current issues in emergency medicine, reviews, opinion and curbside consults

It’s well accepted that the window for acute atrial fibrillation cardioversion of atrial fibrillation ends at  48 hours post onset. We did a whole episode on that very point.  The 48 hour window is now being challenged by the biggest study to date looking on  this topic.

Time to Cardioversion for Acute Atrial Fibrillation and Thromboembolic Complications was published as a letter to JAMA on August 13, 2014. Ryan Radecki sent the first FOAMed shot across the bow with this review.  You can stop now and check out Ryan's review; he's far more erudite than I. If you need more info, read on...

Study in a nugget: This was a retrospective study from Finland that looked at around 2500 patients with a primary diagnosis of atrial fibrillation (AF), aged 18 years or older, with successful cardioversion in the emergency department within the first 48 hours of AF onset.  The primary outcome, a thromboembolic event, was defined as a clinical stroke or systemic embolism confirmed by computerized tomography or magnetic resonance imaging, surgery, or autopsy. Time to cardioversion was determined as the difference between the beginning of arrhythmic symptoms to the exact time of cardioversion. There were 3 groups: less than 12 hours, 12 hours to less than 24 hours, and 24 hours to less than 48 hours.

Thromboembolism Rates


Under 12 hours: 0.3%

24 to 48 hours: 1.1%.

It seems like 12 hours is the inflection point when risk went up and a CHADS VASC score of greater than 1 increased risk.

I’m not sure where this leaves us, maybe risk stratification in ED cardioversion? This was observational, retrospective, and did not include post cardioversion anticoagulation as an intervention. There is no definitive answer or management change from this letter. It does raise the question of whether we should anticoagulate cardioverted AF patients with over 12 hours of symptoms, or those with a CHADS VASC over 1. However, there is no evidence that a post cardioversion anticoagulation strategy would decrease thromboembolic event rate. Also, the incidence of post cardioversion thromboembolic events in this letter is far higher than reported in other literature.

Rob's practice changers

Cunningham Technique

Loop Abscess Drain Technique

Delayed Sequence Oxygenation

Swami's  practice changers

Nasal Cannula Apneic Oxygenation

Tranexamic Acid for Mucosal Bleeds


Nuotio, Ilpo, et al. "Time to cardioversion for acute atrial fibrillation and thromboembolic complications." JAMA 312.6 (2014): 647-649.

CABO CME Retreat December 5-9, 2014

Primary Care RAP

Direct download: A_fib_cardioversion_.output.mp3
Category:podcasts -- posted at: 3:51 AM

How often do you see patients who tell you they are having a sinus headache need antibiotics. There are so many things wrong with that, not the least of which is the antibiotics part, but ….what about the cause of the headache in the first place?

 Is this headache a migraine?

2006 JAMA Rational Clinical Exam Series: Does This Patient With Headache Have a Migraine or Need Neuroimaging?

If you have a patient who has some scomoata, maybe shimmering lights that start small, get bigger, a little nausea followed by headache-  what is that? it’s a migraine. Done. But it’s not always so clear cut.

The POUNDing mnemonic can help sort this out.

  1. Is it a Pulsating head- ache?
  2. Does it last between 4 and 72 hOurs without medication?
  3. Is it Unilateral?
  4. Is there Nausea?
  5. Is the headache Disabling? Disabling headaches are those that disrupt a patient’s daily activities.

If the patient answers “yes” to 4 or more of the 5 ques- tions, the LR is 24. We like to see a positive likelihood ration of at least 10 to indicate something is useful. Twenty four: is very useful.  For 3 criteria, the LR is 3.5, not too impressive. For 1 or 2 criteria, the LR is 0.41, weak.

What about photophobia, the absence of photophobia makes migraine less likely, we know that migraines can cause debilitating photosensitiy, but interestinly, the presence f photophobia doesn’t make migraines MORE likely because in the great headache ven diagram, there is tremendous overlap in symtoms, and photophobia is one of those symptoms that many headaches share.

Sinus headaches. What's in a name?

Sinus headache, so easy to say, it just rolls off the tongue. We say it, patients say it, but is it really a sinus headache?

Arch Intern Med. 2004 Prevalence of Migraine in Patients With a History of Self-reported or Physician-Diagnosed "Sinus" Headache.

Study Bottom Line: About 3000 patients, most carrying a diagnosis of sinus headaches. The overwhelming majority of patients met International Headache Society migraine headache criteria.

