then rapid improvement) and discussing more conservative comfort measures like icing and patching are sufficient.

Lastly, I want to discuss the treatment for simple and non-simple corneal abrasions. It is unclear whether or not the patients in this study were treated with topical antibiotics. It is possible that patients with simple corneal abrasions were sent home with a 24 hour supply of tetracaine and no topical antibiotics. Without an epithelial barrier, the underlying corneal stromal is prone to infection. Topical antibiotics act as a preventive measure and are particularly important if a patient is using topical anesthetic, which could mask the pain of infectious keratitis. Although not all sources agree, there is general consensus among ophthalmologists that all corneal abrasions require topical antibiotics at the time of diagnosis.

In conclusion, I agree that a 24 hour prescription of topical anesthetic in a simple corneal abrasion is likely safe. However, given the rapid healing time, consideration should be made to counseling patients on pain expectation and comfort measures in place of topical anesthetic. Lastly, prescribing more than a 1 day supply of topical anesthetic is unnecessary given the rapid improvement in pain after the first 24 hours


Dr. Glaucomflecken, MD

How To Cite This Post

[Peer-Reviewed, Web Publication] Hung J,  Klein M. (2019, July 8). Tetracaine. [NUEM Blog. Expert Commentary by Dr. Glaucomflecken]. Retrieved from

Other Posts You May Enjoy


  1. Verma A, Khan FH. Corneal abrasion. MedscapeAvailable at: Accessed November 1, 2017.

  2. Waldman N, Densie IK, Herbison P. Topical tetracaine used for 24 hours is safe and rated highly effective by patients for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial. Acad Emerg Med 2014;21:374–82.

  3. Chang YS, Tseng SY, Tseng SH, et al. Cytotoxicity of lidocaine or bupivacaine on corneal endothelial cells in a rabbit model. Cornea 2006;25:590–6.

  4. Swaminathan A, Otterness K, Milne K, Rezaie S. The Safety of Topical Anesthetics in the Treatment of Corneal Abrasions: A Review. J Emerg Med. 2015;49(5):810-815. 

Posted on July 8, 2019 and filed under Ophthalmology.

Sink or Swim: The management of submersion injuries

Written by:  Michael Conrardy , MD (NUEM PGY-2)  Edited by:  Gabby Ahlzadeh, MD (NUEM ‘19)  Expert commentary by : Kristina McAteer, MD

Written by: Michael Conrardy , MD (NUEM PGY-2) Edited by: Gabby Ahlzadeh, MD (NUEM ‘19) Expert commentary by: Kristina McAteer, MD


If you are an emergency physician, you likely will see submersion injuries often throughout your career. In the United States, from 2005-2014, there are approximately ten deaths per day from unintentional drowning, and about 3,536 annually. This number increases to eleven per day if you include boating-related deaths. One in five deaths involve children under the age of fourteen, and drowning is the second leading cause of death for children ages 1-14 [1,2]. Approximately 80% of all victims are male [2], and when considering adolescents and adults, alcohol is involved in up to 70% of cases [3]. Statistics for nonfatal drowning events are difficult to obtain, but studies estimate that they may occur several hundred times more frequently than reported deaths [4,5].

Example Case

While working in the emergency department on Friday night, three college students are brought in by EMS after “drinking alcohol and jumping in Lake Michigan.” Patient #1 received CPR for ten minutes en route, has a temperature of 32 degrees Celsius, signs of head trauma, and a cervical collar in place. Patient #2 experienced a short period of submersion and is in mild respiratory distress. Patient #3 was submerged for only a brief period of time and is completely asymptomatic.

Emergency Department Management of Submersion Injuries
Patient #1 - Severely Symptomatic Patients

Initial Management:

In serious cases of drowning, top concerns are hypoxemia, hypothermia, subsequent cardiac arrest, and other signs of trauma.

  1. If in cardiac arrest, start ACLS and consider underlying causes such as hypoxemia or hypothermia

  2. Remove wet clothing and use rewarming techniques

  3. Chest x-ray, blood gas, labs, end tidal CO2. Initial CXR is often normal but can be helpful in tracking the patient’s condition.

  4. Assess for signs of trauma and obtain appropriate imaging. It is important to note that cervical spine injuries are uncommon (<5%) in cases of drowning, and cervical collars should not distract from airway management [6].

Management of airway, ventilation, oxygenation:

Fluid aspiration can lead to loss of surfactant, pulmonary edema, and hypoxemia from V/Q mismatch. Hypoxemia is the primary cause of end-organ damage in submersion injuries (typically cardiac and neurologic) and treating it should be your top priority. Here are some general guidelines:

  • Airway: Intubate patients if unable to protect airway, O2Sat < 90% despite supplemental O2, or PaCO2 >50

  • Ventilation: Positive pressure opens alveoli and improves ventilation in drowning.

    • Unable to protect airway: Start with bag-valve-mask and then intubate. Use ARDS settings of Vt 6-8 mL/kg, Pplateau < 30mmHg, and increased PEEP.

    • Able to protect airway: Use non-invasive positive pressure ventilation in alert, symptomatic patients for goal O2Sat > 94% [6].

  • Oxygenation: Use maximum available supplemental O2 initially and wean as tolerated.


No medications need to be routinely used for submersion injuries. Bronchospasm can occur, and if suspected should be treated with inhaled beta-adrenergic agonists. Glucocorticoids have not been shown to be helpful in preventing subsequent lung injury and may interfere with healing, and not enough data exists to support routine administration of exogenous surfactant. Antibiotics should only be used in cases where signs of infection develop or if the patient was submerged in grossly contaminated water [7].


Data on use of ECMO to treat patients with severe pulmonary edema or signs of ARDS are extremely limited, although initial results are encouraging [9]. This is an area of ongoing research, and perhaps we may eventually see early initiation of ECMO as standard practice for severely symptomatic patients.

Patient #2 - Mildly Symptomatic Patients

The main takeaway from patient #2 is that all patients who are symptomatic on arrival to the ED (requiring ventilatory assistance or supplemental O2) should be admitted to the hospital. Airway, ventilation, and oxygenation should be managed as above, and serial chest x-rays can help monitor for development of pulmonary edema in symptomatic patients [6].

Patient #3 - Asymptomatic Patients

Although most research on safe discharge has been in children, it is generally accepted that asymptomatic patients can be safely discharged after 4-6 hours of monitoring. Patients should have normal pulmonary exam, SaO2>95% on room air, and GCS>13 [6,10]. Some clinicians advocate for observing up to eight hours based on a study that observed one pediatric patient who did not develop symptoms until seven hours post-submersion [11], although six hours in the ED with return precautions is probably adequate in most cases. Many clinicians obtain basic labs on all patients and a chest x-ray prior to discharge to confirm that there are no signs of pulmonary edema, although no strong evidence supports these practices.

Key Takeaways:

  • Hypoxemia is the main cause of harm, prioritize the airway and use positive pressure

  • Initial chest radiographs are often normal, but can be used to track a patient’s clinical status

  • Blood gas is the most useful laboratory test in symptomatic patients, additional testing (e.g. ECG, CBC, chem, troponin) is particularly useful in patients with altered mental status

  • Asymptomatic patients may be safely discharged after six hours of monitoring

Expert Commentary

The terminology can be confusing with such terms as drowning, nonfatal drowning, submersion injury, dry drowning, wet nonfatal drowning, and so on.  Most recently (2010) the AHA recommended a more straightforward approach and supported the Utstein definition which hopefully offers some clarification, relieves some of the angst when approaching this population, and standardizes research and reporting.  The Utstein defines a drowning as “a process resulting in a primary impairment from submersion or immersion in a liquid medium.” [1]

The key is to keep it simple.  Is your patient symptomatic from the exposure?  If so, focus on the ABC’s and get to work! 

You will often see pediatric patients as drowning victims.  Drowning is a leading cause of accidental death in children under 5 years of age, particularly in states where swimming pools or beaches are more accessible. The states of California, Arizona and Florida lead the way [2].  The second peak is in older ages (15-25 yo), primarily males, and involves more rivers, lakes and beaches. [3].  The distinction between fresh and salt water drownings is no longer considered important as the volume of aspirated water is so small that the theorized electrolyte shifts do not have any real physiological impact [4]. Both wash out pulmonary surfactant.  

As appropriately pointed out it is often is not the drowning that causes mortality. It is therefore necessary to consider concomitant trauma, toxic ingestions (at the very least alcohol leading to impaired judgment!), and hypothermia.  Hypoxemia and the resultant hypoxia is ultimately the cause for death, often impacting multiple organ systems, and thus it is your job to reverse the hypoxemia as quickly as possible!  Supplemental oxygen, BIPAP (Bilevel positive airway pressure), endotracheal intubation and if necessary, ECMO (extracorporeal membrane oxygenation) are management options.  There is a neuroprotective effect of hypothermia and in some cases patients make a complete recovery despite a prolonged resuscitation.  Age > 14, duration of submersion > 5 minutes, time to basic life support > 10 minutes, resuscitation duration > 25 minutes, GCS (Glascow coma scale) <5, persistent apnea and requirement of CPR in the emergency department and arterial blood pH <7.1 have all been associated with a poor prognosis.  [5]

  1. Vanden Hoek TJ, Morrison LJ, Shuster M, et al. Part 12: Cardiac Arrest in special situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergent Cardiovascular Care. Circulation 2010; 122: S829.

  2. Brenner Ra. Prevention of drowning in infants, children, and adolescents. Pediatrics 2003; 112:440.

  3. DeNivola, LK, Falk, JL, Swanson ME, et al. Submersion injuries in children and adults. Crit Care Clin 1997;12:477.

  4. Orlowski JP, Szpilman D. Drowning, Resucue, resuscitation and reanimation. Pediatr Clin. North Am 2001. 48:627.

  5. Quan L, Mack CD, Schiff MA.  Association of water temperature and submersion duration and drowning outcome. Resuscitation 2014.85:790.


Kristina McAteer, MD

Assistant Professor of Emergency Medicine

Brown University

How To Cite This Post

[Peer-Reviewed, Web Publication] Conrardy M,  Ahlzadeh G. (2019, July 1). Sink or Swim: The management of submersion injuries. [NUEM Blog. Expert Commentary by McAteer Kristina]. Retrieved from

Other Posts You May Enjoy


  1. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-based Injury Statistics Query and Reporting System (WISQARS) [online]. Available from: URL:

  2. CDC. Wide-ranging online data for epidemiologic research (WONDER). Atlanta, GA: CDC, National Center for Health Statistics; 2016 [online]. Available at

  3. Driscoll TR, Harrison JA and Steenkamp M. Review of the role of alcohol in drowning associated with recreational aquatic activity. Inj Prev. 2004; 10: 107-13.

  4. Bierens JJ, Knape JT and Gelissen HP. Drowning. Curr Opin Crit Care. 2002; 8: 578-86.

  5. Orlowski JP. Drowning, near-drowning, and ice-water drowning. JAMA : the journal of the American Medical Association. 1988; 260: 390-1.

  6. Schmidt AC, Sempsrott JR, Hawkins SC, Arastu AS, Cushing TA and Auerbach PS. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Drowning. Wilderness Environ Med. 2016; 27: 236-51.

  7. Layon AJ and Modell JH. Drowning: Update 2009. Anesthesiology. 2009; 110: 1390-401.

  8. Chandy D, Weinhouse GL. Drowning (submersion injuries). UpToDate. Danzl DF, Grayzel, J (Ed). 2017.

  9. Burke CR, Chan T, Brogan TV, et al. Extracorporeal life support for victims of drowning. Resuscitation. 2016; 104: 19-23.

  10. Causey AL, Tilelli JA and Swanson ME. Predicting discharge in uncomplicated near-drowning. The American journal of emergency medicine. 2000; 18: 9-11.

