Knowledge Translation: SUSPEND(ing) medical expulsive therapy belief

Editor’s Note: This week we are fortunate to get a great review of the recent SUSPEND article on medical expulsive therapy (MET) in the setting ofunnamed acute renal colic. We are doubly lucky to have the post reviewed by a urologist, Dr. Michael Leveridge (who not only is a great surgeon but knows how to rock a moustache). He reveals some of the thoughts of colleagues who participated in the #urojc twitter journal club on the article. This kind of cross-disciplinary collaboration is something we are looking forward to doing more of at BoringEM in the year to come! 


Pickard, R., Starr, K., MacLennan, G., Lam, T., Thomas, R., Burr, J., … & McClinton, S. (2015). Medical expulsive therapy in adults with ureteric colic: a multicentre, randomised, placebo-controlled trial. The Lancet.


Renal colic is a common cause for emergency room visits, with men and women having a lifetime incidence of 12% and 7% respectively [1]. Pain in these patients is theorized to be a result of increased pressure within the urinary tract proximal to the stone, causing an increase in peristalsis and smooth muscle spasm in the ureter and the release of pain mediators such as prostaglandin from distension of the renal capsule. [2] In addition to pain management, selective alpha-1 receptor antagonists such as tamsulosin and calcium channel blockers such as nifedipine are widely used off-label as medical expulsive therapy (MET) for ureteral stones. The rationale for this use is the inhibition of ureter spasm, which allows for more efficient peristalsis, relaxation of the ureterovesical junction and faster stone clearance. Tamsulosin achieves this through blockade of alpha-1-adrenergic receptors, which are highly concentrated in the distal ureters. Similarly, CCBs (mostly nifedipne) inhibit calcium influx, thus preventing smooth muscle contraction in the ureter wall. [2]

The evidence behind this practice, however, is highly controversial. A number of systematic reviews and meta-analyses have concluded that MET is effective, resulting in greater rates of stone expulsion, thus the use of MET for renal colic is recommended. [3,4] These reviews have been criticized for the inclusion of poor quality, heterogeneous studies that have small sample sizes, inadequate blinding, and poor methodological design. [5,6,7] Given the lack of high quality, blinded, randomized controlled trials assessing the effects of MET, the SUSPEND trial was initiated.

Clinical Question

Does either tamsulosin or nifedipine increase the likelihood of spontaneous stone passage compared to placebo, and if so, which is more effective?

Population18-65 years of age presenting with ureteric colic and a stone of =<10mm confirmed by CT KUB.

*exclusions: those needing immediate intervention, septic patients, eGFR <30mL/min, already on or unable to take alpha-blocker or calcium channel stabilizer. Over 65 excluded due to need for titration of nifedipine dosing.
InterventionSelf administration of either tamsulosin 400 mcg or nifedipine 30 mg orally once daily until spontaneous passage occurred, need for intervention was agreed upon, or for 4 weeks, whichever came first.
Outcome1. Spontaneous passage of stone in 4 weeks, defined as absence of need for intervention to assist passage.

2. 1. Number of days of analgesic use, visual analogue pain scale at 4 weeks, time to stone passage, health status, safety


n=1167 with 31 lost to follow-up

Primary Outcome

The spontaneous passage of stones within 4 weeks  occurred in 81% of the tamsulosin group, 80% in the nifedipine group and 80% in the placebo group.

InterventionAdjusted Odds Ratio (95% CI)p-value
MET vs placebo1.06 (0.70-1.60)0.78
Tamsulosin vs placebo1.09 (0.67-1.78)0.73
Nifedipine vs placebo1.03 (0.68-1.58)0.88

Secondary Outcomes

Days of analgesic use

  • Mean: Tamsulosin 11.6 days vs nifedipine 10.7 days vs placebo 10.5 days
  • MET vs placebo difference = 0.6 (-1.6-2.8); p=0.45

VAS Pain Scale at 4 weeks

  • MET vs placebo difference 0 (-0.4 to 0.4); p=0.96

Time to Stone Passage

  • Mean time: Tamsulosin 16.5 days vs nefedipine 16.2 days vs placebo 15.9 days
  • Adjusted MET vs. placebo difference 0.6 (-2.6 to 4.0) days, p=0.71