We’re not talking about patients with fever and purulent discharge. This is the patient with sinus pressure, sinus pain, even nasal congestion. So that sinus headache may not be a sinus headache after all, but a migraine with pain localized to a sinus area. But, you say, there’s overlap between sinus and migraine headaches,. That is true, but a 2008 study from Laryngoscpoe of patients seen at an ENT clinic with a previous diagnosis of sinus headache (either from a physician or themselves)  suggests that many sinus headaches do not have objective evidence of sinusitis AND get better with migraine treatment. Patients with a negative workup by exam, nasal endoscopy and CT scan were treated with triptans and the majority, over 80%,  got better. Migraine treatment made what was previously diagnosed as sinus headache better.

Maybe triptans help with sinus headaches, but maybe, and the evidence suggests this, many of what we and our patients call  sinus headaches are actually migraines.


Check out Primary Care RAP

Check out the CABO CME Retreat


Direct download: Ercast_headaches.output_1.mp3
Category:podcasts -- posted at: 2:38 PM

An unruly, intoxicated and violent patient rolls into the ED. The situation and the patient are both in need of control. How do you go about it? Redirection? Calming words? Sometimes those things aren't quite enough and chemical sedation is in order. When it comes to choice of sedating agent, everyone seems to have their secret formula. We canvassed the planet to see how chemical takedowns are done across the globe.

Our Panel

ZdoggMD Art of the chemical takedown FOAMed World Premier

Scott Weingart  5mg of droperidol and 2mg of midazolam mixed together in a syringe with 11⁄2 inch needle and jabbed into whatever large muscle is available. Wait a few minutes. If necessary, will repeat once. Then establish IV

Minh Le Cong Ketamine  IV, IM, or IO.

Cliff Reid Ketamine

Chris Nickson Benzo, olanzipine or droperidol

Sean Nordt The B-52.  5mg Haldol, 2mg Ativan and 50mg of benadryl mixed together in a single syringe and given IM

Katrin Hruska abusive patients are asked to leave the emergency department

Amit Maini 5mg of IM droperidol. Repeat in 5-10 minutes if needed

Sa'ad Lahri: lorazepam (4 to 8 mg IV) and haloperidol (5mg IV)

Yosef Leibman midazolam, droperidol. Starting to use clotiapine -  a dibenzothiazepine anti-psychotic and a phenothiazine with anti-anxiety properties.

Gerry O'Malley Burly security guards and a show of force. If that doesn't work- benzodiazepine

Ray Moreno:  Toxin related or sympathomimetic: midazolam 5 - 10mg IM. Psychiatric related- olanzipine. No idea what's causing the agitation- midazolam

Chris Richards- The B-52.  5mg Haldol, 2mg Ativan and 50mg of benadryl mixed together in a single syringe and given IM

Bonus section:

Droperidol,  QTc prolongation, and the Black Box with toxicologist Sean Nordt....

When droperidol was 'black boxed' in the US, it sent shockwaves across the emergency medicine community because this drug was, for many of us, the go to agent for sedation of combative and agitated patients. Over the past several years, the pendulum has swung away from the black box and toward increasing use of droperidol. Why is that? Have we all gone mad? Are we putting patients in danger?

The history (or the conspiracy, depending on how you look at it) is expertly explained in the below article. It involves big pharma, outlier case reports of patients given much higher doses than are used in the ED for either nausea or sedation, and suspicious timing. There is no doubt that butyrophenones can influence the QTc, but so can a lot of other meds we use (that are not black boxed).

Sean Nordt's approach to giving droperidol in the agitated patient

  1. Give the med
  2. When the patient has calmed, get an EKG.
  3. If the QTc is prolonged, put the patient on a cardiac monitor

Horowitz, B. Zane, Kenneth Bizovi, and Raymond Moreno. "Droperidol—behind the black box warning." Academic Emergency Medicine 9.6 (2002): 615-618.


Interested in checking out the best emergency medicine CME and CNE on the planet?


EM:RAP RN Edition

Direct download: Art_of_the_chemical_takedown_podcast.output.mp3
Category:podcasts -- posted at: 5:05 PM

Rich Levitan, pioneer in airway management, talks about operator stress response in the difficult airway. Referenced in this discussion: The laryngeal handshake,  books On Combat and Warrior Mindset. Rich offers several courses including the one of a kind Practical Emergency Airway Management Course and the Advanced Airway Endoscopy Course in Yellowstone.


Interested in a truly unique CME experience? Join Rich Levitan, Scott Weingart, Matt Dawson, Mike Mallin, Andy Sloas and me December 6-8, 2014 for a 5 star, all inclusive vacation in Cabo San Lucas and earn your CME credits in style. The 2014 Cabo CME Retreat will focus on the newest emergency medical practices and technologies in the areas of ultrasound and airway medicine. Our lineup of leading emergency doctors and medical speakers will present at Secret’s Resort, the newest all inclusive luxury resort in San Jose del Cabo. Secrets Puerto Los Cabos Golf & Spa Resort boasts five gourmet restaurants, incredible views, infinity pools, and world renowned golf courses designed by Greg Norman and Jack Nicklaus. At this limited-access retreat, you will experience a CME conference unlike any other.