  11. Noonan L, Howrey R and Ginsburg CM. Freshwater submersion injuries in children: a retrospective review of seventy-five hospitalized patients. Pediatrics. 1996; 98: 368-71.

Posted on July 1, 2019 and filed under Environmental.

Not All Ankle Sprains are Created Equal


Written by:  William Ford, MD, MBA (NUEM PGY-4) Edited by: Simiao Li-Sauerwine, MD (NUEM ‘18) Expert commentary by: Matthew Levine, MD


Ankle injuries are commonly seen in emergency medicine, and serious injuries can be found in the setting of a negative X-ray. The “high ankle sprain” involves the structure of the ankle called the syndesmosis. Isolated ligamentous disruption to the syndesmosis is uncommon, though when it occurs, it is frequently missed. This can lead to serious consequences, including long-term ankle dysfunction and the need for surgery [1]. Identifying these injuries in the ED can improve recovery and facilitate prompt follow-up.

What is the Syndesmosis?

The syndesmosis is the distal articulation of the tibia and the fibula and it keeps the joint stable. For the purposes of this discussion, the focus will be on the ligamentous parts of the syndesmosis not seen on an ankle X-ray.

There are four syndesmotic ligaments: the interosseous ligament (IOL), the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), and the inferior transverse tibiofibular ligament (ITTFL) [2].

How Does Syndesmotic Injury Occur?

The motion often involved in syndesmotic injury is external rotation of the foot. Commonly, it is a combination of external rotation of the foot and excessive dorsiflexion of the ankle [3-6]. This is frequently encountered in high-speed collisions, uneven terrain, and cutting and jumping sports [1]. In most cases, syndesmotic injury will occur concurrently with a fracture, but sometimes, ligamentous injury may occur in isolation [7-8].

How Can I Diagnose Syndesmotic Injury?

Since this diagnosis is difficult to make without an MRI, providers must rely on a high index of suspicion. First, ask yourself if the mechanism of injury is consistent with syndesmosis disruption. Localizing the areas of tenderness on physical exam can also be helpful. Anterolateral or posteromedial ankle tenderness, as opposed to direct lateral or medial pain inferior to the malleoli, can suggest syndesmotic involvement. Finally, in accordance with the name “high ankle sprain”, more proximal pain may be indicative of a syndesmotic injury [1].

There are a few provocative tests described for diagnosing syndesmotic injuries. None are slam-dunk maneuvers, but a constellation of positive findings can be helpful in making the diagnosis.

  1. Squeeze test: With the patient sitting at the edge of the bed and knee bent at 90 degrees, a strong compressive force is applied to the tibia and fibula proximal to the mid-calf. Pain indicates a positive finding.

  2. External rotation stress test: If the pain is reproduced with manual external rotation of the foot and ankle relative to the tibia, this test is positive. It is important to make sure the tibia is stabilized while performing this test.

  3. Cotton test: This test is performed by attempting to translate the talus laterally under the tibia. Increased translation compared to the contralateral side or increased pain with this maneuver is a positive finding.

  4. Fibular translation test: Stabilize the tibiotalar joint with one hand, translate the fibula anteriorly and posteriorly with the other hand. Increased pain and translation compared to the contralateral side equals a positive test.

X-ray diagnosis can also be difficult, except in the presence of frank tibiofibular diastasis [1].


Not all ankle sprains are created equal. High ankle sprains involving the syndesmosis can mean triple the recovery time of a regular sprain, chronic instability, or definitive treatment with surgery. Increased awareness and knowledge of how to diagnose these injuries is important to ensure quality care for patients.

Expert Commentary

Ankle injuries are the most common orthopedic complaint we see in the ED.  While most of these presentations are simple sprains, there are other more severe injuries that will resemble uncomplicated sprains.  Given the sheer volume of ankle injuries we see, we undoubtedly have all missed some of these more complicated injuries.  A high ankle sprain is one of these injuries.  Another classic injury that resembles an ankle sprain is the Snowboarder’s fracture. This is a fracture of the lateral process of the talus that occurs from ankle inversion and dorsiflexion.  Snowboarder’s fractures clinically resemble ankle sprains and x rays miss up to 40% of these fractures!  I have seen radiology miss some of these and then found the fracture by going back and magnifying the area of the lateral talus distal to the lateral malleolus on the AP and mortise views. 

Regardless, plain films will not detect all Snowboarder’s fractures or high ankle sprains.  It is tempting to quickly wrap and discharge all ankle “sprains” after a negative x ray.  It is important, however, to discuss with these patients what is a normal healing progression and timeline.  Emphasize that if 10 days go by and there is still significant pain, functional impairment, or reliance on the crutches or air cast, they need to follow up with orthopedics.  Provide them with the means to arrange this follow up. It is not realistic to be able to diagnose every ankle sprain mimic in the ED, but it is our duty to provide every patient (not just ankle sprain patients) with the proper instructions for follow up in case we have missed something.

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Matthew Levine, MD

Assistant Professor of Emergency Medicine

Northwestern Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Ford W, Li-Sauerwine S. (2019, May 27). Not All Ankle Sprains are Created Equal. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from

Other Posts You May Enjoy


  1. Hunt KJ, Phisitkul P, Pirolo J, et al. High Ankle Sprains and Syndesmotic Injuries in
    Athletes. Journal of the American Academy of Orthopaedic Surgeons. 2015;23(11): 661-73.

  2. Fibular translation test: Stabilize the tibiotalar joint with one hand, translate the fibula anteriorly and posteriorly with the other hand. Increased pain and translation compared to the contralateral side equals a positive test.

  3. Ogilvie-Harris DJ, Reed SC, Hedman TP. Disruption of the Ankle Syndesmosis: Biomechanical Study of the Ligamentous Restraints. Arthroscopy: The Journal of Arthroscopic & Related Surgery. 1994;10(5): 558-60.

  4. Lin C-F, Gross MT, Weinhold P. Ankle Syndesmosis Injuries: Anatomy, Biomechanics, Mechanism of Injury, and Intervention. J. Orthop. Sport. Phys. Ther. 2006;36(6): 372–384. doi:10.2519/jospt.2006.2195.

  5. Dattani R, Patnaik S, Kantak A, et al. Injuries to the tibiofibular syndesmosis. J. Bone Jt. Surg. 2008;90–B(4): 405–410. doi:10.1302/0301-620X.90B4.19750.

  6. Brosky T, Nyland J, Nitz A, et al. The Ankle Ligaments: Consideration of Syndesmotic Injury and Implications for Rehabilitation. J. Orthop. Sport. Phys. Ther. 1995;21(4).

  7. Hopkinson WJ, Pierre P St., Ryan JB, et al. Syndesmosis Sprains of the Ankle. Foot Ankle. 1990;10(6): 325–330.

  8. Miller CD, Shelton WR, Barrett GR, et al. Deltoid and Syndesmosis Ligament of the Ankle without Fracture Injury. Am. J. Sports Med. 1995;23(6): 746–750.

  9. Hunt KJ. Syndesmosis injuries. Curr. Rev. Musculoskelet. Med. 2013;6: 304–312. doi:10.1007/s12178-013-9184-9.

Posted on May 27, 2019 and filed under Orthopedics.

Corneal Abrasions

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Written by: Julian Richardson, MD, MBA (NUEM PGY-2) Edited by: Andrew Moore, MD (NUEM ‘18) Expert commentary by: Brad Sobolewski, MD, MEd

A 40 yo construction worker comes to Emergency Department with a foreign body sensation in his left eye for two days. He states that he forgot to wear his eye protection while sanding a plank of wood the other day and felt like something has been scratching his eye ever since. Upon entering the room, his left eye is hyperemic and the patient appears to be in discomfort.


Approach to the painful red eye with foreign body sensation

The initial differential diagnosis to a painful red eye is broad and includes entities such as keratitis, corneal abrasions, corneal ulceration, acute angle glaucoma, iritis, chemical burn, scleritis, subconjunctival hemorrhage, and conjunctivitis. The patient’s history is particularly concerning for corneal abrasion, corneal ulceration, or globe rupture. A simple test to distinguish these diagnoses is the fluorescein exam.


Fluorescein exam

Fluorescein has been used in ophthalmology since the 1880s. This exam should be included for all patients where there is a suspicion of abrasion, foreign body, or infection. Fluorescein absorbs light in blue-wavelengths and emits energy in green wavelengths. It fluoresces in alkaline environments, for example Bowman’s membrane which is located below the corneal epithelium. It does not fluoresce in acidic environments such as the tear film over intact cornea.  Because of this, defects in the cornea increase fluorescein uptake and assist in locating corneal damage.

The eye should first be numbed usually with the use of a topical anesthetic drop, such as tetracaine. Next, take a fluorescein strip and place one drop of saline or local anesthetic to the strip. Place this strip inside the lower lid, remove, and ask the patient to blink. The key to a good exam is to produce a thin layer covering the surface of the eye. If too much is applied, the excess can easily be removed by asking the patient to blot their eye while closed with a tissue. The eye should then be examined using a Wood’s lamp, blue filter of a slit lamp, or penlight with a blue filter

Warning! this dye will permanently stain soft contact lenses and clothing. Be sure to remove any contacts and have plenty of gauze or other absorbant material available prior to instillation. Irrigating the excess dye out the eye after examination will help minimize staining the patient’s clothing.

Corneal Abrasion



  • Scratch to the epithelium that comprises the cornea and exposes the basement membrane. Patients generally complain of a foreign body sensation, pain, photophobia, and some vision loss. On physical exam, the clinician may find injected conjunctiva, and decreased visual acuity (if the defect is large or lies in the visual axis).

 Fluorescein Exam

  • Typically, abrasions are seen at the central part of the cornea due to limited protection of closure of the patient’s eyelids. The margins are sharp and linear in the first 24hrs. Circular defects suggests an embedded foreign body is present and may persist for greater than 48hrs. Foreign bodies can also produce vertical linear lesions and the upper lid should be lifter up to look for a foreign body under the eyelid


  • Treatment with antibiotics have become the standard of care. Antibiotics are particularly indicated for abrasions caused by contacts (cover for pseudomonas), foreign bodies, or history of trauma with infectious or vegetative matter due to a higher risk of infection. Ophthalmic antibiotic therapy include: erythromycin ointment or sulfacetamide 10%, polymyxin/trimethoprim, ciprofloxacin, or ofloxacin drops (4 times a day for 3-5 days). Pain relief can be provided with oral or topical pain meds. Topical NSAIDs include .1% indomethacin, .03% flubiprofen, .5% ketorolac, 1% indomethacin, and .1% diclofenac.  If symptoms persist greater than 24 hours after treatment the patient should follow-up with a physician. If the abrasion has not healed in 3-4 days the patient should be evaluated by an ophthalmologist.


Corneal Ulceration

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  • When a defect in the corneal epithelium becomes infected with bacteria or fungi it is defined as a corneal ulceration. This is a common complication of corneal abrasions and if left untreated can result in a corneal perforation.

Fluorescein Exam

  • Corneal staining with infiltrate or opacification around the lesion should raise suspicion for ulceration. Contact lens wearers raise the suspicion of a Pseudomonal infection. Many Pseudomonal organisms fluoresce when exposed to UV light and fluoresce prior to fluorescein application.


  • Concern for ulceration requires an urgent ophthalmology consultation within 24hrs. Discharged patients should be treated with antibiotic drops or ointment.

Globe Rupture


  • Full thickness injury to the cornea, sclera, or both secondary to penetrating of blunt trauma.

Fluorescein Exam

  • Seidel test: instill a large amount of fluorescein onto eye and looking for small stream of fluorescent blue or green fluid leaking from the globe.