  • 3 adverse reactions in the nifedipine group (flank pain/diarrhea/vomiting, malaise/chestpain/headache, severe chest pain/SOB/arm pain)
  • 1 adverse reaction in placebo group (headache/dizziness/abdominal pain)


Urologic intervention as surrogate for efficacy:

  • The primary outcome was determined by lack of any required intervention to assist stone passage. While this is pragmatic and fits in with the study design, it is an imprecise measurement of the exact influence of MET on stone passage. While the patient-reported time to stone passage was assessed as a secondary measure (more on that below), this is an imprecise measure of stone passage following drug therapy.
  • Furthermore, 74.6% of the stones identified through the study were ≤5 mm in size, and stones of such size rarely necessitate an intervention. Thus the data should be interpreted with caution for patients with larger stones.

Secondary outcomes had low response rates (62% of participants):

  • The fact that attrition was relatively high for the 4-week follow-up survey, the collection of secondary outcome data was incomplete. Thus, secondary outcomes should be interpreted with appropriate skepticism. While the authors note there were no differences between the two groups, they noted younger people were less likely to return questionnaires, potentially introducing bias. Nonetheless, the primary outcome was well powered.


Author conclusions

“The results of our trial… showed that use of tamsulosin and nifedipine did not affect the proportion of patients needing further intervention to clear their stone during 4 weeks. “

“We found no evidence that the drugs reduced pain, hastened time to stone passage, or improved health state.”

Our Thoughts

Ultimately, this study generates evidence that tamsulosin or nifedipine have minimal role in the acute setting of renal colic. While there are a few arguable points regarding subgroups and statistical methodology (see discussion about this on EM Literature of Note) [8], the completion of this rigorous, high-quality study shows that benefits from the routine use of MET are insignificant.

Take Home Points

  • This blinded, randomized controlled trial indicated no benefit to the use of MET for ureteric stone, showing it to be no better than placebo at improving likelihood of stone clearance
  • This study showed no reduction in pain or decrease in time to passage as reported by patients
  • There study showed no significant benefit to using MET to improve stone clearance for stones


  1. Worcester EM, Coe FL. Nephrolithiasis. Prim Care. 2008;35(2):369-91, vii.
  2. Golzari SE, Soleimanpour H, Rahmani F, et al. Therapeutic approaches for renal colic in the emergency department: a review article. Anesth Pain Med. 2014;4(1):e16222.
  3. Lu Z et al. Tamsulosin for ureteral stones: a systematic review and meta-analysis of a randomized control trial. Urologia Internationalis 2012; 89(1):107-115
  4. Campschroer T, Zhu Y, Duijvesz D, Grobbee DE, Lock MTWT. Alpha-blockers as medical expulsive therapy for ureteral stones. Cochrane Database of Systematic Reviews 2014, Issue 4.
  5. Available at: Accessed September 9, 2015.
  6. Available at: Accessed September 9, 2015.
  7. Available at: Accessed September 9, 2015.
  8. Available at: Accessed September 9, 2015.

Image from Wikipedia

Author information

Jared Paty

Jared Paty

The post Knowledge Translation: SUSPEND(ing) medical expulsive therapy belief appeared first on BoringEM and was written by Jared Paty.

Medical Concept: Hyphema

The Case

A 25 year old man presents 5 hours after an injury sustained in an intense racquetball match. He states that he had not been wearing protective eyewear at the time and that a ball hit him directly in his left eye. He reports occular pain and immediate blurry vision that has progressively worsened since his injury. A quick pen light examination of the left eye reveals an obvious hyphema filling just over a third of the anterior chamber.

What is a hyphema?

Hyphema refers to the presence of blood in the anterior chamber of the eye.  A microhyphema is a hyphema visible only with the aid of a slit lamp examination. In the examination of a patient with ocular trauma, a hyphema is an injury that can portend both acute and long term sequelae as well as being associated with other devastating ocular injuries that must be addressed in a timely manner.