To register and/or find out more, go to the Cabo CME homepage

Direct download: Psychology_of_the_difficult_airway.output.mp3
Category:podcasts -- posted at: 6:22 PM

Cardiac arrest. It seems so easy. Just follow the algorithm on the reference card, and all cardiac arrest issues will be solved. The truth is that codes can be messy, chaotic and scattered. On this episode of ERcast, we hear from the RAGE podcast  experts on how to take control of the room and run an effective resuscitation.

The medicine isn't always the hard part. Being an effective leader,  communicating well,  and making things happen are often the bigger challenges. And speaking of Making things happen. Click that link for one of the greatest medical lectures. Ever.


Adenosine vs Verapamil Articles

Adenosine versus Verapamil for termination of SVT (AVNRT)

Comparison of adenosine and verapamil for termination of paroxysmal junctional tachycardia

Adenosine versus verapamil in the treatment of supraventricular tachycardia: A randomized double-crossover trial

Comparative clinical and electrophysiologic effects of adenosine and verapamil on termination of paroxysmal supraventricular tachycardia.

Contemporary management of paroxysmal supraventricular tachycardia.




Direct download: How_to_run_a_code.output.mp3
Category:general -- posted at: 4:42 PM

Which is more effective for pain and fever control: Acetaminophen or Ibuprofen? Should a patient in the emergency department with upper GI pain be started on an H2 blocker or a proton pump inhibitor? Special guest Anand 'The Swami' Swaminathan joins ERCast to explore these and many more medical quagmires. 

Bonus segment: How can a medical students present themselves well during critical rotations? In this case, we are talking about emergency medicine rotations.

Rob Says

  1. Work hard, always be curious, donʼt stress getting out right on time
  2. Presenting patients is one of your critical skills as a medical student
  3. Get the Emergency Medicine Secrets book so you know a rational approach to common medical emergencies, and keep the EMRA ddx card/ book in your pocket
  4. Present to the attendings but don't be a kiss ass
  5. Present patients the same way each time. Be concise with pertinent positives and negatives. When you give your differential diagnosis,, ALWAYS starting with the life threats based on the chief complaint. Even itʼs a typical migraine, emergency medicine is in the business of ruling out the life threats. As one of my internal medicine colleagues says, EM is in the business  of 'not to lose'
  6. As attendings, we want to know that the student ʻgetsʼ emergency medicine

Swami Says

  1. Show up to work on time. By on time, I mean the Joe Lex on time – 15 minutes early
  2. Recognize when it’s too busy and go into helper mode. This means not taking patients primarily (which is more work for us). Starting IVs, do EKGs, draw blood, sew lacerations, etc.
  3. Work hard. It’s as simple as that. When I work, I rarely sit, I keep moving all time. I should see the same from the students.
  4. There are three unforgivable sins in emergency medicine – laziness, stupidity and arrogance. It's preferable to have none of these. If you have one, you may be able to squeak by. If you have two, you are a waste of space. 

Acetaminophen versus Ibuprofen

Perrott DA et al. Efficacy and safety of acetaminophen vs ibuprofen for treating children’s pain and fever: a meta-analysis. Arch Pediatr Adolesc Med 2004; 158(6): 521-6.

2004 meta-analysis - summarized the findings from 17 randomized, controlled trials comparing the two drugs in children <18 years of age. Three studies involved pain, 10 involved fever, and all 17 involved safety. 


1. Pain – no difference between ibuprofen 4-10 mg/kg vs. APAP 7-15 mg/kg

2. Fever – ibuprofen 5-10 mg/kg superior to APAP 10-15 mg/kg (at 2 hours and more pronounced at 4-6 hours)

15% more children were likely to have reduced fever with ibuprofen compared to acetaminophen. 

When selecting for studies using only the 10mg/kg dose of ibuprofen, there was a doubling of the effect in support of ibuprofen. 

Safety: there was no evidence that one drug was less safe than the other (or placebo). The authors determined that this data was inconclusive and that more large studies would be needed to identify small differences in safety 

Pierce CA et al. Efficacy and safety of ibuprofen and acetaminophen in children and adults: a meta-analysis and qualitative review. Ann Pharmacother 2010; 44(3): 489-506.

First meta-analysis looking at the question in adults.

Qualitative review revealed that ibuprofen was more effective than acetaminophen for pain and fever reduction, and that the two were equally safe. 

From the quantitative data, the authors found that for pain, ibuprofen was superior in children and adults. For fever, ibuprofen was superior in children, but conclusions could not be made for adults due to insufficient data.