  • Once suspected, avoid further examination or manipulation, make the patient NPO, and place an emergent ophthalmology consultation. These patients also require broad spectrum IV antibiotic coverage with a 3rd generation cephalosporin or aminoglycoside and vancomycin to prevent post-traumatic endophthalmitis.

In summary, all patients with eye pain, particularly with a foreign body sensation, warrant a fluorescein exam. A wealth of information can be gained by this simple test and will guide the management of the patient.

Expert Commentary

This is a very comprehensive review of a common complaint in the Emergency Department. You correctly identified that one must be careful to avoid instilling too much fluorescein so as to cause a false positive result. Though a drop of tetracaine or saline dilutes the fluorescein from the strip somewhat the quantity is hard to control at times – especially in noncompliant patients (like the children I usually examine in the Pediatric Emergency Department). Excess fluorescein can collect across the eye making identification of small abrasions challenging. If you put too much in rinse the eye and try again. It is also incredibly important to not sent the patient home with tetracaine drops, as too frequent use may lead to further corneal injury. The evidence is based on animal models and case series and is far from complete. Read more on this great R.E.B.E.L. EM post (link:

One of the main pitfalls to the use of fluorescein strips is the risk of actually causing an abrasion. The method noted in this article – placing the strip inside the lower lid margin and asking the patient to blink – can cause an abrasion if the edge of the strip touches the cornea. This is particularly challenging to do in children, since even with proper restraint the blink reflex and their tendency to recoil is high. Therefore I recommend doing one of the following:

  1. Hold the patient’s eyelids open. Drip the tetracaine or saline down the strip and allow it to drip into the eye, being careful to avoid touching the strip to the eye.

  2. Make a fluorescein dropper. This is well detailed in the Tricks of the Trade: Fluorescein application techniques for the eye form Academic Life in Emergency Medicine (link: The Angiocath dropper allows for better control of droplet size and makes it easier to instill fluorescein into the squinting eye without the risk of touching the cornea.


Brad Sobolewski, MD, MEd

Associate Professor, Assistant Director - Pediatric Residency Training Program

Division of Emergency Medicine

Cincinnati Children's Hospital Medical Center

How To Cite This Post

[Peer-Reviewed, Web Publication] Richardson J, Moore A. (2019, May 20). Corneal Abrasions [NUEM Blog. Expert Commentary by Sobolewski]. Retrieved from

Other Posts You May Enjoy


  1. Images courtesy of

  2. Marx, J. A., & Rosen, P. (2014). Rosen's emergency medicine: Concepts and clinical practice (8th ed.) Ch. 71. Opthamology. Philadelphia, PA: Elsevier/Saunders

  3. Yanoff, M., Duker, J. S., & Augsburger, J. J. (2009). Ophthalmology. Ch 4, Corneal anatomy, physiology, and wound healing. Edinburgh: Mosby Elsevier.

  4. Roberts, J. R., In Custalow, C. B., In Thomsen, T. W., & In Hedges, J. R. (2014). Roberts and Hedges' clinical procedures in emergency medicine. Ch 62. Opthalmologic procedures.

  5. Gardiner, M. F. Overview of eye injuries in the emergency department. Retrieved September 16, 2017, from

  6. Jacobs, D. S. Corneal abrasions and corneal foreign bodies: management. Retrieved September 16, 2017, from

  7. Waldman, N., Winrow, B., Denise, I., Gray, A., McMAster, S., Giddings, G., & Meanley, J. (2017). An observational study to determine whether routinely sending patients home with a 24-hour supply of topical tetracaine from the emergency department for simple corneal abrasion pain is potentially safe. Annals of Emergency Medicine, 02(016).


Posted on May 20, 2019 and filed under Ophthalmology.

C-spine Clearance with Negative CT: Are We There Yet?

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Written by: M. Terese Whipple, MD (NUEM PGY-3) Edited by: Quentin Reuter, MD (NUEM ‘18) Expert commentary by: Matthew Levine, MD

We have excellent decision rules for clinically clearing cervical spine injury in low risk patients without imaging. However, a frustrating situation arises when a CT of their c-spine is obtained and negative, but they are having persistent midline pain. What do we do then? Are we forced to order an MR of the c-spine even when they have no neurological deficits and our gestalt tells us there is no clinically significant injury? MR often means admission, worsening of already overwhelming ED crowding, and unhappy patients when they cannot remove the c-collar for at least several more hours. Recent data and recommendations suggest that this may not be the case; a negative CT may be enough to rule out clinically significant injury. This blog post will explore some of the historical and recent data on the subject of cervical spine clearance after CT scan alone.  

There has been great historical debate over the best management for patients with persistent midline pain after negative CT, however that evidence is beyond the scope of this post. Current common practice and the recommendation of the American College of Radiology leads down the path of cervical spine MR when this situation arises [1]. Due to the cumbersome logistics of MR, much work has been done to determine if MR truly adds value to the patient’s workup. Is MR catching clinically significant injury missed by CT that changes clinical management? The majority of studies have concluded that the answer to that question is no.  

In 2015 the Eastern Association for the Surgery of Trauma (EAST) sought to tackle this question by reviewing all studies to date examining C-spine evaluation in obtunded patients [2]. They evaluated 11 studies with a total of 1718 obtunded patients who underwent C-Spine imaging with CT. None were ultimately found to have unstable fractures or unstable ligamentous injury missed by CT. There was a 9% incidence of stable injuries missed on CT and found on follow up MR, flex-x, upright XR, or clinical follow up. They found a cumulative 100% NPV for unstable C-Spine injury with CT and 91% NPV for stable injury. They did rate the quality of evidence as low for various reasons, including non-comparable imaging protocols, inconsistently reported and variable outcomes, publication bias, and an overall inability to perform a meta-analysis with the data.  However, they rated the data from which they derived the NPV as moderate quality as the NPV was consistently 100% throughout all of the trials. Based on their analysis they provided the following recommendation for obtunded blunt trauma patients:

“We conditionally recommend cervical collar removal after negative high-quality c-spine CT scan results alone.”

 They went on to further clarify,   

“It should be acknowledged that cervical collar removal can result in neurological change and even paralysis, although this may be underreported in the literature. However we cannot continue indiscriminate two-stage sequential screening for C-spine injuries if the injury rate is near 0% for the first test and the second adjunctive test results in false positives and inconsistent treatment plans.”

But the real question that is more pertinent to us as EM physicians (obtunded MR’s are usually dealt with upstairs), is:  if we can remove the c-collars of obtunded patients after negative CT, why couldn’t that be extrapolated to awake patients?  Well, they commented on that too:   

“Therefore, if collars are to be removed in a high risk obtunded population […] cervical collar removal can be logically argued for any population-obtunded or not.” [2]

 They finally call for multicenter prospective research on the subject, again citing the low quality of evidence that they used for their recommendation. That call was answered in 2017 by the Western Trauma Association. The group completed a multi institution trial with 10,000 patients who were getting a CT for evaluation of cervical spine injury prospectively enrolled at 17 centers [3]. They found only 3 CT scans that missed clinically significant injury (.03%). All of those patients had focal neurological abnormalities on exam. There was no clinically significant injury missed by CT and exam combined. CT scan alone had an NPV of 99.97%, and an NPV of 100% when combined with clinical exam. Therefore, they proposed this diagnostic algorithm:


Most trials have found similar results, with a few exceptions. Two trials prior to the publication of the Western Trauma Association (WTA) paper found that CT missed a few clinically significant injuries in patients with no neurological symptoms. Both trials enrolled significantly fewer patients than the WTA paper, and only enrolled patients with negative CT who would be evaluated with MR, meaning they couldn’t comment on the overall sensitivity of CT in unstable c-spine injury. The ReConect trial in 2016 found 5 of 767 patients (.6%) with injuries requiring surgical intervention that were missed on CT [4].  Another study with similar methods published in Annals of Emergency Medicine in 2011 evaluated those who had a negative CT but were MR’ed for persistent midline C-Spine tenderness [5]. They found that out of 178 patients, 5 had injury requiring operative management that was missed on CT but found on subsequent MR (2.8%) [5].  The Annals paper is certainly an outlier, with a considerably higher rate of missed clinically significant injury than the remainder of the literature, with rates usually between 0-1% [6-18]. The authors believe this may be due to more stringent methodology.  For instance, they required MR to be performed within 48 hours when it is the most sensitive for edema, and only enrolled patients with midline tenderness rather than subjective pain [5].  While this may be true, the results have not been replicated in subsequent studies.


With the publication of the WTA paper, evidence certainly seems to be tipping in favor of CT clearance of cervical spine in neurologically intact patients. However, a few questions remain. In every study discussed here, MR resulted in discharge with hard collar in a portion of patients. Indications ranged from stable injury to persistent pain with no evidence of injury on MR. It is unclear whether hard collar placement makes a difference in the clinical course of these patients, if their stable injuries would have become unstable without it, or if it has any long term impact on outcomes such as chronic pain. This is an important question not yet adequately addressed in the literature.  The majority of these trials were also completed at trauma centers with radiologists well trained in reading c-spine imaging and high quality CT scanners. It could be difficult to generalize this data to centers with older scanners or whose radiology departments are not as expert in trauma radiology.

Incredibly high quality and reproducible evidence is required to change practice when high stakes, such as potentially missed cervical spine injury, are involved. So far we have multiple trials showing an NPV of close to 100% when CT and good neurological exam are combined, and the conditional recommendation by the EAST group. Time will tell if recommendations in the future remove the “conditional” portion as CT technology continues to improve, further studies with stringent methodologies are conducted, and the results of the WTA paper are hopefully replicated.

Expert Commentary

Thank you Dr Whipple for that really practical review of a real-life common clinical question we face all the time: Can we remove the collar?  Some important takeaways are:

  1. There is a robust and growing body of evidence that removing the collar after a negative high-quality CT is safe if the patient is neurologically intact.

  2. This practice is endorsed by two major trauma organizations, EAST and WTA. 

The endorsement by respected major trauma societies is important in translating evidence into practice.  It seems like all that is left at this point for widespread implementation is overcoming culture.  This would likely require addressing the outlier studies listed by Dr Whipple to win over those still skeptical.  Part of overcoming culture would involve buy-in from neurosurgical societies.  What do neurosurgical societies say regarding clearing these patients?  There are many instances in which a patient is discharged with recommendations from the neurosurgeon to wear a hard collar despite a negative CT and MRI.  On the surface this seems like defensive medicine and impractical for the patient.  Is the patient really going to comply with this until follow up?  Is this collar really protecting them and preventing further injury which, after negative CT and MRI and with a normal neuro exam, seems exceedingly unlikely?  Does evidence support this practice?

In the end, decision rules should be used when you want evidence to support your clinical decisions, such as removing the C collar after negative imaging in a neurologically intact patient.  Do not use decision rules, however, to overturn or replace sound clinical judgement.  If there is something about a case that makes you still feel like you could be missing an outlier injury by removing the collar, listen to that voice inside of you. It is that sound clinical judgement that will guide you through your career, not decision rules.

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Matthew Levine, MD

Northwestern Medicine, Assistant Professor of Emergency Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Whipple T, Reuter Q. (2019, May 13). C-spine clearance with negative CT: Are we there yet? [NUEM Blog. Expert Commentary by Levine M]. Retrieved from

Other Posts You May Enjoy


  1. American College of Radiology. ACR appropriateness criteria on suspected spine trauma. Available at:

  2. Patel MB, et al. Cervical spine collar clearance in the obtunded adult blunt trauma patient: A systematic review and practice management guideline from the Eastern Association for the Surgery of Trauma. J Acute Care Trauma Surgery. 789(2): 432-441.