The most common cause of a hyphema is trauma, usually blunt, wherein vessels of the iris and ciliary body are torn and blood enters the anterior chamber [1]. A paper studying the epidemiology of hyphema found the median age of patients to be 23 years old, with 88% of patients being male. The largest single cause of injury was sports or recreation with the majority of injuries being preventable with proper eyewear [2]. Hyphemas can also occur spontaneously without trauma as a result of a variety of disease processes. Selected causes include leukemia/lymphoma, ocular neoplasms, neovascularization of the iris, herpetic keratouveitis, complications with artificial lens implants and post-surgical hyphemas [3]. Coagulapathies and the use of anticoagulant medications are often provoking factors for other underlying causes but rarely cause hyphemas by themselves [4].

Approach and Considerations

A thorough history in a patient with ocular trauma should pay careful attention to the mechanism of injury, detailing the time, force, direction and potential for intraocular foreign bodies. Patients with hyphema commonly experience ocular pain and decreased visual acuity. The extent of visual loss and its time course should be elicited from the patient. Delayed or evolving loss of vision following the initial injury should raise suspicion for rebleeding or raised intraocular pressure [3]. A past medical history of sickle cell disorder, recent ocular surgery and the use of anticoagulant medications should be sought.

In the setting of trauma to the eye, care should be taken to consider other potential injuries including:

  • Open globe injury
  • Traumatic iritis
  • Lens dislocation
  • Corneal abrasion
  • Retinal detachment
  • Vitreous hemorrhage
  • Orbital floor blow out fracture

A good history and physical examination can help to rule out some of these concomitant injuries. Traumatic iritis, presents within a few days of a blunt ocular injury with photophobia, redness, and ocular pain not completely relieved by topical tetracaine drops. Slit lamp examination typically reveals perilimbial conjunctival injection or “ciliary flush” and cells and flare in the anterior chamber. Diplopia may be present with either a lens dislocation or extraocular muscle entrapment from an orbital floor fracture. Diplopia from entrapment of one of the ocular muscles results in a binocular diplopia, or double vision, that resolves when one of the eyes is closed. Lens dislocation would result in monocular diplopia. Other signs of an orbital floor or “blow out” fracture includes enopthalamos, limitation of upward gaze, and sensory loss over the cheek and upper lip. Retinal detachments may also occur following blunt trauma and presents with classic signs of flashes of light, floaters and visual field cuts such as the “gray curtain” effect. Open globe injuries can be obvious or occult. Siedel’s sign is useful in the identification of an open globe injury:

Physical examination specific to hyphemas in the emergency department should include visual acuity assessment, measurement of intraocular pressure (once an open globe injury has been ruled out) and a slit-lamp examination to measure the extent of the bleed and for the presence of clotted, dehemoglobinzed blood.

Hyphemas can be graded on the following scale:

MicrohyphemaVisible only by use of a slit lamp, often only circulating red blood cells floating in the anterior chamber are seen
Grade 1Less than one third of the anterior chamber
Grade 2Between one third and one half of the anterior chamber
Grade 3Greater than half of the anterior chamber
Grade 4“8 Ball” hyphema with the entirety of the anterior chamber filled with clotted blood. Hyphemas that fill the entire anterior chamber with fresh blood may become smaller once clotting occurs

This grading system has prognostic implications and can help determine the decision for admission [5].

Consideration of screening for sickle cell disease should also be made in the appropriate patient population. Patients with sickle cell disease are at increased risk for secondary glaucoma by occlusion of the trabecular meshwork by sickled red blood cells, blocking the regular drainage of aqueous humor from the anterior chamber and leading to a rise in intraocular pressure. The use of carbonic anhydrase inhibitors such as acetazolamide is contraindicated in these patients as they may promote sickling of red blood cells by lowering the pH in the anterior chamber [6].

Management and Disposition

The emergency department management of hyphema centers on control of any ongoing bleeding within the eye, prevention of any subsequent bleeding and the anticipation and treatment of hyphema complications. A number of treatment modalities for the treatment of hyphema have been traditionally described, however there is often little evidence that these measures improve final visual acuity [7].