What about alternating acetaminophen and ibuprofen?

Malya RR. Does combination treatment with ibuprofen and acetaminophen improve fever control? Ann Emerg Med 2013; 61(5): 569-70.

1. Identified 4 studies that the author deemed high-quality and relevant to emergency practitioners.  

2. Three of the four studies found that the combination was more effective at reducing fever than either alone.

One study that looked at alternating regimens over 24 hours found that 6-13% of parents exceeded the maximum number of recommended doses (Hay, 2008). 

There is suggestion that the two drugs could act synergistically to cause renal tubular injury; however, acetaminophen and ibuprofen have different pathways of metabolism, and adverse effects in patients taking both have only been described in rare case reports.

EM Lyceum Review of APAP (acetaminophen) vs NSAIDS (ibuprofen). This review also includes a breakdown of PPIs vs H2 blockers, medical treatment for vertigo, and calcium channel blockers versus beta blockers for atrial fibrillation with rapid ventricular response (RVR)

Check out the RAGE podcast. In this episode of ercast, we discuss a recent round table on managing SVT (AVNRT) with verapamil versus adenosine.

Direct download: APAP_vs_NSAIDs.output.mp3
Category:general -- posted at: 6:25 PM

Interview with hematologist Dr. Tom Deloughery about a smattering of clotting quagmires...Superficial Thrombophlebitis, Recurrent Pulmonary Embolism, Calf Vein DVT, Clotted PICC Lines, Starting (loading) dose of warfarin, low molecular weight heparin, widowmaker clots.

Quandary 1. Recurrent pulmonary embolism

Your patient is on warfarin, INR is therapeutic and has another PE. What do you do?

Make sure it’s truly recurrent. If it is...

  1. How long have they been on anticoagulation? If it’s only a week, then the warfarin may not have had time to provide any benefit.
  2. If longer than a week and their INR has been therapeutic the whole time, consider that a warfarin failure. Start LMWH. This is a worrisome sign for an underlying malignancy or coagulopathy. LMWH is superior to warfarin for recurrent thromboembolic disease.
  3. On warfarin for years and has a recurrent PE. Do they get life long LMWH? Give LMWH for 3-6 months and, if they’re stable, restart the oral anticoagulant.

First dose of warfarin

1. How long to you need to wait to start warfarin after the first shot of LMWH? You can start both meds at the same time.

2. Is there a need for a loading dose of warfarin? Sort of....Dosing and effect are unpredictable. As a general rule, Tom gives young and otherwise healthy patients 10mg as a first dose. Over 65 or young and frail, first dose 5mg.

3. If your patient needs to restart warfarin after being off it for a while, do you need to bridge with LMWH until the INR is therapeutic?  In the setting of DVT and PE, yes. In atrial fibrillation, you probably don’t .

Superficial thrombophlebitis

Can  clot in the saphenous vein progress to DVT? Yes. 5-10%. Non saphenous vein clots progress to DVT at a rate of about 1%. As saphenous vein clot gets closer to the femoral vein, risk rises of it becoming a deep clot, but there are also perforator veins all along the saphenous vein that connect it to the deep system. Clot can connect from  the superficial (saphenous) vein to deep vein through a perforator at any point, but it’s less of a worry than deep propagation directly into the femoral vein near the groin.

Treating superficial thrombophlebitis needs to take into account the ‘thrombo’ (clot) and ‘itis’ (inflammation)

Tom’s approach

NSAIDS decrease rate of inflammation and clot extension

Therapeutic vs prophylactic LMWH: both decrease rate of inflammation and clot extension - outcomes are equal, so prophylactic LMWH is preferred (once a day, lower dose)

Small, under 5-7cm and not proximal (not upper half of thigh) NSAIDS

Larger than 5- 7cm or proximal, prophylactic dose of LMWH or fondaparinux (40mg daily)

Duration of therapy

There is uncertainty as to the optimal duration of therapy. Tom treats for two weeks. If patients are still symptomatic, treat for another two weeks.

Upper extremity thrombophlebitis

It is thought that upper extremity superficial thrombophlebitis has a more benign course. Treat with NSAIDS and hot packs. If this isn’t working, transition to LMWH.

What should you do with a PICC line clot?

Anticoagulation does not help with recannalization. Pull the line.

Putting in a new PICC right away - high rethrombosis rate.

Calf vein DVT

15-30% will grown and cause PE. Follow up ultrasound to check for extension is an option.

Unless there is a contraindication, treat with anticoagulation. ACCP recommends 3 months of treatment, Tom treats for 6 weeks.