  3. Inaba, K et al. Cervical Spine Clearance: A Prospective Western Trauma Association Multi-Institutional Trial. J Trauma Acute Care Surg. 2016 Dec: 81(6): 1122-1130.doi: 10.1097/TA.0000000000001194

  4. Maung A, et al. Cervical spine MRI in patients with negative CT: A prospective, multicenter study of the Research Consortium of New England Centers for Trauma (ReCONECT). J Trauma Acute Care Surg. 82 (2): 263-269.

  5. Ackland HM, et al. Cervical Spine Magnetic Resonance Imaging in Alert, Neurologically Intact Trauma Patients With Persistent Midline Tenderness and Negative Computed Tomography Results. Ann of Em Med. 2011 Dec. 58 (6): 521-530.

  6. Chew B, et al. Cervical spine clearance in the traumatically injured patient: is multidector CT scanning sufficient alone? J Neurosurg Spine. 2013. 19: 576-581

  7. Bush L, et al. Evaluation of cervical spine clearance by computed tomographic scan alone in intoxicated patients with blunt trauma. JAMA Surg. 2016; 151 (9): 807-813

  8. D’Alise  et al. Magnetic resonance imaging for the evaluation of the cervical spine in the comatose or obtunded trauma patient. J Neurosurgery  (Spine 1) 1999; 91:54-59.

  9. Resnick S, et al. Clinical relevance of magnetic resonance imaging in cervical spine clearance: a prospective study. JAMA Surg. 2014; 149 (9): 934-9.

  10. Menaker J, Philp A, Boswell S, Scalea TM. Computed tomography alone for cervical spine clearance in the unreliable patient--are we there yet? J Trauma. 2008; 64(4):898–903.

  11. Chew BG, Swartz C, Quigley MR, Altman DT, Daffner RH, Wilberger JE. Cervical spine clearance in the traumatically injured patient: is multidetector CT scanning sufficient alone? Clinical article. J Neurosurg Spine. 2013; 19(5):576–81.

  12. Como JJ, Leukhardt WH, Anderson JS, Wilczewski PA, Samia H, Claridge JA. Computed tomography alone may clear the cervical spine in obtunded blunt trauma patients: a prospective evaluation of a revised protocol. J Trauma. 2011; 70(2):345–9. discussion 9-51.

  13. Khanna P, Chau C, Dublin A, Kim K, Wisner D. The value of cervical magnetic resonance imaging in the evaluation of the obtunded or comatose patient with cervical trauma, no other abnormal neurological findings, and a normal cervical computed tomography. J Trauma Acute Care Surg. 2012; 72(3):699–702.

  14. Schuster R, Waxman K, Sanchez B, Becerra S, Chung R, Conner S, Jones T. Magnetic resonance imaging is not needed to clear cervical spines in blunt trauma patients with normal computed tomographic results and no motor deficits. Arch Surg. 2005; 140(8):762–6.

  15. Anekstein Y, Jeroukhimov I, Bar-Ziv Y, Shalmon E, Cohen N, Mirovsky Y, Masharawi Y. The use of dynamic CT surview for cervical spine clearance in comatose trauma patients: a pilot prospective study. Injury. 2008; 39(3):339–46.

  16. Brohi K, Healy M, Fotheringham T, Chan O, Aylwin C, Whitley S, Walsh M. Helical computed tomographic scanning for the evaluation of the cervical spine in the unconscious, intubated trauma patient. J Trauma. 2005; 58(5):897–901.

  17. Harris TJ, Blackmore CC, Mirza SK, Jurkovich GJ. Clearing the cervical spine in obtunded patients. Spine (Phila Pa 1976). 2008; 33(14):1547–1553.

  18. Steigelman M, Lopez P, Dent D, Myers J, Corneille M, Stewart R, Cohn S. Screening cervical spine MRI after normal cervical spine CT scans in patients in whom cervical spine injury cannot be excluded by physical examination. Am J Surg. 2008; 196(6):857–862.

Posted on May 13, 2019 and filed under Trauma.

Anticoagulation in Distal DVT

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Anticoagulation in Distal DVT

Written by: William LaPlant, MD (NUEM PGY-3) Edited by: William Ford, MD (NUEM PGY-4) Expert commentary by: Kelsea Caruso, PharmD

Currently there is significant heterogeneity in the treatment of distal deep vein thromboses (DDVTs), which are DVTs that occur distal to the popliteal fossa. What is the best course of action when a reasonably healthy patient has a new calf DVT?

The CACTUS trial was a randomized, placebo-controlled, double-blinded trial prospectively assessing anticoagulation for calf DVTs [1]. Notably, the trial was met with slow enrollment resulting in termination of the study prior to enrollment of the prespecified sample size, meaning that it was underpowered to detect a significant difference between the groups. It only enrolled about half of the participants it had intended to, with an initial 90% power to detect a 70% risk reduction in the composite outcome: development of a proximal DVT or symptomatic PE by day 42. This power study assumed a 10% incidence of the primary outcome in the placebo group.


As you can see, in both groups the progression to proximal DVT or PE was quite low. As there were only 12 total composite events (DVT extension, PE), making a comparison between groups with any degree of certainty impossible. This study met neither their enrollment goals (only enrolling half the participants) nor the predicted incidence of the composite outcome (half the projected amount), so it was quite significantly underpowered to detect a difference.

Notably, the study also did not enroll pregnant women, patients with a previous DVT, recent PE, or recent malignancy. These patients were likely not enrolled due to their higher risk of progression, which may have biased the results towards treatment. As such, the results of this trial could never be applied to these groups.

Unfortunately, given the slow recruitment in the CACTUS trial as well as the low event rate of the composite outcome, the likelihood that this will be studied again in a prospective, double-blinded manner is unlikely. As such, we will need to put the CACTUS trial into context of retrospective evidence to try to identify an ideal practice pattern.

With regard to the retrospective data available:

In a 2016 metanalysis, the incidence of PE from DDVT was 0% to 6.2% [median 1.1%] [2], which is in line with the results from the CACTUS trail. As you can see in the chart below, there is some heterogeneity to the results, likely due to the wide variety in study methodology.

Based on the above evidence, what are the best management options? A recent review article (which includes data from CACTUS) offers two suggestions [3]:

  1. The most conservative management will still be anticoagulation of the isolated DDVT. This should be standard for patients with cancer or other pro-thrombotic state that would place the patient at high risk for the development of DVT.

  2. Deferred anticoagulation with follow up ultrasound can be used for patients without significant thrombotic risk factors. You can engage in shared decision making and discuss the risks for bleeding in your patient against the 4-5% risk for clot progression and 1% risk for PE (based on the CACTUS trail as well as retrospective data).

If you decide against anticoagulation in the emergency department, follow up imaging would be recommended in 1-2 weeks to evaluate for progression. This tight follow up window would help to ensure clot progression is identified early and would allow the patient to readdress anticoagulation with his/her primary care physician.

Expert Commentary

Thank you for this really great summary! I think you are bringing up a dilemma that we see quite often in the Emergency Department and one that, unfortunately, still doesn’t have much data to help guide our treatment recommendations. The CHEST guidelines for VTE disease were most recently updated in 2016 and do not include the results of the CACTUS trial or the results of the mentioned meta-analysis. Their recommendation is to treat an unprovoked DVT (distal or proximal) with anticoagulation for at least 3 months.

 The CACTUS trial questioned if this is required for all patients, primarily focusing on those with an isolated calf DVT. The CACTUS trial had some interesting results, but, like you mentioned, a huge patient population was excluded.. We can only extrapolate this data to a very small group of people: young (average age ~50 years old in the trial), healthy and without any risk factors for VTE. Also, the study drug utilized in the trial was nadroparin, a low molecular weight heparin, which is not available in the US. It would have been more applicable to clinical practice if this trial had utilized a direct-oral anticoagulant like rivaroxaban or apixaban. If these were used the safety results could have potentially been reduced.

So the question remains… to anticoagulate or not to anticoagulate? Here are my final thoughts:

  1. The patients you can think about deferring anticoagulation are those without any VTE risk factors (cancer, obesity, immobility, those on estrogen therapy etc.).

    • As mentioned, this should be a discussion with the patient so they understand the risk of deferring anticoagulation. They should have adequate follow-up and understand the signs and symptoms of a pulmonary embolism.

  2. The patients that should be anticoagulated are those that have any risk factor for VTE or patients from the previous point that choose treatment.

    • The anticoagulant should be selected by keeping patient specific factors in mind like past medical history, renal function and current medications

    • Unlike the CACTUS trial, try and prescribe oral therapy. Your patients will thank you if they don’t have to inject themselves daily.

kelsea caruso.png

Kelsea Caruso, PharmD

Emergency Medicine Clinical Pharmacist

Northwestern Memorial Hospital

How To Cite This Post

[Peer-Reviewed, Web Publication] LaPlant W, Ford W. (2019, May 6). Anticoagulation in distal DVT. [NUEM Blog. Expert Commentary by Caruso K]. Retrieved from

Other Posts You May Enjoy


  1. Righini M, Galanaud J, Guenneguez H, et al. Anticoagulant therapy for symptomatic calf deep vein thrombosis ( CACTUS ): a randomised , double-blind , placebo-controlled trial. 2017;3(December 2016). doi:10.1016/S2352-3026(16)30131-4.

  2. Wu AR, Garry J, Labropoulos N, Brook S. Incidence of pulmonary embolism in patients with isolated calf deep vein thrombosis. J Vasc Surg. 2016;5(2):274-279. doi:10.1016/j.jvsv.2016.09.005.

  3. Robert-ebadi H, Righini M. Management of distal deep vein thrombosis ☆. Thromb Res. 2017;149:48-55. doi:10.1016/j.thromres.2016.11.009.

Posted on May 6, 2019 and filed under Hematology.

Ultrasound in Pediatric Distal Forearm Fractures

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Written by: Jason Chodakowski, MD (NUEM PGY-3) Edited by: Logan Weygandt, MD (NUEM ‘17) Expert commentary by: Rachel Haney, MD (NUEM ‘17)

Why use Ultrasound?

Distal forearm fractures are common fractures in the pediatric population. Although plain radiographs of the forearm are still considered the gold standard for definitive diagnosis, there is growing interest in using ultrasound for diagnosis because it provides zero radiation exposure, it can be used to guide local pain control, and it can confirm reduction success at the bedside. Ultrasound is easy to teach and provides value under circumstances when plain radiography might be unavailable (pre-hospital environment, disaster areas, or in developing countries).

A recent meta-analysis of 12 studies, which included 951 children 18 and younger, found that physician performed bedside ultrasound detected distal forearm fractures with a pooled sensitivity of 98% and a specificity of 96% when compared with the gold standard plain radiographs.[1] The pain associated with ultrasound use was also significantly less.[2]


How do I use Ultrasound?

To evaluate musculoskeletal pathology use the high-frequency linear array transducer employing the six-view ultrasound technique as shown below. You may detect a fracture as an apparent discontinuity or irregularity (divots, step-offs, distortion) of the hyperechoic and continuous bony cortex. Disruptions as small as 1mm can be detected.

Six-view technique (Herren et. al. 2015)

Six-view technique (Herren et. al. 2015)

Normal Cortex (Crosby et. al. 2014)

Normal Cortex (Crosby et. al. 2014)

Distal radius fracture (

Distal radius fracture (

Distal radius fracture (

Distal radius fracture (


In children the evaluation of bones is complicated by the open physes, which may be mistaken for fractures. The difference is that physes will appear as smooth, downward-sloping curves unlike fractures, which will have abrupt step-offs.

Normal open tibial physis (Crosby et. al. 2014)

Normal open tibial physis (Crosby et. al. 2014)

What else is Ultrasound Good For?

