Boring Question: Does this medication cause long QT? (with Bonus: Tiny Tips!)

The Clinical Case

A 70-year-old female presents to the emergency department with new palpitations and 2 syncopal episodes, witnessed by her son. These episodes have started within the past 10 days. Her past medical history includes diabetes, hypertension, depression, dyslipidemia and atrial fibrillation. She is a long-standing diabetic and is followed by a nephrologist for her diabetic nephropathy. Her medications included: metformin, atorvastatin, aspirin, warfarin and sertraline. She was recently seen in hospital for similar symptoms and sotalol was used for her atrial fibrillation.

On physical examination, her vitals were:

Temp: 37.2, HR: 130, RR: 18,  BP: 144/72, O2: 97% on room air.

On examination, she was alert and orientated to time, place and person. Her neurological assessment, which included cranial nerve examination, power assessment, fine/gross touch discrimination and cerebellar evaluation was unremarkable. Her cardiac examination revealed an irregularly, irregular pulse with a systolic murmur at the apex without radiation. Her respiratory examination revealed good air entry bilaterally. Atrial fibrillation was confirmed on 12-lead ECG. Her QTc was calculated to be 500 ms.

 Your attending asks you which of the patient’s medications may be the cause of her syncope?

The Clinical Question

What is the QT interval on an ECG, why is it important to assess and which medications cause QT interval prolongation?


The QT interval is measured from the start of the QRS complex to the end of the T wave on an electrocardiogram (ECG) (1). The interval represents ventricular depolarization and subsequent repolarization, which is dependent on positively charged ions. The rapid inflow of positively charged ions (sodium and calcium) results in normal myocardial depolarization (1). When this inflow is exceeded by outflow by potassium ions, repolarization occurs. A malfunction of these ion channels results in an intracellular excess of positively charged ions, resulting in QT interval prolongation (1). This can be the result of a congenital defect in the ion channels, pharmacologic agents and changes in a patients electrolyte levels (1).

The QT interval is influenced by the heart rate of a patient. In cases of a slower heart rate or bradycardia, the QT interval can be prolonged. In cases of a faster heart rate, the interval can be shortened. As a result, the Bazett formula can be used, where the QT interval is divided by the square root of RR, generating a corrected QT or QTc (1). The normal QTc is less than 440 ms (2). Any value over this is considered prolonged. If the interval is more than 500 ms, it is considered moderately prolonged and any value greater than 550ms is considered markedly prolonged (2).   NB: For more details on how to calculate QT intervals, I highly suggest you consider reviewing Al-Khatib et al (2003) which demonstrates the corrected QT calculation in both normal sinus rhythm and atrial fibrillation.

Some signs and symptoms for patients who may have prolonged QT on an ECG can include dizziness, syncope, congenital deafness and palpitations (3). The workup can include ECG, additional cardiac monitoring, full electrolytes including extended lytes, toxicology screen and imaging such as echocardiography (3).

QT prolongation typically occurs from a congenital cause, medication or electrolyte abnormalities such as hypokalemia. Congenital etiology for patients with prolonged QT can include an autosomal recessive form associated with deafness (Jervell and Lange–Nielsen syndromes) or an autosomal dominant form not associated with deafness (Romano–Ward syndrome) (3). There are several medications that have also been associated with prolonged QT intervals.

The Tiny Tips:  The “Anti” list & The “SAD Qu-pid” Mnemonic

In attempting to remember these drugs, several mnemonics have been generated.

One is the ‘Anti’ mnemonic, where one can remember some of the broad classes to consider:



Another is known as the “Sad Qupid” mnemonic.






The table below highlights some of the medications that have the potential to cause a prolongation of the QT interval.

Screen Shot 2014-09-06 at 5.57.02 PM

Table 1-Adapted from Al-Khatib et al 2003  (For more up-to-the-moment lists,

Very probable refers to more than 50% of respondents in this paper stating they would check an ECG prior to starting the medication. Probable is 40-49% of respondents indicating their preference to check an ECG with improbable referring to 40-49% of respondents stating that they did not feel the need to check an ECG before starting the medication.

Returning to the case

When initiating therapy for a patient with a medication that is known to potentially cause QT prolongation, an assessment of risk and benefit must be considered. It is also important to understanding the drug’s pharmacology and clearance prior to prescribing. For instance, a medication that has renal clearance such as Sotalol needed to be prescribed with caution in a patient with impaired renal function.

It is also imperative to understanding the risk factors which include elderly women, advanced heart disease, patients with history of sudden death and those on complex drug regimens that can influence modulate drug elimination (4). Patients on the above listed medication should also be warned to inform a health provider of symptoms such as syncope or new palpitation. In high risk situations, more serial ECGs can also be considered to assess the patient (4).