Factor V Leiden mutation

9% prevalence in Portland, OR. Mostly a caucasion disease. Raises risk of first clot 3 fold (more DVTs than PE). Having this mutation does not increase risk of DVT recurrence.

Bonus point of the day

The SUPERFICIAL femoral vein is a DEEP vein. Perhaps the worst anatomic name ever. If you get a report that your patient has clot in the superficial femoral vein, that is a DVT, not superficial thrombophlebitis.


Direct download: Superficial_thrombophlebitis.output.mp3
Category:general -- posted at: 6:09 AM

The 4th anniversary of ERcast recognizes some of the luminaries who have helped and inspired me since the show's inception.

Direct download: ERCAST_Hall_of_fame_4th_anniv_special.output.mp3
Category:general -- posted at: 5:44 AM

We learn about the MUD PILES, the causes of anion gap acidosis, as medical students. And it gets even further drilled into us in residency. But sorting out a gap acidosis can be real challenge, even with a nifty mnemonic. To help us get smarter in understanding some of the nuance of gap acidosis, Sean Nordt, MD, PharmD.

Case: Alcoholic, diabetic with a blood glucose of 295, bicarbonate of 12, and an anion gap 28. Is this alcoholic ketoacidosis (AKA), diabetic ketoacidosis (DKA), toxic alcohol, something else? What is the cognitive process for sorting out this anion gap acidosis? 

 Nordt: Without additional history, send...

-Ethanol level
-Serum ketones (acetone and beta hydroxybutyrate) if possible
-Serum calcium- a good surrogate marker for ethylene glycol. Most hospitals have a volatile alcohol screen looking for methanol and isopropanol, but not ethylene glycol. To detect ethylene glycol, you’ll need to look at surrogate markers.
-Start IV fluids

Case continues: The patient has a normal mental status. Heart rhythm is sinus tachycardia in the low 100s. To treat this sinus tachycardia, he gets the sinus tachycardia antidote - 3 liters of normal saline. Since AKA (a starvation and volume depletion ketosis) is high on the differential diagnosis, he also gets a hamburger and apple juice. His labs are rechecked and few hours later and his bicarbonate is unchanged at 12 and anion gap drops slightly from 28 to 24.

How fast should the anion gap and serum bicarbonate to correct in AKA?

Nordt: It should start to improve in 1-2 hours and takes about 5-7 hours to reverse. If the anion gap and bicarbonate aren’t improving (or getting worse) in an hour or two, think about an alternate diagnosis.

Case continues: Since there’s not much improvement in the gap acidosis after several hours of re-feeding and fluid resuscitation, maybe this is not a case of AKA. Could it be DKA? Probably, but it could also be one of the many other causes of anion gap acidosis.  With a persistent gap acidosis, or maybe one that’s hard to figure out, are there clues to look for or other tests that can help?

Let’s go through the different things that we use, or tests we order, to sort out the gap.


Urine Ketones: May or may not be helpful. IN AKA, the predominate ketone is beta-hydroxybutyrate. The UA only looks for acetone. Also not helpful with toxic alcohols. May he helpful in later states of AKA.

Osmolar gap: A challenge to use effectively. For toxic alcohols, it’s only high early in the ingestion. When the alcohol gets metabolized, the osmolar load is less because the toxic metabolites don’t contribute to the osmolar load. If you forget to account for ethanol in your equation, you can have an elevated osmolar gap. A confounding factor is that the normal osmolar gap ranges from -14 to +14. So if your patient drank ethylene glycol but had a non-intoxicated osmolar gap of 0, they might get their gap up to 10 which, for them, is high, but within the normal laboratory range.

Ethanol: If the level is higher than 100, it’s less likely (not impossible) that there’s a toxic alcohol on board. If there was enough ethanol on board before a toxic alcohol ingestion, the patient shouldn’t make many toxic metabolites. If the ethanol is less than 100, toxic alcohols should still be on the differential. A high ETOH level does not completely rule out a toxic alcohol, it just makes it less likely. In other words, there should not be a metabolic acidosis unless the toxic alcohol was ingested before ethanol. In that case, the toxic alcohol would already have been metabolized and the ETOH would not be protective.

Serum Lactate: Helpful in sepsis. Confounder- one of the metabolites of ethylene glycol can cause a falsely elevated lactate on the lab assay.

Urine Calcium Oxalate Crystals: Looking for dihydrate (envelope shaped) crystals. The presence of crystals raises concern for a toxic alcohol ingestion. Absence of crystals does not help. The limitation of crystals is that if your patient is early in the poisoning, they may be acidemic but not have crystals. It takes a while for crystals to form

Woods lamp urine: Mostly useless. Normal urine can fluoresce, especially with high urine phosphorous. What might help is using the Woods lamp on their clothing to look for spill patterns as would come from drinking antifreeze.