  • Confirming reductions

    Ultrasound is also utilized by emergency physicians to determine successful realignment of pediatric distal forearm fractures after closed reduction.[4]

Fracture reduction (Socranksy et. al. 2016)

Fracture reduction (Socranksy et. al. 2016)

  •  Achieving adequate pain control

    Ultrasound can also be used to guide hematoma blocks. The hematoma block is a technique wherein the physician injects an anesthetic solution into the hematoma between the fractured bone fragments (see image below). It has been shown to be effective, safe, faster, and uses fewer resources with no significant difference in pain scores when compared to procedural sedation in both adults and children with distal forearm fractures.[6,7]

Clean skin and place a sterile cover over the transducer. Using 5-10cc of 1-2% lidocaine inject into the hematoma between the fractured bone fragments using an 18-22 gauge needle.

Visualization of needle (N) entering between fracture bone fragments (U) (

Visualization of needle (N) entering between fracture bone fragments (U) (

Take Home Points

  • Ultrasound is most useful in evaluating long bone fractures such as the femur, clavicle, ribs, or distal radius and ulna.

  • A reliable alternative to the plain radiograph is the proper six-view method it, with the advantages of being portable and radiation-free.

  • Ultrasound can also be reliably used to confirm fracture reduction, as well as for guiding forearm fracture hematoma blocks. 

Thank you for providing a concise summary of the utility of Point-of-care Ultrasound (POCUS) for pediatric forearm fractures.  

I’d like to mention a few key points regarding the use of POCUS for pediatric fracture assessment.

  • If you do a lot of adult scanning and not much pediatric scanning it is important to keep in mind that children may not be as cooperative (or stationary) as adults.

    • Smaller children may be afraid of the transducer therefore introducing the transducer to the patient as an object that will not hurt them is key. You should hand the probe to the patient, allow them to touch it and even scan themselves initially in order to get them more comfortable with the probe.

  • While the 6-view scan you describe will certainly improve sensitivity, adequate sensitivity can be achieved with a 2-view approach. Additionally, the 6-view technique may be prohibitively time-intensive in a busy Emergency Department.

    • In order to increase sensitivity with the 2-view approach, always start imaging at the point of maximal tenderness, initially in the longitudinal plane with the cortex of the bone parallel to the probe surface. Slide distal and proximal to the point of tenderness. Then rotate the probe 90 degrees to view the cortex in the transverse plane. Fractures are noted as cortical disruptions or step-offs. Fractures are most visible on POCUS when the fracture line is perpendicular to the angle of insonation.

  • Another key pearl is to use copious gel in order to optimize the focal point of the image. The focal zone on the screen is the part of the image with the highest resolution secondary to convergence of the US beams. The focal point can be changed depending upon your machine, but is typically no more shallow than about 1-cm below the probe surface, therefore if you place a good layer of gel about 1cm thick, you will place the cortext of the bone at the optimal focal point. Using copious gel is also important in reducing any potential discomfort caused by pressure from the probe.

    • If gel is a limited resource, you can use a water bath as well.

  • While POCUS is a wonderful tool, especially for fracture detection, I want you to keep in mind that the sensitivity of POCUS for fractures is the highest (low-mid 90s) for the diaphysis of long bones (femur, humerus, radius and ulna). Sensitivity is significantly lower for detecting fractures of other bones and fractures near joint lines secondary to the curvilinear nature of the metaphysis as well as the presence of cartilaginous epiphyseal plates in children.

    • While POCUS can supplant the use of radiography in austere environments, in a well-resourced emergency department, POCUS should be an adjunct to radiography. In this setting, POCUS can have utility in patients in whom you suspect occult fracture despite negative XRs or for real-time fracture reduction assessment before sedation wears off. Unless you are a pediatric POCUS expert, I would order XR’s as usual for a pediatric patient you suspect has a fracture. In the meantime- continue scanning patients with normal anatomy and documented fractures in order to develop your POCUS expertise! Happy Scanning!


Rachel Haney, MD

NUEM ‘17

Ultrasound Fellow at Massachusetts General Hospital

How To Cite This Post

[Peer-Reviewed, Web Publication] Chodakowski J, Weygandt L. (2019, April 28). Ultrasound in pediatric distal forearm fractures. [NUEM Blog. Expert Commentary by Haney R]. Retrieved from

Other Posts You May Enjoy


  1. Douma-den Hamer, Djoke, et al. "Ultrasound for Distal Forearm Fracture: A Systematic Review and Diagnostic Meta-Analysis." PloS one 11.5 (2016): e0155659.

  2. Chaar-Alvarez FM, Warkentine F, Cross K, et al. Bedside ultrasound diagnosis of nonangulated distal forearm fractures in the pediatric emergency department. Pediatr Emerg Care 2011; 27:1027.

  3. Herren C, Sobottke R, Ringe MJ, et al. Ultrasound-guided diagnosis of fractures of the distal forearm in children. Orthop Traumatol Surg Res 2015; 101:501.

  4. Dubrovsky, Alexander Sasha, et al. "Accuracy of ultrasonography for determining successful realignment of pediatric forearm fractures." Annals of emergency medicine 65.3 (2015): 260-265.

  5. Socransky, Steve, et al. "Ultrasound-Assisted Distal Radius Fracture Reduction." Cureus 8.7 (2016).

  6. Fathi, M. et al. Ultrasound-guided hematoma block in distal radius fracture reduction: a randomized clinical trial. Emerg Med J. 2014 Jul 12.

  7. Bear, David M., et al. "Hematoma block versus sedation for the reduction of distal radius fractures in children." The Journal of hand surgery 40.1 (2015): 57-61.

Posted on April 29, 2019 and filed under Ultrasound.

Top 5 Blog Posts of 2018

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As the long and cold Chicago winter wanes and Spring begins, let’s take a look at the most popular NUEM blogs from 2018. While we value all of our residents’ and experts’ hard work, we are highlighting these 5 posts which earned the most pageviews in calendar year 2018:

5) Auricular Hematoma Drainage

Andrew Berg, Elizabeth Byrne, and Chris Beach take us through the intimidating but fortunately uncommonly needed auricular hematoma drainage.

4) Hand Exam

Terese Wipple, Victor Gappmaier, and Avi Giladi (current Hand surgeon and my former college roommate who got me through organic chem) provide a usable guide to both basic and comprehensive hand exams, and important and common test for an important body part. You’ve really got to respect what they did here.


3) Beta Blocker Toxicity

Spencer Lang, Rachel Haney, and Patrick Lank review beta-blocker toxicity, including but far from limited to the fancier topics of high insulin euglycemic therapy and intralipids.

2) Migraine Cocktail

Headaches can be, well, a headache in the ED. Vidya Eswaran and Danielle Miller put together a comprehensive and digestible infographic collating key points of ED headache management, replete with tips & references. Also fun for me to have space to rant about my practice.


1) HiNTS Exam

Dizziness is one of the most frustrating entities we see in EM, with a handful of needles in a frustrating haystack with few tools to separate the two without turning our hospitals into full time MRI centers. The HiNTS exam gained popularity in the past few years, but has important limitations: easily applied to the wrong dizzy patients and can also be technically difficult to perform in already-dizzy patients. Will LaPlant, Mitali Parmar and Phillip Chang give a comprehensive but concise review of the key points – including how to document your findings. A well-deserved top spot for 2018, and sorry everyone, but it wasn’t even close.


Seth Trueger, MD, MPH, FACEP

Assistant Professor, Emergency Medicine Northwestern University


Posted on April 22, 2019 and filed under Top 5 2018.


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Written by: Alex Ireland, MD (NUEM PGY-3) Edited by: Gabrielle Ahlzadeh, MD (NUEM PGY-4) Expert commentary by: Gary Lissner, MD

Expert  Commentary

The author has written an excellent illustrated review of the technique of lateral canthotomy and cantholysis for traumatic orbital compartment syndrome due to a significant retrobulbar hemorrhage. As with any procedure it is crucial to understand the indications and contraindications of the procedure. In these cases, the indication is the saving or restoring of vision lost due to excessive intraorbital pressure, and the contraindication is generally an opened globe.  This is a difficult situation because there is usually limited information and there is a limited amount of time to relieve the orbital compartment syndrome. The timing of the onset of the retrobulbar hemorrhage that created the critical pressure to cause loss of vision is often unknown.  The decision to decompress is usually based solely on a clinical examination without having time to obtain orbital radiologic studies and before an ophthalmologist can arrive to evaluate the patient. However, the clinical exam could be limited if the patient is not cooperative or is not conscious.

Initially a determination has to be made if the globe is lacerated or ruptured which could preclude the performance of the canthotomy and cantholysis .  Either a ruptured globe or an orbital compartment syndrome can cause loss of vision.  A ruptured globe can occur along with a retrobulbar hemorrhage. If the eyeball is opened, no additional external pressure should be placed on the lids or globe in order to prevent additional damage to the eye. An opened globe could be determined by seeing a laceration of the globe, seeing protruding intraocular contents, finding a very soft eye, and/or finding a distorted eye. If the eyeball is opened, a sturdy shield should be placed resting on the surrounding orbital bone to protect the eye from external pressure, and the aide of an ophthalmologist should be sought.

If it is determined that the globe is intact, a decision has to be made on clinical examination findings if a significant retrobulbar hemorrhage exists that would create enough pressure in the orbit to cause  loss of vision. There is usually not enough time to wait for imaging studies to be done. The trauma could create a large enough orbital fracture that could decompress the orbital pressure and the orbital compartment syndrome. On the other hand, an orbital fracture can create orbital emphysema. Blowing of the nose by the patient can increase the emphysema and further increase the intraorbital pressure, creating a sight-threatening orbital compartment syndrome.  

Acute vision loss is the key clue to a significant orbital compartment syndrome, but many trauma patients may not be able to cooperate for visual testing.  The reaction of the pupil to light can be used as a sign of visual loss even in the uncooperative patient. With an orbital compartment syndrome, the pupil of the involved eye will not react well to a bright light and will have an afferent defect. However, if the patient was given narcotics the pupils can become miotic and pupil testing becomes difficult.  Visual loss is not diagnostic of an orbital compartment syndrome because the trauma can create other damage that can cause visual loss including intraocular bleeding, retinal disorders, traumatic optic neuropathy, or a lacerated or ruptured globe.  Trauma can cause edema and ecchymosis of the lids, but tense proptosis with very firm retropulsion of the involved eye is a key diagnostic finding of a significant retrobulbar hemorrhage. As the orbital bleeding continues, the eye is pushed forward against the tight eye lids and the intraocular pressure increases.  A significant intraocular pressure increase can be used as another sign of an orbital compartmental syndrome.  Checking the intraocular pressure can be difficult in the presence of massive eyelid swelling.  Pulling the lids opened especially if the patient is squeezing can transmit the external pulling pressure to the eye, creating a false reading of a raised intraocular pressure.  Using curved instruments, or the blunt end of bent paper clips as shown by the Blog’s author, can help open the lids. Using a topical anesthetic to reduce eye discomfort, or using injectable local anesthetic to relax the orbicularis muscle action can also help to more easily open the eyelids to obtain a more accurate intraocular pressure. Orbital compartment syndrome will limit extraocular motility on the involved side, but the unconscious patient’s motility cannot be easily tested. A significant increase of the orbital pressure and the intraocular pressure can cause pulsation of the retina arteries and full retina veins which can help with the diagnosis of an orbital compartment syndrome if the fundus is viewed.