Reviewing with Staff:  Dr. James Ahn |  Click here to reveal

Dr. James Ahn, MD (University of Chicago, Associate Program Director)

As the article states, the main concern of long QT is torsades de pointes, which is a largely preventable disease in emergency medicine. The main issue with long QT is the recognition of this potentially deadly ECG abnormality. Although understanding the Bazett formula is useful and we are taught to naturally mistrust computer interpretations, the interval calculations provided are accurate and will save time for the provider. As mentioned above, the dangerous zone for a prolonged QT beings after 500ms.

Providers will undoubtedly obtain ECGs in a history concerning for ischemia and hypothermia. However, physicians should have a low threshold to obtain an ECG in situations without classic indications as these can scenarios can prolong the QT interval. For example, any scenario where the patient may have electrolyte abnormalities (e.g. gastroenteritis), increased ICP (e.g. intracranial hemorrhage), or troublesome medication administered should have an ECG obtained

Seemingly, every medication can prolong QT and memorizing these can prove to be as confusing as the coagulation pathway. However, providers should be aware of certain commonly prescribed medications, such as anti-emetics, antibiotics, and antipsychotics, that can prolong the QT interval. For more esoteric drugs, a website such as can be helpful – this site in particular organizes medications in order of likelihood to prolong QT.

In summary, maintaining vigilance with ordering ECG and the QT interval can prevent torsades de pointes in vulnerable patient populations.



1. Al-Khatib SM, Allen LaPointe NM, Kramer JM, Califf, RM (2003).What Clinicians should know about the QT Interval. JAMA. 289: 2120-2127

2. Wong K, Ubogagu E, Francis D. (2010) Cardiology to Impress: The Ultimate Guide for Students and Junior Doctors. London. Imperial College Press

3. Schaider JJ et al. (2010) Rosen and Barkin, 5 Minute Emergency Medicine Consult. New York. Lippincott Williams and Wilkins

4. Wood AJJ. (2005). Drug Induced Prolongation of the QT Interval. NEJM. 350: 1013-1022.



Author information

Jatin Kaicker
Jatin Kaicker
Jatin Kaicker is a Family Medicine resident at McMaster University.

The post Boring Question: Does this medication cause long QT? (with Bonus: Tiny Tips!) appeared first on BoringEM and was written by Jatin Kaicker.

Tiny Tip: PREeclampsia

Preeclampsia is a common complication in pregnancy, affecting 3-5% of pregnant women in the general population, and up to 25% of pregnant patients with pre-existing chronic hypertension [1].

It’s common enough that you’re likely to see it in the emergency department if you are rotating through a site without a primary obstetrics triage area. It’s important to recognise preeclampsia early in the emergency department, because unrecognised it can lead to eclampsia and increase the risk of early induced labour, placental abruption, and foetal growth restriction [2].


The classic preeclampsia triad can be remembered using the mnemonic PRE:

P roteinuria

R ising blood pressure

E dema


If you’ve done a urine dipstick in the emergency department, you can reasonably suspect significant proteinuria with a result of 1+. Formal diagnostic criteria require a 24-hour urine collection showing 0.3g/day or 30mg/mmol in a random urine sample [3].

If you suspect hypertension in the emergency department (systolic blood pressure 140 mmHg or diastolic pressure 90 mmHg), be sure to confirm by taking at least 2 measurements in the same arm, waiting at least 15 minutes between measurements [3].

As for edema, swelling of the legs and feet is pretty common in pregnancy, but residents and staff in obstetrics and gynaecology tell me that facial swelling is the hallmark of preeclampsia edema…and it can happen overnight, so it’s usually noticed and reported by patients and partners!

Reviewing with the Staff (by T. Chan)

Staff Review by Teresa Chan MD FRCPC

Thanks for the great piece, Luckett. One thing I wanted to call out was to ensure that readers remember one key clinical pearl: It’s good to remember what preeclampsia looks like so that you can treat it! Therefore, I have two bonus tips that I would like to highlight:



Remember, (full) eclampsia should be treated with magnesium sulphate (2014 SOGC recommendation 116) [3]. Magnesium sulphate should also be given to preeclamptic patients with severe preeclampsia (2014 SOGC recommendation 117) and may be considered as prophylaxis in women with non-severe eclampsia and at least one of the following symptoms [3]:

  • severe hypertension,
  • headaches/visual symptoms,
  • right upper quadrant/epigastric pain,
  • platelet count < 100 000 × 109/L,
  • progressive renal insufficiency,
  • elevated liver enzymes (I-C)

Please note that this list is VERY SIMILAR to the HELLP syndrome, but slightly different – and thus learners should be flagged to the obvious confusion that this might cause. (Good thing you have previously also reviewed HELLP for Tiny Tips recently! :D)



The dose of Magnesium sulphate for prophylaxis of eclampsia is 4 g IV load (over 20 min) and then 1 g / hr [4].