Serum Calcium: You can’t get calcium oxalate crystals without calcium. As more crystals form, the patient will become increasingly hypocalcemic. Diuresing your patient can also cause the calcium to drop, but not significantly.

Case continues:

Working through the MUD PILES on this patient...


Methanol - Still possible

Uremia- No. Renal function normal

DKA- Still possible

P- Propylene Glycol. Possibly. Propylene glycol gets metabolized to lactic acid. Excessive propylene glycol from medications is unlikely in the ED (unlike the ICU where patients get many injectable meds), but can be found in pet friendly antifreeze.

INH- No       Iron- No          Infection-No evidence of this

Lactic acidosis- Still possible. He takes metformin but renal function is normal

Ethylene Glycol - Still possible

Salicylates- Salicylate level negative

The remaining MUD PILES...

  1. Methanol
  2. DKA
  3. Lactic Acidosis
  4. Propylene glycol
  5. Ethylene Glycol

How do we figure out the answer? We don’t always have to have the right answer in emergency medicine, but we shouldn’t be wrong.


Methanol- if you can’t get a level, it’s going to be a challenge because there aren’t good surrogate markers. Methanol is very osmotically active so, early on, it’s likely to elevate the osmolar gap.


Lactic Acidosis

Propylene glycol- if the lactate is getting worse or is severely elevated, think propylene glycol

Ethylene Glycol- when they get sick, they often have single digit bicarbonates. Watch  their calcium level (hypocalcemia is a surrogate marker). Patients with toxic alcohol ingestions get sick quick and continue to get sicker. If in doubt, start fomepizole.

Direct download: mind_the_gap_podcast.output.mp3
Category:podcasts -- posted at: 9:11 PM

What do lung nodules have to do with emergency medicine? Weʼd like to see ourselves as full time resuscitationists and while thatʼs one of our master skills, much of our job involves  taking care of non-critical patients and, even more so, having conversations with patients and their families. But arenʼt pulmonary nodules someone elseʼs problem, like the pulmonologist? Yes, and no. The pulmonologist is going to manage things in the long term, but the overwhelming majority of nodules are going to be incidental findings that land in your lap.

Clinical scenario:

You get a phone call from the radiologist on a CT chest, “Thereʼs no PE or sign of dissection, but thereʼs a 5mm non-calcified pulmonary nodule in the right upper lobe” What does that mean? Do you need to pay attention to it? Can you ignore it? What do you tell the patient?

The conversation often goes something like this, “Good news Mr. Jones, we donʼt see a blood clot and, oh by the way, the radiologist saw a small nodule.” For you, someone who is used to getting reports of an incidental pulmonary nodule, itʼs no big deal. For the patient, what they heard is, “You have cancer.” That may sound like hyperbole, but itʼs most patientsʼ first reaction.

Mr. Jones may or may not have cancer and Mr. Jones may or may not ask you questions. We donʼt want to do is to induce fear in the patient by our ignorance but we also donʼt want to dismiss the findings and ignore a possible malignancy.

Is this a bad nodule?

  1. Assessing risk and determining a long term follow-up/treatment plan for a patientʼs pulmonary nodule is beyond our scope of practice. But there are some background points that may help in your conversation.
  2. Around 5% of pulmonary nodules turn out to be cancer.
  3. The bigger the nodule, the higher the risk of malignancy. In smokers risk of a 5mm nodule being malignant is  1/500, 10 mm is 1 in 50, and  20mm is 1 in 10.
  4. Pulmonary nodules are common- half of smokers over 50 have at least one nodule. Up to 150,000 patients in the United States have a pulmonary nodule diagnosed each year.
  5. Young patients (<35) have a very low incidence of lung cancer (<1%)
  6. Complete calcification in a small nodule suggests benign etiology. When your radiologist says, “A 4mm completely calcified nodule in the right lower lobe,” thatʼs code for, “probably benign, but clinical correlation recommended.”
  7. The false positive rate for chest CT lung nodules varies by geographic location. The midwest has the highest false positive rate because of granulomatous disease.
  8. Risk factors: Itʼs no secret that non-smokers can get lung cancer, but smokers have 10 times the lung cancer risk of non-smokers. There are other risk factors like asbestos, radon and genetics, but smoking is by far the most heavily weighted. Also, the older the patient, the more likely a nodule is malignant.

Who needs follow-up and when should they get it?

This comes down to risk and benefit. Risk  that this nodule is malignant, the benefit of follow up imaging versus the risk of extra radiation, unnecessary biopsies, surgeries, anxiety, and medical bills. While it’s not well known in emergency medicine,  The Fleischner Society is a group in radiology that develops an evidence based consensus guideline on how to follow up  pulmonary nodules.