The Blog gives a precise pictorial and written description of the lateral canthotomy and cantholyisis technique.  However, unlike the author’s demonstration photos, most cases with significant traumatic orbital compartment syndrome have massive lid ecchymosis and subconjunctival hemorrhage and a proptotic  eye that is pushed forward tightly against the lids. Therefore, there is frequently little room to insert the instruments at the lateral canthal angle. Extreme care must be taken to avoid unwanted damage.  The author’s “tip” to insert a Morgan lens (a sclera shell if available can also be used) onto the patient’s eye is a good idea to help protect the eye, but the tight space in some cases can prevent the insertion of the lens.  It is important that when working in the  tight space to always work with the instruments pointing away from the eye and orbit to prevent injury to the globe, lateral rectus, lacrimal gland, or deeper orbital tissues.  Always aim anteriorly toward the anterior orbital boney rim during the canthotomy.  As the author suggests, the lids should be pulled or lifted away from the eyeball. Pulling the eyelid nasally and anteriorly helps tighten the crus of the lateral canthal tendon, thus making it easier to feel or strum the crus and cut it during the cantholysis. Always keep the tip of the scissors pointed away from the globe.

An orbital compartment syndrome can also occur with retrobulbar hemorrhage after surgery in the region. In such cases it can be advisable to first open the surgical wounds to determine if release of blood and clots from the depths of the wounds relieves the problem and thus eliminating the need for the canthotomy and cantholysis.  In cases of retrobulbar hemorrhage after sinus or nasal surgery, the removal of nasal or sinus packing could release the blood and relieve the orbital compartment syndrome.

The Blog’s author presents a good list of potential complications from the canthotomy and cantholysis procedure. Many of the patients with significant retrobulbar hemorrhage are elderly patients who fall on their face.  This group of patients can be on anticoagulants that could have potentiated the initial orbital hemorrhage and could create a problem of continued bleeding. The patients have to be observed after the canthotomy and cantholysis for continued or recurrent orbital bleeding and also for the possibility of a newly created surgical site eyelid bleeding that may not stop spontaneously. Additional surgery could be needed to stop the bleeding.  Also to be considered as a complication is the fact that the release of the lateral canthal tendon lid support could cause lower lid ectropion, lid retraction, or lateral canthal deformity. Such deformities sometimes have to be surgically repaired.

In conclusion, the author has written a Blog which gives an excellent guide to perform a canthotomy and cantholysis.  It can be difficult to make the decision if the procedure is needed to be done to prevent permanent loss of vision of an eye. The decision has to be based on clinical examination findings and the procedure if needed should not be delayed. After the procedure the patient needs to be observed and to have an evaluation by an ophthalmologist.


Gary S. Lissner, MD

Associate Professor, Chief Ophthalmic Plastics Service, Department of Ophthalmology, Northwestern University Feinberg School of Medicine



  1. Yung CW, Moorthy RS, Lindley D, Ringle M, Nunery WR.  Efficacy of lateral canthotomy and cantholysis in orbital hemorrhage.  Ophthalmic Plast Reconstr Surg. 1994 June; 10(2):137-41.

  2. Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D.  Orbital compartment syndrome: the ophthalmic surgical emergency.  Surv Ophthalmol. 2009 Jul-Aug; 54(4): 441-9.

  3. Kent TL, Morris CL, Scott IU, Fekrat S. Evaluation and management of orbital hemorrhage.  Eye Net magazine. 2018 July.

  4. Jaksha AF, Justin GA, Davies BW, Ryan DS, Weichel ED, Colyer MH. Lateral canthotomy and cantholysis in operations Iraqi Freedom and Enduring Freedom: 2001-2011.  Ophthalmic Plast Reconstr Surg. 2018 Jul 3. [Epub ahead of print].

How To Cite This Post

[Peer-Reviewed, Web Publication] Ireland A, Ahlzadeh G. (2019, April 15). Canthotomy [NUEM Blog. Expert Commentary by Lissner G]. Retrieved from

Other Posts You May Enjoy


Posted on April 15, 2019 and filed under Ophthalmology.

Pediatric ECMO: Beyond the Basics of Pediatric Resuscitation

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Written by: Steve Chukwulebe, MD (NUEM PGY-4) Edited by: Spenser Lang, MD (NUEM ‘17) Expert commentary by: Leah Harris, MD and Kiona Allen, MD


A 38-year-old G8P6 female at 39-weeks gestation presents to your emergency department in active labor. The patient has gotten all her prenatal care at your institution, but has not made it to her due date. She reports her water breaking about 2 hours ago. She describes that the ruptured fluid was not clear but dark yellow/green, and she is now experiencing contractions every 2 minutes.

Your bedside doppler reveals reassuring fetal heart tones at a rate of 152. On your initial exam, the cervix is fully dilated and effaced…and you see the baby’s head.  As your obstetric colleagues are several minutes away, you check your pulse, dust off the radiant warmer, and prepare your resources for an ED delivery. 

The mother delivers within the next few minutes with your OB colleagues still en-route. While she has minimal complications, the newborn is now not doing as well.


Neonatal Exam

Constitutional: Full term boy, covered in meconium

Skin: Appears blue gray, cool to touch

Respirations: For the most part apneic and at times grunting

CV: Heart rate 100

Tone: Flaccid


You take over the resuscitation of the neonate immediately as he is delivered given the above exam. Attempts at stimulation, drying, oral suctioning, and warming still yields a 1-minute APGAR of 3.



As per the algorithm below, with continued apnea and SpO2 in the 50’s you begin positive pressure ventilation and continued stimulation [1]. At 15 minutes, despite your attempts with continued PPV, suctioning, and stimulations, the SpO2 continues to be in the 60’s and the heart rate begins trending towards from 100 to the 60’s as well. You decide to intubate the patient, and the tube is passed successfully. Tube placement is confirmed and the x-ray shows fluffy infiltrates bilaterally in both lung fields but no evidence of barotrauma. Attempts at bagging yields minimal resistance, however the highest SpO2 the patient reaches is in the low 80’s at 40 minutes, with improved heart rate to the 120’s. At this point, your pediatric colleagues have found their way to the ED and are ready to take the neonate to the NICU. Two hours later into your shift, you read that the neonate was placed on veno-venous extracorporeal membrane oxygenation (ECMO) and is doing better. After your shift is over, you find your way over to the NICU and you see a pink sedated baby under a radiant warmer and connected to a large ECMO circuit.


Diagnosis: meconium aspiration syndrome complicated by pulmonary vascular hemorrhage and ARDS.  

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Had this neonate been in your ED, and your resuscitative measures have been exhausted, at what point do you consider ECMO in the neonatal or pediatric patient?  I will review briefly the emergence of ECMO in the neonatal and pediatric literature, as well as its indications and the limited data on its utility in the emergency department setting.


From theory to practice

The first cardiac bypass circuit was created by John Gibbon in 1936 in the operating suite. ECMO is defined as a mechanical circuit outside the body where blood oxygenation and carbon dioxide removal can occur for patients with reversible cardiac or respiratory failure [2].  Through the 1950-1970s, many researchers studied various materials and techniques to further improve membrane oxygenation and attempted to increase the length of time a patient could remain on bypass. However, it was not until 1976 in which Bartlett et al. reported on the first neonate suffering from meconium aspiration syndrome to be successfully treated ECMO [3]. Since then, ECMO has grown and been used in various forms as treatment of respiratory failure in the neonatal and pediatric ICU settings.  ECMO is to be considered for any reversible pathologic process that is impeding adequate tissue oxygenation and ventilation.


Indications for ECMO in children


  1. Primary pulmonary hypertension of the newborn

  2. Meconium aspiration syndrome

  3. Persistent fetal circulation

  4. Congenital diaphragmatic hernia


  1. Respiratory failure

    1. Bronchiolitis

    2. RSV

    3. Pneumonia

    4. ARDS

    5. Aspiration

    6. Status asthmaticus

  2. Sepsis

  3. Cardiac arrest

    1. with reversible conditions or amenable to heart transplantation

    2. with favorable neurologic outcomes, some studies show better outcomes with CPR initiated in up to 95 minutes [5], key being excellent CPR with ETCO2 > 10 and early recognition and initiation of eCPR (extracorporeal cardiopulmonary resuscitation)

  4. Hypothermia (cold water drowning)


In general, pediatric ECMO has been found useful in the above settings, however Gehrmann et al. reviewed the indications across various institutions when patients have been refractory to medical therapies. These indications are shown in the table below.


ECMO comes in two types: venoarterial (VA) and venovenous (VV). While the early VA ECMO circuits utilized the roller pump to provide non-pulsatile flow of oxygenated blood, its limitations for infants included the necessity to cannulate the artery via either an open sternotomy or open cannulation of the carotids with the risk of losing a unilateral carotid artery due to ligation [4]. VV ECMO is the newer of the two modalities and rather than accessing a major vein and a major artery, the circuit requires access to either 2 major veins or a single major vein using a double-lumen catheter.  However, each modality has its associated risks and benefits as described in the chart below [2].

Outcome Data


Neonates generally have better survival and outcomes on ECMO than older children and adults. One single center retrospective study in the journal of pediatric critical care published that of the 264 neonates placed on ECMO, 211 (80%) survived to discharge and 10-year survival was 71% [5]. The study had 2 cohorts and followed both neonatal and pediatric patients, collecting both demographic and survival data from patients placed on ECMO from 1987 to December 2013. Of those neonates that were alive at 90 days, at a 10-year follow up (ie.10-year conditional survival) 93% were alive. Of the common indications for neonatal ECMO, the 90-day survival and 10-year conditional survival are as follows respectively:

  • meconium aspiration syndrome (99% and 100%)

  • congenital heart anomalies (58% and 86%)

  • congenital diaphragmatic hernia (68% and 74%)

  • neonatal infection (72% and 100%)

Furthermore, patients who underwent VV ECMO had better 90-day survival and 10-year conditional survival rates than VA ECMO, 92% vs. 69%, and 98% vs. 87% respectively.



The same study followed 136 pediatric patients as well showing that the 90-day survival rate was 66% (90 patients) and that the 10-year conditional survival rate was 89%.  The study divides the 90-day survival rates for ECMO by splitting it between pneumonia (bacterial, viral, and aspiration, 66, 76, and 83% respectively), other causes of sepsis (33%), trauma (100%), and other respiratory etiology (63%). Again, patients who underwent VV ECMO had better 90-day survival rates than VA ECMO, 78% vs. 50% respectively.

Other retrospective studies report similar survival rates to discharge when ECMO is used for severe respiratory failure, with rates from 39% to 83% depending on the pulmonary diagnosis, with status asthmaticus having survival rates of 83-100% on ECMO [2,6].


Data in ED

While data on emergency department utilization of pediatric ECMO is limited, one study mentions the outcomes from its two cases [7]. The first case was a 3-year-old previously healthy girl who presented with nausea and developed cardiogenic shock in the department from viral myocarditis. This patient was placed on ECMO in the ED and transferred to the cardiac intensive care unit. She was taken off the circuit after 4 days with improved contractility, and eventually discharged home 10 days later neurologically intact. The second case was similar in etiology: a 17-year-old male who presented in respiratory distress and suffered a PEA arrest. This patient achieved ROSC, was placed on ECMO in the ED and was eventually discharged home 31 days later with a favorable neurological outcome.



While some centers continue to grow their extracorporeal membrane oxygenation programs to expand their resuscitative efforts, still few places have the equipment to start the circuit or even at times an on-call staff to prime the machine. In general, few studies report the usage of ECMO in the emergency departments as a means for cardiopulmonary resuscitation of a reversible etiology, and only case reports exist in the pediatric literature. However, even if the ability to start neonatal/pediatric ECMO may not be ever be present in one’s emergency department, prompt recognition and early disposition to tertiary care centers that offer these services could potentially be lifesaving in many appropriate cases.

Expert Commentary

While ECMO (extracorporeal membrane oxygenation) may seem a foreign concept for ED management, it is important to recognize that as recently as the 2009 H1N1 epidemic, utilizing this intervention as a rescue therapy to treat acute severe hypoxic respiratory failure associated with influenza resulted in cases of ECMO initiation in emergency rooms across the world. Your review introduces meconium aspiration – a frequent clinical indication – as a platform to review this technology. Critical to the understanding of ECMO is first to be able to determine the appropriate candidates for this support, then to pick the correct mode (veno-arterial versus veno-veno) and to learn your own institution’s interpretations of inclusion and exclusion criteria.   For the purposes of this commentary, we will break down the review into five sections sections: types of ECMO, who goes on ECMO, how to measure and trend hypoxemia, what can you do in the ED to maximize success on ECMO and new advances in ECMO.