1. Seely, E. W., & Ecker, J. (2011). Chronic hypertension in pregnancy. New England Journal of Medicine, 365(5), 439-446. PMID: 24637432

2. Arulkumaran, N., & Lightstone, L. (2013). Severe pre-eclampsia and hypertensive crises. Best Practice & Research Clinical Obstetrics & Gynaecology, 27(6), 877-884. PMID: 23962474 

3. Magee, L. A., Pels, A., Helewa, M., Rey, E., von Dadelszen, P., Audibert, F., … & Sebbag, I. (2014). Diagnosis, Evaluation, and Management of the Hypertensive Disorders of Pregnancy: Executive Summary. Journal of obstetrics and gynaecology Canada: JOGC= Journal d’obstetrique et gynecologie du Canada: JOGC, 36(5), 416-438.  PMID: 23962474

4.  Altman, D., Carroli, G., Duley, L., Farrell, B., Moodley, J., Neilson, J., & Smith, D. (2002). Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet359(9321), 1877-1890.  PMID: 12057549

Author information

Sarah Luckett-Gatopoulos
Sarah Luckett-Gatopoulos
Junior Resident Editor at BoringEM
Luckett is a resident at McMaster University. Newbie to the #FOAMed world. Interested in literacy, health advocacy, creative writing, and near-peer mentorship.

The post Tiny Tip: PREeclampsia appeared first on BoringEM and was written by Sarah Luckett-Gatopoulos.

#TipsforEMexams: Exam Study Tips Series

As September arrives, my thoughts always turn towards memories of being in school.  The fun, the initial excitement… but then… with memories of school comes memories of exams.

Inspired by the “How I work smarter series” this series will outline study tips for EM exams. They may seem a bit targeted towards the Canadian RC emergency medicine exam (because that’s the exam I wrote), but  I’m hoping that most of the tips from this series will generalize towards the CCFP-EM or even ABEM exams though.  Also, much like ALiEM’s “Work Smarter” series, the writer will tag his/her friends to see if they can create a similar post, so I hope that eventually we will tag people with different backgrounds and perspectives, all whom have conquered various examinations. On Twitter we’ll use the hashtag #TipsforEMexams to track the conversation.  Hopefully with everyone’s help we can get a great assortment of exam study tips.

So without further ado, here are my tips:


Name:     Teresa Chan, Survivor of the 2013 RC emergency medicine exam

Where are you now?
Assistant Professor, McMaster University. BoringEM Managing Editor


Five tips for prospective examinees:

1. Organize yourself – Random studying will make you case-by-case smarter, but programmatic studying will be more important as you start to study for examinations. Remember, the point of the exams is to ensure you have a broad understanding of key emergencies – and as such, it is advantageous to work through a good list of topics. Taking Rosen’s, Tintinalli, and other key textbooks, I compared their content to my program’s academic half day schedule to augment what I had learned over the past 3 years. Then I stuck to this study schedule, 2-3 topics at time – summarizing, reviewing, extracting what I could into my notes. I’m super duper glad I did this audit since there were several areas that were missing from my end-of-PGY-3 notes that ended up being on my exam.

2. Start early (if you can) – I started studying for the RC exam in PGY4. That’s not to say I didn’t study before then, but I was more opportunistic about studying around cases and things that were clinically relevant from my shifts or rotations. In PGY4 though, I sat down at least 2-3 times per week and powered through various topics, brushing up my study notes, reading and gathering materials (key papers, etc.). In PGY5, we turned up the heat, going through all these materials again once more.

3. Study social – Group studying has been proven in a number of studies to be highly beneficial for learning outcomes. Likely this stems from collaborative learning – forcing participants to practice and revisit external representations of the knowledge they hold to be true. Regardless of HOW it works (that’s why I started Masters in Health Professions Education), you merely need to know THAT it works and harness this for its advantage. This means orienting your life to ensure that you can meet up and discuss your material with others – aligning study topics or practice questions is key. Moreover, don’t fool yourself about tandem studying (i.e. studying alongside someone else quietly). That is NOT group studying, and doesn’t help your learning in the same manner.

4. Use the Cloud – It pays to have a back up of your notes. My study group had a group study Google Drive where we shared and collaborated on exam study notes. (Nerdily, we wrote it up as a brief educational report in CJEM.) We also made a set of one-page mock oral case scenario guides and exchanged them via this Google Drive. Beyond that, I sometimes studied with colleagues via Skype or Google Hangouts (e.g. my friend Janice all the way in Vancouver or my friend Serena in the neighbouring city). This made it much easier to study with others, while never having to change out of my pyjama pants.