Fleischner Criteria


Nodule size and patient risk factors are the principle elements that determine timing and type of follow-up study needed. There are two main pieces of the Fleischner Criteria that are germane to emergency providers:

  1. Almost all pulmonary nodules are going to need a follow up CT scan. When that happens depends on risk factors and nodule size.
  2. Low risk (meaning a minimal or absent history of smoking and other known risk factors) patients with small nodules ≤4 mm do not need follow up.

These guidelines suggest that the likelihood of a small (≤4mm) nodule being cancer in low risk patient is so low that no further follow up is needed. Will some of these nodules turn out to be cancer? Yes, but striving for a zero miss rate in this group is not risk-benefit favorable. The likelihood of the patient having negative sequelae (radiation, unnecessary biopsy, surgery, financial hardship) is greater than the chance of the nodule being cancerous. Itʼs analogous to striving for a 0% MI miss rate. Cost far outweighs benefit.

The Other Side of the Fleischner Coin

Not everyone follows the Fleischner guidelines.  Some radiologists recommend follow-up imaging, or at least discussion, for every patient with a newly diagnosed nodule. Pulmonary nodules are a complex topic with multiple factors and variables that dictate the best course of action (or no action). These patients need follow up, preferably with a pulmonologist, to discuss risk level and decide what to do next. When weʼre talking about a one millimeter difference dictating a follow up scan versus doing nothing, one of my colleagues who is a chest radiologist, has this to say, “Depending on how much coffee Iʼve had to drink, I can measure the same nodule 20 times and have it be different every time, so trying to make separate recommendations for nodules that are ≤4mm or 4-6mm is silly to me. 

Tips for communicating with patients

  1. Emphasize that pulmonary nodules are a common finding but donʼt appear unconcerned. While you are trying to demystify and normalize the finding, avoid acting as if itʼs ʻnothing at allʼ.
  2.  Give simple explanations. Avoid confusing medical terminology
  3.  Itʼs OK to mention the possibility of cancer, even if itʼs remote. Donʼt avoid the elephant in the room (cancer). Your patient will probably start out with the idea that their nodule is cancer and prefer to have an honest conversation about it.
  4.  You will not know all of the answers but that wonʼt stop them from asking questions.
  5.  There is no correlation with the patientʼs actual risk of cancer and their level of concern. A 2 mm nodule in a 30 year old can evoke as much fear as a 2 cm nodule in a 60 year old smoker.
  6.  Reassure your patients they are not alone. Nodules are a common incidental finding and, after the patient leaves the the ED, a pulmonologist, PCP, etc will help guide them along the way.
  7.  If you donʼt think news of a nodule impacts your patientʼs psyche, here is a quote from a patient with a newly diagnosed nodule, not diagnosed cancer, but a nodule, “I actually gave notice at my job ... and spend more time with my kids. I donʼt know whatʼs going to happen and I donʼt want to miss anymore.”

What are you going to say to the patient?

Here are some example scripts for delivering the news of a newly diagnosed nodule...

“Mr Jones, good news, there's no blood clot. The radiologist did mention that he saw a small spot on your lung. The medical term for it is a nodule. It's 5mm, which is about half the width of your little finger or the size of a pea. We see these all the time and 95% turn out to be completely harmless so I don't want you to lose any sleep over this. You will, however need to make sure someone takes a look at this again with a CAT scan to make sure it's not growing. Iʼm going to refer your to our pulmonologist, a lung specialist, who is an expert in lung nodules and will help guide you the rest of the way.”

Maybe Mr. Jones is low risk.... “The chance of this nodule being anything serious is extremely low. The nodule is small, you donʼt smoke and youʼre young. The risk isnʼt zero, but itʼs pretty close. I still think you should follow up to discuss all of the options, but in all likelihood, this will not cause you any problems.”

Bottom line:

The overwhelming majority of pulmonary nodules are benign. The bigger they are, the higher the chance of malignancy. There is debate as to whether a very small lung nodule in a low risk patient needs follow up at all. Should an emergency provider make the call that no follow up is needed? I think there is too much uncertainty in sorting out all of the variables that go into risk factor assessment. I refer all patients with newly diagnosed nodules for follow up, risk stratification, and further discussion with their PCP or a pulmonologist.

Patients almost always have questions about the significance of their newly diagnosed pulmonary nodule. What they really want to know is if they have cancer. You canʼt know that looking by at a nodule one time. For a small nodule, itʼs about how it grows (or doesnʼt) on repeat studies. The things that make cancer more likely and follow up more urgent include size >4mm, age over 35, history of smoking, and nodules that are not completely calcified.