ECMO modes:

ECMO is temporary cardiopulmonary bypass used to support a patient with either heart or lung failure. Originally developed from modifications of cardiopulmonary bypass and subsequently adapted for prolonged support, an ECMO circuit has both an oxygenator and a pump and a rate by which the blood passes across the oxygenator filter and has carbon dioxide removed.   Children with heart or lung failure who do not respond to conventional medical therapies may be candidates for ECMO support. The ECMO circuit drains blood from the body, exchanges oxygen and carbon dioxide on the red blood cell, warms the blood and pumps it back into the body. Placing a child on ECMO allows time for the heart and/or lungs to improve or to serve as a bridge to other long-term extracorporeal support or transplant.

In this very simple model, the oxygenator functions as the lungs, the pump takes over the work of a beating heart and the flow of the blood across the oxygenator mimics a respiratory rate and removes the carbon dioxide. If a patient’s heart is still adequately functioning as a pump and the indications for ECMO are due to oxygenation and/or ventilation defects, then utilizing ECMO as an isolated pulmonary bypass is preferred and veno-venous cannulation is warranted. Blood is therefore removed from a vein, red blood cells are oxygenated and carbon dioxide removed, and then blood is returned to a vein for the heart to pump. This approach allows for an adequate mixed venous saturation and tissue oxygenation. More importantly it allows for the heart to perfuse the coronary arteries with antegrade flow, does not require that an artery be sacrificed for access, permits a pulsatile waveform to be sensed by organs and can often be performed with a single dual-lumen catheter.  Most frequent sites are internal jugular vein or femoral vein. Cannulation can be accomplished by either using 2 separate cannulae or by utilizing a dual lumen internal jugular cannula that spans from superior vena cava (SVC) to inferior vena cava (IVC) in order to remove blood via end and side ports in the cavae and return blood via a side port of the second lumen that is positioned in the right atrium and directed towards the tricuspid valve.

If the patient has had any indications of cardiac injury including but not limited to cardiac arrest, arrhythmias, severe pulmonary hypertension, or evidence of significant cardiac dysfunction, then venoarterial cannulation is indicated as the patient’s heart can no longer be relied upon to pump blood.

ECMO Candidates:

The review elegantly lists criteria for candidacy but there are few others to be considered including mediastinal masses with airway compression and complex airway disease. Usually ECMO is on stand-by for these cases in the operating room. 


Measurement of hypoxemia:

While many are using P/F ratio (as Steve commented on in his review), the gold standard remains calculating and trending oxygenation index as a surrogate marker for severity of hypoxemia. Patients with an OI > 25 x 6 hours are demonstrating refractory severe lung failure and should be considered for ECMO.


Pre-ECMO Studies:

If you have a patient scenario develop in the Emergency Department with a high likelihood of progression to ECMO, there are handful of tests/treatments to be ordered prior to initiating ECMO that will make the decision to proceed with ECMO easier for the inpatient team:

1.           Is there any evidence of a CNS abnormality or bleed? Order a head ultrasound on the infant or a head CT on the child if able – you want to rule out any CNS bleed that would be worsened by anti-coagulation.  

2.           Does the child have an underlying congenital heart lesion? Order an ECG and ECHO on every patient – you want to rule out any congenital cardiac lesions and to quantify pulmonary hypertension.

3.           Is there any evidence of pulmonary hypertension – regardless of whether this is acquired or idiopathic? If “yes” – then start iNO – you can presume that all mechanisms of respiratory failure are coupled with worsening pulmonary hypertension in the child.

4.           Order a type and screen and a CBC. While not ideal, a baby with a hemoglobin of 14 g/dL can be placed on a saline-primed ECMO circuit emergently with the recognition that this will dilute and drop their Hg and interfere with oxygen carrying capacity. For smaller children where the total volume of the ECMO circuit can exceed their own intravascular volume, best to be able to prime the ECMO circuit with blood before placing the patient on the ECMO pump.

New Advances in ECMO:

The ECMO world is pushing the envelope and recognizing that preventing deconditioning and minimizing de-recruitment of both lung tissue and muscle mass is key to recovery or to eventual organ transplantation. Centers across the US and Europe now have their patients walking on ECMO. Who knows, one may walk into an ER near you some day!!


Kiona Allen, MD

Assistant Professor of Pediatrics, Cardiology


Leah Harris, MD

Professor of Pediatrics, Pediatric Clinical Care

How To Cite This Post

[Peer-Reviewed, Web Publication] Chukwulebe S, Lang S. (2019, April 8). Pediatric ECMO: Beyond the basics of pediatric resuscitation [NUEM Blog. Expert Commentary by Harris L & Allen K]. Retrieved from

Other Posts You May Enjoy


  1.  Pediatrics AA, Association AH. Textbook of neonatal resuscitation. 2006.

  2. Gehrmann LP, Hafner JW, Montgomery DL, Buckley KW, Fortuna RS. Pediatric Extracorporeal Membrane Oxygenation: An Introduction for Emergency Medicine Physicians. J Emerg Med. 2015;49(4):552-60.

  3. Bartlett RH, Gazzaniga AB, Jefferies MR, Huxtable RF, Haiduc NJ, Fong SW. Extracorporeal membrane oxygenation (ECMO) cardiopulmonary support in infancy. Trans Am Soc Artif Intern Organs 1976;22:80—93.

  4. Mok YH, Lee JH, Cheifetz IM. Neonatal Extracorporeal Membrane Oxygenation: Update on Management Strategies and Long-Term Outcomes. Adv Neonatal Care. 2016;16(1):26-36.

  5. Alsoufi B, Osman A, Nazer R, et al. Survival outcomes after rescue extracorporeal cardiopulmonary resuscitation in pediatric patients with refractory cardiac arrest. J Thorac Cardiovasc Surg 2007; 134:952–9.

  6. Swaniker F, Kolla S, Moler F, et al. Extracorporeal life support outcome for 128 pediatric patients with respiratory failure. J Pediatr Surg. 2000;35(2):197-202.

  7. Nevet A, Polak T, Dagan O, Waisman Y. Extracorporeal Membrane Oxygenation as a Resuscitation Measure in the Pediatric Emergency Department. Isr Med Assoc J. 2015;17(10):639-41.

Posted on April 8, 2019 and filed under Pediatrics.

Visual Guide to Splinting

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Written by: Danielle Miller, MD (NUEM PGY-4) Edited by: John Sarwark, MD (NUEM ‘16) Expert commentary by: Matthew Pirotte, MD

Visual Guide to Splinting HR Simplified with Lines Trueger 5-2-19.jpg

Expert Commentary

Great work by the authors to create such a handy guide to splinting. Like so many procedures in the emergency department, splinting is like snowboarding – easy to learn difficult to master! My love for emergency ortho has led me to really work on my own splinting techniques and to have a healthy respect for this skill.

The only quibbles that I would have for the otherwise excellent chart (and they are minor) are the following:

1.           Mid-shaft humerus: Rare will the patient be who can manage this with just a sling. There is tons of painful fracture movement to deal with here. The appropriate splint (a coaptation splint) is extremely challenging to place but worth it for the patient with such a painful fracture

2.           Distal radius fractures: After reduction I really like a double sugar-tong splint as opposed to a single. I worry about elbow extension (even involuntary at night) degrading the integrity of my splint and therefore my reduction.

My biggest teaching point with respect to splinting in the ED is the under-appreciated art of molding splints. Getting the plaster or fiberglass correctly placed, padded, and wrapped is really the easy part. The emergency provider must grasp the critical orthopedic concept that “crooked splints make straight bones.” Your splint needs to be working for you not just sitting there observing! If you have made a reduction your splint generally needs to be keeping in in place. This sounds more complicated than it is, follow my 3-step plan to learn how to make and mold splints:

Step 1: understand the concept of a 3-point mold.

 The concept of the 3-point mold creates a fulcrum proximal to the fracture site and bends the splint to keep the reduction from falling away. The 3-point mold looks like this.

Credit: Orthobullets

Credit: Orthobullets

Sharp-eyed readers might have noted that this is a pediatric fracture but have no fear, the splinting and molding is very similar to that of an adult. As you can see above the splint needs to be pushed and molded while it dries to keep that distal fragment from falling back. Start going into rooms with ortho residents and you’ll grasp this concept very quickly.


Step 2: start doing your own distal radius fracture reductions and splinting

Quentin Reuter MD (NUEM ’18) splinting a DRF

Quentin Reuter MD (NUEM ’18) splinting a DRF

Unless there is nerve entrapment or some other complicating factor there is rarely a need to consult on DRF fractures in the emergency department. I basically taught myself to splint by really learning how to manage distal radius fractures. There are any number of high-quality videos out there. This is a good one that demonstrates my favorite molding technique as well. The nice thing about a DRF is that with a good hematoma block you can take the time to get it right. A pair of finger traps thrown in your shift bag is a good trick, they are a high-theft item so watch out for prowling residents. The nice thing about reducing DRFs is that you end up needing to place and mold a relatively complex splint. I like a double sugar tong followed by a good mold incorporating 3-points along with some mild flexion and ulnar deviation at the wrist. You also need to pay attention to what is going on at the elbow. Putting in all together for your mold you must manage the position of the elbow, wrist flexion, and wrist ulnar deviation all while putting good pressure on your mold points., It takes a bit of time to get right but your patients (and consultants) will thank you!

Step 3: build on what you’ve learned and apply it to other common fractures

Once you understand the principles of reduction, splinting, and molding you are ready to tackle a host of other fractures. Bimalleolar/trimalleolar ankle fractures, both bone midshaft forearm fractures in school aged kids, and boxer’s fractures are all great places to start. This is a fun and rewarding part of our practice that any emergency provider can do with a bit of practice.

Always remember to check and document your nerve function after splint placement!



Matthew Pirotte, MD

Assistant Program Director, Northwestern Emergency Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Miller D, Sarwark J. (2019, April 1). Visual Guide to Splinting [NUEM Blog. Expert Commentary by Pirotte M]. Retrieved from

Other Posts You May Enjoy

Posted on April 1, 2019 and filed under Orthopedics.

The Seriousness of Deliriousness: Delirium in the ED

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Written by: Nery Porras, MD (NUEM PGY-2) Edited by: Katie Colton, MD (NUEM PGY-4) Expert commentary by: Lee Lindquist, MD


Imagine: you arrive to your shift, surrounded by the beeping and buzzing of monitors, an intoxicated patient already on the bed in front of your computer.  You gamely walk in to the room of your first patient, a 74 year-old man for whom the tracking board reads “something is not right.”  You see a quiet, subdued elderly man who looks at first glance generally well.  The family member in the room starts talking immediately, concerned that something is just not right with this man – he seems depressed, and has been forgetting names.  As she talks you hear a commotion from the next room and poke your head around the divider to see if you can help.  There you see an older woman fighting with EMS and her EKG leads, surrounded by nurses trying to keep her from jumping off the stretcher.  These widely disparate presentations potentially represent ends of the spectrum of the important but often missed diagnosis of acute delirium.