5. Drilling yourself is important too, but make it fun! – I’ll be honest, by March of my exam year, I was pretty exhausted and extremely bored – and yet I still felt compelled to study every waking moment. As such, I decided to channel my energies into gamifying my studying. I had created about 1000 flash cards with various important lists from Rosen’s… But they were just sitting there. Enter the Flash Card Advent Calendar (Figure 1). I set up my flashcards in roughly equal decks of materials, and then I put a surprise task at the bottom of each deck (i.e. Buy and eat your favourite cupcake! Go watch a movie!).  This made my last few weeks of studying far more interesting.


Figure 1:  The Exam Flash Card Advent Calendar



Tag! You’re it!

I would now like to ask the following tow people to submit their five exam tips.

1. Rob Woods

2. Heather Murray


Author information

Teresa Chan
Managing Editor at BoringEM
Emergency Physician. Medical Educator. #FOAMed Supporter, Producer and Researcher. Assistant Professor, Division of Emergency Medicine, Department of Medicine, McMaster University. + Teresa Chan

The post #TipsforEMexams: Exam Study Tips Series appeared first on BoringEM and was written by Teresa Chan.

Boring Question: How useful are plain abdominal films for bowel obstruction?

Clinical Scenario

An otherwise healthy 65 year old comes into the emergency department with an 8 hour history of abdominal pain. Her last bowel movement was 3 days ago and she’s not sure if she has passed gas.  She endorses nausea but has not vomited. She has not taken her temperature but does not believe she has been febrile. She’s tried Tylenol for analgesia with little relief. She last ate 12 hours ago and has recently only prepared home cooked meals with no new foods. Her urination has been normal. She has had a number of surgeries including a hysterectomy (1990) and cholecystectomy (1995). There is no family history of colon cancer and she had a normal screening colonoscopy two years ago after an episode of rectal bleeding.

On physical examination, her vital signs were:

Temp: 37.6, HR of 90, RR:18, BP:128/80, O2: 99% on room air.

On exam, she looks uncomfortable moving around on the stretcher. Her abdomen looks slightly distended, you didn’t auscultate her bowel sounds (see why here) and she has diffuse tenderness of the abdomen but no peritoneal signs. She does not have flank percussion tenderness. The rest of her exam is unremarkable. You wonder:


Boring Question:  How useful are plain abdominal films for a patient with abdominal pain and suspected small bowel obstruction?


Radiographs are also ordered in the emergency department for patients with acute abdominal pain. Flat and upright abdominal films, upright chest films and lateral decubitus views can be used to screen for bowel obstruction, constipation or free air (1). Plain abdominal films may demonstrate air fluid levels which may suggest mechanical obstruction. While these levels may suggest an obstruction, they are not pathognomic for such a condition (2). Plain abdominal x-rays also expose patients to about 35 times the radiation as a dose of a chest x-ray (3).

Search Strategy

Using PubMed, three separate searches were performed. These were:

1. “abdominal radiographs” AND “small bowel obstruction”

2. “plain radiographs AND “abdominal pain”

3. “abdominal x rays” AND “acute abdominal pain” AND “emergency department”

The resulting article titles and abstracts were screened with relevant articles reviewed. In addition, the textbook ‘Tintinalli’s Emergency Medicine’ was used. For investigations highlighted in review literature, the primary studies were assessed.

The Evidence

Taylor et al published a scientific article in 2013 that identified five studies, attempting to assess the usefulness of plain radiographs in diagnosing small bowel obstruction (4). Three of these investigations were prospective case studies with two retrospective case studies. All these investigations used the criteria of SBO on x-ray to be two or more air fluid levels in dilated loops of bowel (more than 2.5 cm) (4). The positive likelihood ratio was published to be 1.64 as the collective for these investigations.

A study by Van Randen et al in 2011 discussed a multi-center trial for patients with abdominal pain lasting between 2 hours and 5 days (2). Each patient was clinically assessed with physical examination and laboratory blood work, with subsequent supine abdominal and upright chest x-rays (2). This investigation found a positive predictive value of 54% for patients with a bowel obstruction with the clinical assessment and 61% after radiographs (2).

In the late 1990s, Suri et al conducted a small prospective study, comparing abdominal x-rays with ultrasound and CT to diagnose small bowel obstructions (3, 5). The calculated positive likelihood ratio from their findings is 1.54. Maglinte et al in 1996 also attempted to assess the value of CT and abdominal radiographs in patients with suspected small bowel obstruction (3, 6). For abdominal films, the positive likelihood ratio can be calculated to be 1.60 from their findings.

Bottom Line

From the literature assessed, plain abdominal films and chest radiographs have limited added diagnostic value for patients with abdominal pain and suspected small bowel obstruction.



Review by an Attending

Patients suspected of bowel obstruction are a heterogeneous group and include patients that may have ileus, gastroparesis or gastroenteritis. The gas pattern also varies due to severity, level and duration of the obstruction. It should be no surprise, therefore, that the radiographs can be normal in 1/3 of cases [especially in the setting of partial obstructions]. That said, many of these patients could be treated conservatively with 40-75% resolution.