In the end, it may be cancer, but chances are, your patient is going to be just fine.


Bonus Section... Even more information about pulmonary nodules!

Historic Guidelines

Historically, all patients with non-calcified nodules were recommended to get follow-up chest CTs for 2 years. This was based on the pre helical CT era when most pulmonary nodules were found on chest x-ray. By the time a nodule is seen on CXR, itʼs often big. The old ACCP recommendation for indeterminate solitary nodules was follow up CT at 3-, 6-, 12-, and 24 months. Thatʼs five chest CTs (including the original study), no matter what. When you consider that upwards of 51% of smokers over age 50 have pulmonary nodules, that is a lot of negative CT scans, radiation, unnecessary biopsies, surgeries, anxiety, and money spent. With our ability to diagnose smaller nodules, we needed to change our thinking about what to do with them. Thatʼs what the Fleischner recommendations addressed. Itʼs not one size fits all.

Does it make a difference if the nodule is measured on CT or Chest X-Ray?

These measurements apply only to CT scans. CXR is too inaccurate. The work-up for nodules found on CXR varies depending on the scenario. The first step is to try to get old films to see how long it's been there. If no old films are available, depending on nodule features and clinical story, the patient needs either a CT scan or a short-term follow up CXR (4-6 weeks) to see if it persists. Sometimes it's tough to tell if a nodule is calcified on CXR. If it is obviously calcified, it doesn't need any follow-up.


What does calcification in a nodule suggest? Calcification in a small nodule suggests benign etiology. Mostly. A partially calcified nodule or one with eccentric calcification needs followupMalignancies, like scar carcinomas (from old granulomas), and mucinous adenocarcinomas can have small calcifications.


How should you think about terms like ground glass, semi-solid, and solid? Does appearance make a difference when it comes to determining nodule behavior?

In general...

  • Ground glass - grow slowly
  • Solid nodules- grow quickly
  • Party solid, which is between ground glass and solid- medium growth rate (itʼs also associated with adenocarcinoma)


  1. Known malignancy gets a different workup. A history of cancer means that nodule is more likely to be malignant.
  2. Young patients (<35) have a very low incidence of lung cancer (<1%). The radiation from multiple follow up CTs exposes them to greater risk than older patients
  3. In the setting of unexplained fever, nodular densities may represent infection


1) MacMahon, Heber, et al. "Guidelines for Management of Small Pulmonary Nodules Detected on CT Scans: A Statement from the Fleischner Society1."Radiology 237.2 (2005): 395-400.

2) Wiener, Renda Soylemez, et al. "What Do You Mean, a Spot? Physician Patient Communication About Lung NodulesA Qualitative Analysis of Patients’ Reactions to Discussions With Their Physicians About Pulmonary Nodules."CHEST Journal 143.3 (2013): 672-677.

3) Silvestri, Gerard A. "Lumps, Bumps, Spots, and ShadowsSolitary Pulmonary NoduleThe Scary World of the Solitary Pulmonary Nodule." CHEST Journal143.3 (2013): 592-594.

4) Mehta, Atul C., and Peter J. Mazzone. "An Attempt to Reach the Galaxy of the Pulmonary Nodules." American journal of respiratory and critical care medicine188.3 (2013): 264-265. 5) Slatore, Christopher G., et al. "What the Heck Is a “Nodule”? A Qualitative Study of Veterans with Pulmonary Nodules." Annals of the American Thoracic Society 10.4 (2013): 330-335.

6) Patel, Vishal K., et al. "A practical algorithmic approach to the diagnosis and management of solitary pulmonary nodules: part 1: radiologic characteristics and imaging modalities." Chest 143.3 (2013): 825-839. 7) Patel, Vishal K., et al. "A practical algorithmic approach to the diagnosis and management of solitary pulmonary nodules: part 2: pretest probability and algorithm." Chest 143.3 (2013): 840-846.

8) Shiau, Maria C., Elie Portnoy, and Stuart M. Garay. "Management of solitary pulmonary nodules." Clinically Oriented Pulmonary Imaging. Humana Press, 2012. 19-27. 9) Masciocchi, Mark, Brent Wagner, and Benjamin Lloyd. "Quality review: Fleischner criteria adherence by radiologists in a large community hospital."Journal of the American College of Radiology 9.5 (2012): 336-339.

10) Wiener, Renda Soylemez, et al. "‘The thing is not knowing’: patients' perspectives on surveillance of indeterminate pulmonary nodule." Health Expectations (2012).

11) McWilliams, Annette, et al. “Probability of Cancer in Pulmonary Nodules Detected on First Screening CT.” NEJM 369:10 (2013): 910-919.

Direct download: ERCast_Pulmonary_Nodule.output.mp3
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