Emergency physicians are trained in the diagnosis and initial management of life and limb-threatening medical conditions.  Delirium is an under-recognized but highly morbid condition that we are under-prepared to diagnose and treat in a busy ED.  Trained in pattern recognition, we currently lack an easy and reliable method to diagnose acute delirium.  The DSM-V identifies 5 key features that characterize this diagnosis:

  •  Disturbance in attention and awareness

  • Develops over a short period of time, represents a change from baseline, and tends to fluctuate during the course of the day

  • An additional disturbance in cognition

  • The disturbances are not better explained by another preexisting, evolving or established neurocognitive disorder

  • There is evidence that the disturbance is caused by a medical condition, substance intoxication or withdrawal, or medication side effect


What’s the big deal with a somewhat confused elderly patients?

As the US population ages, elderly Americans are becoming the predominant users of healthcare with over 20 million older American visits to the ED each year (Han, et al 2013); these older patients are preferentially affected by delirium.  One study notes delirium to be present in 8-17% of all elderly ED patients and in 40% of nursing home patients (Inouye 2014).  Acute delirium can be the presentation of potentially life-threatening conditions including metabolic derangements, sepsis, and hypoxia.  Interestingly one study showed that patients in their eighties with myocardial infarction are more likely to present with delirium than chest pain (Inouye 2014).   

The diagnosis of delirium itself confers morbidity beyond the underlying condition that it can reflect.  When comparing groups of elderly patients in the ED, those with delirium were found to be markedly more likely to die within 6 months than those without delirium – 36% versus 10%, respectively (Han 2013).  Another study found that elderly patients diagnosed with delirium had 12-month mortality of 10-26%, rates comparable to sepsis or acute MI (Gower 2012).  Despite the remarkable danger of this condition, emergency physicians are bad at making this diagnosis – per one report missing 57-83% of cases of delirium (Han 2013).


What does a patient with delirium look like?

The fluctuating presentation of delirium makes it difficult to recognize but we should be attentive to certain hallmarks, including alterations in attention and awareness and acute changes in cognition.  These can be associated with hallucinations or other perceptual disturbances.  Collateral information and family input can be critical in detecting changes from baseline function and cognition.  The more acute temporal course of delirium is important to distinguish from underlying dementia, which is itself one of the most important risk factors for delirium.  The most common presentation, the hypoactive form, is a quiet, subdued, withdrawn state. This is distinguished from the hyperactive form notable for hypervigilance, irritability and restlessness. Hypoactive and mixed-type deliriums are the most common presentations in the ED, representing up to 96% of acute cases in the ED (Han 2013). Unfortunately, the hypoactive form is both more commonly missed and associated with a worse prognosis (Inouye 2014).


So, how do I diagnose delirium? Can this be done in the ED? 

As the personal, medical, and financial risks of delirium are increasingly recognized, research has focused on creating better tools for recognition and diagnosis.  Traditionally this diagnosis has required an extended interview and evaluation, usually performed by a psychiatrist or geriatrician; these methods are rarely available in the ED or inpatient setting.  Inouye and her colleagues built upon the DSM definition of delirium to create the Confusion Assessment Method (CAM) tool to quickly and easily screen for delirium.  

The CAM algorithm for diagnosis of delirium, using standardized psychiatric evaluation for delirium for validation, showed a sensitivity of 94%-100% and a specificity of 90%-95% for the diagnosis of delirium (Inouye 1990).  The CAM was later adapted and validated for use in the ED (Lewis 1995) and most recently that CAM has been modified to be even more ED friendly.  In 2013 the Geriatric Emergency Department Guidelines were put together by ACEP, SAEM, AGS (American Geriatric Society) and ENA (Emergency Nurses Association in which they delineate a real-world adaptation of the CAM, the bCAM. In conjunction with the Delirium Triage Screen, these two tools are quick, easy and practical method of assessing for delirium in the ED.  

What should be in your differential diagnosis when you suspect delirium?

 You have made the step of recognizing that your elderly patient is off their baseline; what should you consider as part of your work-up?  Consider the acronym “I WATCH DEATH” (below), a helpful reminder of the broad (and overlapping) differential of diagnoses that exist for acute delirium.  For a more nimble tool particularly useful in the ED evaluation of the delirious elderly patient, the “ABCDEF” acronym (below) was developed by Rosen et al (Rosen 2016) to identify overlooked precipitating causes.



What can I do to acutely de-escalate a delirious patient?

As always, consider non-invasive measures first – recruiting family for this can be critical.  Alleviating pain and discomfort and frequent re-orientation can help calm an acutely agitated patient.

Pharmacological interventions should be reserved for the agitated patient with overt psychotic manifestations. The use of restraints should be avoided if possible as the use of restraints themselves can worsen delirium. If medications are required, low doses of haloperidol of 0.5-1 mg can be used, although caution must be exercised with regard to QTc prolongation in patients with polypharmacy (Gower 2012).  Atypical antipsychotics can be considered as well; the chart below details one potential protocol for pharmacologic management of acute delirium.


Take Home Points:

  • Delirium is under-recognized and under-diagnosed but carries marked increases in morbidity and mortality in the elderly population.

  • This diagnosis can and should be made in the ED; consider diagnostics aids like the CAM.

  • Delirium is often the presenting symptom of an underlying pathology and a broad differential should be consider.

  • Pharmacological interventions are a last resort; if needed low does of haloperidol or other atypical antipsychotics can be considered.

Expert Commentary

I love that delirium in the emergency department is being discussed! As a geriatrician, so many of my older adult patients are brought into the ED with these symptoms and it is vital that delirium is recognized and treated effectively. Delirium is a serious problem among older adults – and their families and supporters. It carries a high risk of extended hospitalizations, morbidity, and mortality. Katie and Nery did an excellent job describing the full spectrum of Delirium – ranging from hypo to hyperactive delirium. The hypoactive delirium symptoms are frequently missed because older adults affected by this are very quiet and often appear distracted.  With “the squeaky wheel getting the grease”, we are more likely to recognize and respond to the older adult with hyperactive delirium instead. 

I fully concur that collateral information is important. I would emphasize that we need to encourage patient families and supporters to stay with the patient – even after the patient is being admitted and moved to the inpatient setting. What can be most frustrating is that families will sometimes leave once the patient is called from the waiting room or after they have been seen by one staff member. We need to reaffirm with families that they need to remain at bedside and continue to remain at bedside when the patient is admitted. Having a loved one nearby will help both physicians in obtaining more information as well as the patient is reorienting and soothing them. I have seen too often that family members will leave from the ED, since the patient is being admitted, and subsequently, the patient’s agitation worsens. Important lesson:  Please tell families to follow the patients to the inpatient floors/rooms and continue to stay with them.  

 Besides the family, collateral information should be obtained from the patient’s prior residence. So many older adult patients are transferred from skilled nursing facilities (SNF), or senior residences/communities (e.g. assisted living, memory care) for worsening confusion and delirium. I would suggest that ED teams contact the SNF nurses to determine collateral information. It would also be helpful to become familiar with the places that house seniors in their area (e.g. set up a tour, ask for clinical/nurse station phone numbers) so that communication can flow more easily.

From a clinical practice, the most common causes of delirium that I see are medication-related (withdrawal, polypharmacy) and dehydration. Doing a medication/brown bag review is always my first step. What I see is that older adults will sometimes start an OTC medication (e.g. diphenhydramine, sleep aid, or a pain medicine/sleep aid combo like a “acetaminophen PM”) and that will cause the acute confusion.   Dehydration is also a common cause for delirium among older adults since we lose our thirst mechanism as we age and do not feel the need to drink. With summer weather, it is easy for a senior to become dehydrated with the first symptoms being delirium.

I would like to point out that UTIs are frequently misdiagnosed as a cause for delirium. What does that mean? We have been taught that UTIs can be the culprit for delirium - but it is usually not.  Actually, checking a UA for confusion alone is no longer recommended by the CDC. The CDC recommends that urinary symptoms (e.g. frequency, dysuria) are present for UA testing. Why? Many older adults have asymptomatic bacteriuria – so much so that UTIs are frequently over-diagnosed in the ED as the culprit for delirium. When the culture comes back days later, there is a lack of evidence for the UTI. Even on the graphic presented by Katie and Nery on infections causing delirium – UTI is not listed.  What I will do is ask for collateral information about any prior urinary symptoms from the families, fevers/chills, leukocystosis, and check for suprapubic tenderness on exam to assess urinary issues as a culprit for delirium.

Lastly, avoid benzodiazepines to treat delirium in older adults. I realize that it is listed on the infographic but this class of medicines are likely to exacerbate the delirium. Benzos can be used for alcohol withdrawal symptoms/delirium tremens but that is it. The ABIM Choosing Wisely Campaign has noted this “Don’t use benzodiazepines or other sedative-hypnotics in older adults as first choice for insomnia, agitation or delirium.”   Non-pharmacologic methods are by far the best to treat delirium.  

Delirium is not fun for our older adults or their families. The quicker we can recognize the symptoms of delirium and ameliorate the cause in the ED, the better everyone’s lives are. I congratulate Nery and Katie for a great discussion of delirium and I hope that it will impact how we treat our seniors with delirium!


  1. ABIM Choosing Wisely – Geriatrics. Available at:

  2. Mody L, Juthani-Mehta M: Urinary tract infections in older women: a clinical review. Jama 2014, 311(8):844-854.

  3. McKenzie R, Stewart MT, Bellantoni MF, Finucane TE: Bacteriuria in individuals who become delirious. Am J Med 2014, 127(4):255-257.

  4. Nicolle L.E., Bradley S., Colgan R., Rice J.C., Schaeffer A., Hooton T.M. Infectious Diseases Society of America Guideline for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin. Infect. Dis. 2005;40:643–654.


Lee Lindquist, MD, MPH

Associate Professor of Medicine

General Internal Medicine and Geriatrics

How To Cite This Post

[Peer-Reviewed, Web Publication] Porras N, Lindquist L. (2019, March 25). The seriousness of deliriousness: delirium in the ED [NUEM Blog. Expert Commentary by Lindquist L]. Retrieved from

Other Posts You May Enjoy


  1. Gower, Lynn, et al. “Emergency Department Management of Delirium in the Elderly.” Western Journal of Emergency Medicine, vol. 13, no. 2 Jan. 2013, pp. 194-201.

  2. Grossmann, Florian F. et al. “Screening, detection and management of delirium in the emergency department – a pilot study on the feasibility of a new algorithm for use in older emergency department patients: the modified Confusion Assessment Method for the Emergency Department (MCAM-ED).” Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, vol. 22, no. 1, 2014, p. 19.

  3. Geriatric Emergency Department Guidelines. (2014). Annals of Emergency Medicine, 63(5). doi:10.1016/j.annemergmed.2014.02.008

  4. Han, Jin H., et al. “Delirium in the Older Emergency Department Patient: A Quiet Epidemic.” Emergency Medicine Clinics of North America, vol. 28, no. 3, 2010, pp. 611-631.

  5. Inouye, Sharon K, et al. “Delirium in elderly people” The Lancet, vol. 383, no. 9934, 2014, pp. 911-922.

  6. Inouye, Sharon K. “Clarifying confusion: The Confusion Assessment Method.” Annals of Internal Medicine, vol. 113, no. 12, 1990, pp. 941-948.

  7. Inouye SK. The Confusion Assessment Method (CAM):Training Manual and Coding Guide. 2003; New Haven: Yale University School of Medicine.

  8. Lewis LM et al. “Unrecognized delirium in ED geriatric patients.” American Journal of Emergency Medicine. vol. 13, 1995, pp. 142-45.

  9. Monette, Johanne, et al. “Evaluation of the confusion assessment method (CAM) as a screening tool for delirium in the emergency room.” General Hospital Psychiatry, vol. 23, no. 1 , 2001, pp. 20-25.

  10. Rosen, Toney, et al. “Assessment and Management of Delirium in Older Adults in the Emergency Department.” Advance Emergency Nursing Journal, vol. 37, no. 3, 2015

Posted on March 25, 2019 and filed under Neurology.

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

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  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.