Radiologists look at more than just the presence [and number] of air-fluid levels and dilated loops of bowel –for example “mean differential air-fluid levels”. Most studies use rad-reads in patients known to have bowel obstruction. So the published test characteristics reflect the best possible scenario. So I believe that an emergency-read plain film will probably perform even less favorably than you have described.

However, plain films may still have a role depending on factors such as resource availability. I would be reluctant to advocate for CT-everybody approach given the risk of radiation and the current global trend of spiraling health costs and ED overcrowding. It appears that ultrasound may now also emerging as a potential alternative to CT. I would advocate for a sit-down between EM, surgery and radiology to derive an algorithmic approach to which modality would best serve patient needs in your center.

- Nadim Lalani  MD FRCPC



1. Tintinalli’s Emergency Medicine-A Comprehensive Study Guide (2011). New York. McGraw Hill Companies Inc

2. Van Randen A, Lameris W, Luitse JSK, Gorzeman M, Hesselink EJ et al. (2011). The role of plain radiographs in patients with acute abdominal pain at the ED. The American Journal of Emergency Medicine. 29 (6). 582-589.

3. Smith JE, Hall EJ. (2009) The use of plain abdominal x rays in the emergency department. Emergency Medicine Journal. 26(3).160-3.

4. Taylor MR, Lalani N. (2013). Adult Small Bowel Obstruction. Academic Emergency Medicine. 20(6). 528-544.

5. Suri S, Gupta S, Sudhakar PJ et al. (1999) Comparative evaluation of plain films, ultrasound and CT in the diagnosis of intestinal obstruction. Acta Radiol 40(4). 422-8.

6. Maglinte DD, Reyes BL, Harmon BH et al (1996). Reliability and role of plain film radiography and CT in the diagnosis of small-bowel obstruction. AJR Am J Roentgenol 167(6). 1451-5.


Author information

Eve Purdy
Medical Student Editor at BoringEM
Fourth year medical student at Queen's University-happily consuming, sharing, creating and researching #FOAMed

The post Boring Question: How useful are plain abdominal films for bowel obstruction? appeared first on BoringEM and was written by Eve Purdy.

Ondansetron vs Placebo vs Metoclopramide: Normal saline as an antiemetic?

This week we review an article comparing ondasetron, metoclopramide and placebo (normal saline).

Title: Antiemetic use for nausea and vomiting in adult emergency department patients: randomized controlled trial comparing ondansetron, metoclopramide, and placebo. PMID: 24818542


Why is this paper important?

Nausea and/or vomiting are common emergency department (ED) presentations. While investigating underlying cause and establishing a diagnosis are important, so too is the goal of relieving the patient’s symptoms. This paper evaluates two commonly prescribed anti-emetic medications and placebo in a head-to-head comparison for the treatment of ED patients with nausea and/or vomiting.

Catching Up

The success of pharmacologic anti-emetic strategies in oncology and post-operative patients (1, 2) was extrapolated to support use in patients with un-differentiated nausea and vomiting in the ED. Four studies (3, 4, 5, 6) have shown success of metoclopramide and/or ondansetron in reducing the severity of nausea in the ED, but the only two placebo controlled studies showed no benefit of these medications over placebo (3, 4). Severity of nausea and vomiting is frequently measured using a visual analogue scale (VAS) and a minimally significant change has previously been defined as 15mm (7). This topic was previously covered by Ryan Radecki in a post “Nausea? We’ve got placebo for that” on EM Literature of Note.

The Study: Ondansetron vs Placebo vs Metoclopramide

Bottom Line

IV ondansetron and metoclopramide are no better than placebo at improving patient perceptions of nausea and vomiting along a visual analogue scale but all three provide a clinically significant improvement in symptoms.

The PICO Question

Population: Adult patients with nausea and vomiting during ED care for which the physician prescribed IV anti emetics.

  • Exclusions: hemodynamic instability, critical intervention needed, pregnancy or lactation, Parkinson’s disease, restless leg syndrome, use of antemtic in last 8 hours, previous IV fluids during ED stay, N/V related to vertigo/chemo/radiotherapy, previous allergy to a study medication


  • Metoclopramide 20mg IV (10mg/2ml x 2-2ml syringes)
  • Ondansetron 4mg IV (4mg/2ml x 1-2ml syringe + 0.9% saline x 1-2ml syringe )


  • 0.9% Saline 4ml (0.9% saline x 2-2ml syringes)


  • Primary: mean change in severity rating on the VAS 30 minutes after administration of study drug
  • Secondary: 
    • Median change in severity on the numeric rating scale
    • Adjectival description of change
    • Change in number of vomiting episodes
    • Need for rescue medication
    • Patient satisfaction
    • Adverse Events

Of 744 patients screened, 385 were eligible for enrollment (see exclusion criteria above) and 270 underwent randomization. Data on 258 patients (96%) was available for analysis. The results after 30 minutes were:

  • Less need for rescue medication in the metoclopramide group (18%) compared to ondansetron (35%) and placebo (36%). No statistically significant differences in the other secondary outcomes.
  • Nine adverse events were reported (3.5%) with six were in the metoclopramide group. Of those, two had akathisia, two had restlessness, one had muscle twitching, and one was diaphoretic. There were also two minor adverse events with ondansetron and one with placebo.


Internal Validity

This study met most of the criteria for high internal validity:

  • Randomisation was centralized and computer generated.
  • Treatment groups were similar at baseline on important factors such as gender, age, clinical cause, number of vomiting episodes and initial VAS score.
  • Patients, care-givers and data collectors were blinded to the intervention through rather elaborate measures to conceal delivered medications. In this case, blinding was particularly important because all other factors of treatment were not perfectly controlled. Physicians were free to implement treatments other than antiemetics at their discretion. We have no data on whether opioids/steroids/other medications were given differently to each group. Since there is no guarantee in the protocol that groups remained similar throughout ED stay, we are left to hope that proper blinding prevented against any systematic confounding bias towards or against a specific treatment.
  • Follow-up was near complete (96%). The 4% lost to follow-up were excluded but the remaining were included analyzed using the intention-to-treat principle. Ideally it would have been nice to see a “best and worse” case scenario analysis with the missing results, but it is still unlikely that this small missing cohort would change the conclusion.
  • The study endpoint was symptoms at 30 minutes, however, nausea often comes in waves rather than being a persistent phenomenon. As such, it would have been helpful to see comparison at a number of different evaluation time points (ie. 60 minutes, 120 minutes) to account for more realistic symptomatology and provide information that may be relevant when considering patient discharge.
External Validity

After confirming that a study internally valid it is important to think about whether or not the results are generalizable. This study is generalizable with a few considerations to keep in mind when applying to your patients.

  • First, the exclusion criteria eliminate (with good reason) a significant number of patients with nausea and vomiting. Before you think about applying the results of this study by skipping on IV anti-emetics make sure that the patient does not meet one of these exclusion criteria.
  • Second, the dosing of medications must also be considered. The recommended dose of ondansetron is 0.15mg/kg so it could be argued that patients were actually underdosed in this trial by receiving 4mg. Conversely, metoclopramide is most often dosed at 10mg (rather than 20mg) so the increased number of side effects may have been attributable to that.
  • Unfortunately this trial did not include anti-emetics delivered PO, IM or SL. We often administer medications this way to avoid an IV. We can’t extrapolate the results from this study for those alternate antiemetic strategies.


So What?

Is normal saline the new ondansetron? This study demonstrates that there was no difference between IV anti-emetics (ondansetron and metoclopromide) and an IV placebo of 0.9% saline in the reduction of undifferentiated nausea &/or vomiting in a convenience sample of ED patients. Given the possible adverse effects and costs associated with antiemetics, should we re-evaluate their role in this patient population? Or is this another study that will not be replicated?

The not so boring question

If it does turn out that ondansetron is no better than placebo,should doctors be able to prescribe a placebo medication? Is it unethical if it works? Why? Why not? What do you think the results would have been for a fourth group with no intervention? Or perhaps the 4ml of 0.9% saline is not actually a placebo. After all, we know normal saline isn’t so normal after all.

Please comment below.

This post was reviewed by Dr. Andrew Petrosoniak (@petrosoniak).


1. Carlisle J., & Stevenson C. (2006). Drugs for preventing post operative nausea and vomiting. Cochrane Anesthesia Group. Accessed online:;jsessionid=55EBBAA09E9A3009F704B0C0A22FC995.f01t04

2. Billio A., Morello E., & Clarke M. (2009). Serotonin receptor antagonists for highly emaetogenic chemotherapy in adults. Cochrane Pain, Palliative and Supportive Care Group. Accesed online:

3. Braude, D., Soliz, T., Crandall, C., Hendey, G., Andrews, J., & Weichenthal, L. (2006). Antiemetics in the ED: a randomized controlled trial comparing 3 common agents. The American journal of emergency medicine, 24(2), 177-182.

4. Barrett, T. W., DiPersio, D. M., Jenkins, C. A., Jack, M., McCoin, N. S., Storrow, A. B., … & Slovis, C. M. (2011). A randomized, placebo-controlled trial of ondansetron, metoclopramide, and promethazine in adults. The American journal of emergency medicine, 29(3), 247-255.

5. Braude, D., & Crandall, C. (2008). Ondansetron versus Promethazine to Treat Acute Undifferentiated Nausea in the Emergency Department: A Randomized, Double‐blind, Noninferiority Trial. Academic Emergency Medicine, 15(3), 209-215.

6. Chae, J., McD Taylor, D., & Frauman, A. G. (2011). Tropisetron versus metoclopramide for the treatment of nausea and vomiting in the emergency department: A randomized, double‐blinded, clinical trial. Emergency Medicine Australasia, 23(5), 554-561.

Author information

Eve Purdy
Medical Student Editor at BoringEM
Fourth year medical student at Queen's University-happily consuming, sharing, creating and researching #FOAMed

The post Ondansetron vs Placebo vs Metoclopramide: Normal saline as an antiemetic? appeared first on BoringEM and was written by Eve Purdy.

Boring Question: How does the sensitivity/specificity of lung ultrasound compare to plain films in diagnosing pneumothorax?

The Case

A 74-year-old male with a history of COPD arrived in the emergency department in respiratory distress. On physical examination, the patient was mildly tachypneic and had an oxygen saturation of 93% on a non-rebreather mask. On auscultation, the patient had wheezing and diminished air movement bilaterally. A supine chest radiograph (CXR) was obtained. A short time later, a radiologist called to confirm the presence of a “moderate sized right pneumothorax” (Figure 1).

Figure 1 - Chest X-ray initially read as a right pneumothorax.

Figure 1 – Chest X-ray initially read as a right pneumothorax.

As a chest tube tray was being prepared, a bedside ultrasound (US) was performed and showed bilateral lung sliding. (Link to Case Video or simply see below.)


The Question

Is lung US more or less sensitive and specific than CXR in diagnosing pneumothorax?

The Answer

Whereas our patient presented with a pneumothorax (PTX) presumably due to COPD, most of the evidence for the sonographic diagnosis of PTX is based in the trauma literature. Four recent meta-analyses have addressed the use of sonography for PTX, and all support ultrasound as vastly superior to supine CXR as evidenced by their sensitivities for diagnosing PTX. For all the included studies, the sensitivity of US and CXR for PTX detection ranged from 78.6-98% and 28-75%, respectively.

Name Year N # of publications included U/S sens CXR sens US spec CXR spec
Wilkerson 2010 606 4 86-98% 28-75% 97-100% 100%
Ding 2011 7569 20 89% 52% 99% 100%
Alrajhi 2012 1048 8 90.9% 50.2% 98.4% 99.4%
Alrajab 2013 1514 13 78.6% 39.8% 98.4% 99.3%


Of note, most patients included in these meta-analyses were trauma patients that underwent supine imaging; it is difficult to judge whether the characteristics of CXR might have improved accuracy if imaging were done in the upright or lateral decubitus positions [4,5]. The gold standard for diagnosis of PTX in each of these meta-analyses was demonstrated PTX on CT scan or a rush of air with chest tube insertion.

The Test

Now that we know US is more sensitive and specific than CXR in diagnosing PTX, how do we perform the test? The authors of a recent publication found that in supine patients, most pneumothoraces were located beneath the 5-8 intercostal spaces [7], which makes that the best place to start scanning. The most commonly taught sign of PTX on lung US is the absence of lung sliding.


In lung sliding, the visceral-parietal pleural interface (VPPI) appears as a hyperechoic (white) line beneath the cross-sectional cut of the ribs and moves back and forth with respiration. In PTX, this white line will not move with respiration. Recall that the patient in our vignette had bilateral lung sliding despite a CXR that showed moderate right sided PTX’. [Video 2: Moderate Pneumothorax]


The presence of lung sliding effectively rules out a PTX, but its absence does not necessarily rule one in (Figure 2), so correlating your sonographic findings with the clinical exam is important.

Figure 2 - Causes of no lung sliding.

Figure 2 – Causes of no lung sliding.


If you don’t see lung sliding, the presence of comet tails or b-lines can be used to help rule out a PTX, since these artifacts originate from the visceral pleura [8]. [Video 3:  B-lines with no lung sliding.]


One sign thought highly specific for PTX is the lung point. This represents the limit of the PTX and is identified when both lung sliding and the absence of lung sliding are seen in one area. If this is present you will see the hyperechoic (white) pleural line sliding normally and right next to it an area that is not sliding within the same intercostal space.  [Video 4:  Lung point]


You can see a more detailed description of one here). Some physicians use m-mode in diagnosing PTX by US, but m-mode really has no role unless you need to print out a still image proving a PTX. A recent publication found that using m-mode decreases accuracy in diagnosing PTX versus using b-mode (i.e., normal US mode)[1].

The Bottom Line

When evaluating a patient with respiratory distress, ultrasound is vastly superior to supine or semi-recumbent CXR for diagnosing pneumothorax.

Back to the Case

Because of the presence of lung sliding on US, a CT scan was performed. This showed emphysematous changes, worse in the right hemithorax, without pneumothorax (Figure 2). The patient avoided an unnecessary tube thoracostomy that likely would have caused deterioration from an iatrogenic pneumothorax. The cause of the false positive CXR finding was a skin fold combined with diminished lung markings peripherally due to emphysema.  The patient was subsequently treated as a COPD exacerbation, and improved clinically.

This post was edited by Sarah Luckett-Gatopoulos @SLuckettG


1.  Adhikari S, Zeger W, Wadman M, Walker R, Lomenth C. Assessment of a human adaver model for training emergency medicine residents in the ultrasound diagnosis of pneumothorax. Biomed Res Int. 2014. (Epub ahead of print)

2.  Alrajhi K, Woo MY, Vailancourt C. Test characteristics of ultrasonography for the detection of pneumothorax: a systemic review and meta-analysis. Chest 2012;14:703-8

3.  Alrajab S, Youssef AM, Akkus NI, Caldito G. Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: Review of the literature and meta-analysis. Crit Care 2013;17:R208

4.  Beres RA, Goodman LR. Pneumothorax: detection with upright versus decubitus radiography. Radiology. 1993;186 (1): 19-22

5.  Carr JJ, Reed JC, Choplin RH, Pope TL Jr, Case LD. Plain and computed radiography for detecting experimentally induced pneumothorax in cadavers: implications for detection in patients. Radiology. 1992;183(1):193.

6.  Ding W, Shen Y, Yang J, He X, Zhang M. Diagnosis of pneumothorax by radiography and ultrasonography: A meta-analysis. Chest 2011;140:859-66

7.  Mennicke M, Gulati K, Olivia I, Goldflam K, Skali H, Ledbetter S, Platz E. Anatomical distribution of traumatic pneumothoraces on chest computer tomography: Implications for ultrasound screening in the E.D. Am J Emerg Med 2012;3:1025-31

8.  Volpicelli G, Elbarbary M, Blaivas M, Lichtenstein DA, Mathis G, Kirkpatrick AW, Melniker L et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38:577-591

9.  Wilkerson RG, Stone MB. Sensitivity of bedside ultrasound and supine anteroposterior chest radiographs for the identification of pneumothorax after blunt trauma. Acad Emerg Med 2010;17:11-7

Review by an Attending
Expert Review by Dr. Paul Olszynski, University of Saskatchewan

This is a great write-up! Well written, good flow with key findings clearly explained.

As Jacob states, most of the cited studies looked at supine films. The authors of one meta-analysis [1] did make note this may underestimate the performance of non-supine chest radiographs (upright and semi-upright). Conventional medical teaching (yikes!) and the above-mentioned evidence suggest that upright posterior-anterior films are superior to supine chest radiographs. By how much? Hard to say, but I suggest it’s worth addressing.

Emergency physicians regularly diagnose spontaneous pneumothoraces in their dyspneic/short of breath (SOB) patients using upright chest films (inspiratory, expiratory—you name it!). Many have come to trust these images much more than supine films, and l suspect many of our colleagues will want to know how the different types of chest radiographs measure up (not to mention how well pleural ultrasound performs in assessing the SOB differential: effusion, consolidation, edema, etc…a post for another time I suppose!).

The performance of an upright posterior-anterior chest radiograph for the detection of pneumothorax is oddly difficult to find. One study from the American Journal of Roentgenology (AJR) [2] allows us to (slightly) side-step that question by instead comparing upright CXR to ultrasound in 285 patients who had undergone lung biopsy. With the limitations of being a small study, and these pneumothoraces being iatrogenic, the authors showed ultrasound was at least as good as an upright CXR.

Where does this leave us? As Jacob points out, in the supine patient, pleural ultrasound is superior to chest radiography. As for our non-supine patients (the ones with those spontaneous pneumothoraces that usually present and remain upright during bedside assessment), the limited evidence for ultrasound looks promising. I’d suggest you place them supine, have a good look as described in the post, and prepare yourself to know a lot more about your dyspneic/SOB patients, the risks they are facing before leaving for tests, and their disposition, long before they get that upright CXR.

Paul Olszynski, MD, MEd, CCFP (EM)


1. Alrajab S, Youssef AM, Akkus NI, Caldito G. Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: Review of the literature and meta-analysis, 2013.

2. Sartori S, Tombesi P, Trevisani L, Nielsen I, Tassinari D, Abbasciano V. Accuracy of Transthoracic Sonography in Detection of Pneumothorax after Sonographically guided Lung Biopsy: Prospective Comparison with Chest Radiography. AJR, Jan 2007.

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Jacob Avila
Jacob Avila

The post Boring Question: How does the sensitivity/specificity of lung ultrasound compare to plain films in diagnosing pneumothorax? appeared first on BoringEM and was written by Jacob Avila.