Use of an eye shield is recommended for prevention of any potential further trauma to eye. Elevation of the head of the bed to 35-40 degrees helps to promote settling of blood inferiorly and prevent occlusion of the trabecular meshwork by red blood cells [3]. In the past, patients were admitted and put on bed rest to minimize the risk of rebleeding, however there is significant controversy regarding the benefits of this intervention [7],. Most patients are now counseled to refrain from strenuous activity and managed as outpatients, with frequent follow-up examinations.

Topical anti-fibrinolytic drugs including aminocaproic and transexamic acid have been used in hyphemas and help to reduce the occurrence of rebleeding[8]. However there is no definite evidence suggesting they help to improve final visual acuity[7] and these are now rarely used.

A cycloplegic, such as atropine 1%, is often used with the intent of preventing pupillary movement thus limiting further movement of torn iris vessels and promoting tamponade [6]. The agent of choice is generally best directed by the consultant ophthalmologist, as certain eye drops such as atropine have a long duration of action.

Pain management is best accomplished by acetaminophen. The use of platelet inhibiting drugs is not recommended.

Recognition and management of raised intraocular pressure is of paramount importance as bleeding may block the trabecular meshwork of the eye and prevent the normal drainage of aqueous humor leading to secondary glaucoma. The normal intraocular pressure (IOP) of the eye is between 10 and 20 mmHg of mercury. Elevations above this range, especially above 35mmhg, are concerning and can lead to damage to the optic nerve. Treatment of raised IOP is usually accomplished initially with the use of a topical β-blocker such as 0.5% timolol, which acts to decrease the production of aqueous humour. Topical α2-agonist therapy with an agent such as brimonidine can also be used. Acetazolamide, a carbonic anhydrase inhibitor, also decreases production of aqueous humor at a dose of 500mg IV or PO. Hyperosmolar therapy with mannitol reduces total volume of aqueous humour through the generation of an osmotic gradient, drawing fluid into the intravascular space. Dosing is at 1 to 2 g/kg IV [3].

All patients with hyphema deserve prompt consultation by an ophthalmologist, as some complications may not be apparent until several days after the injury. Rebleeding commonly presents within the first few days following the initial injury as initial clotting retracts [3], and is associated with a worse prognosis. A hyphema may also lead to the development of membranous anterior or posterior synechiae secondary to the inflammatory process in the eye, whereby the iris may become adherent to the cornea or the lens respectively. Corneal staining by blood and angle recession glaucoma are other potential complications.


  1. Rosen’s Emergency Medicine: Concepts and Clinical Practice (8thed) 2014. Philadelphia. Elsevier Saunders Inc. – Chapter 71
  2. Khan-Farooqi, H. R., Chiranand, P, Edelstein, S.L. (2010). Epidemiology and Outcome of Traumatic Hyphema: A Retrospective Case Series. Investigative Opthalmology and Visual Science, 51(13), 1314.
  3. The Wills Eye Manual: Office and Emergency Room Diagnosis and Treatment of Eye Disease (6th ed) 2012. Ovid Technologies, Inc. – Chapter 3
  4. Bagnis, A., Lai, S., Lester, M., Bacino, L., Traverso, C. E. (2008). Spontaneous Hyphema in a Patient on Wafarin Treatment. Br J Clin Pharmacol. 66(3), 414-415.
  5. Shammas, H.F., Matta, C.S. (1975). Outcome of Traumatic Hyphema. Ann Ophthalmol. 7(5), 701-706.
  6. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide (7thed) 2011. New York. McGraw Hill Companies Inc. – Chapter 268
  7. Gharaibeh A, Savage HI, Scherer RW, Goldberg MF, Lindsley K. Medical interventions for traumatic hyphema. Cochrane Database of Systematic Reviews 2013, Issue 12. Art. No.: CD005431. DOI: 10.1002/14651858.CD005431.pub3
  8. Crouch, E.R. Jr, Williams, P.B., Gray, M.K., Crouch, E.R., Chames, M. (1997) Topical Aminocaproic Acid in the Treatment of Traumatic Hyphema. Arch Ophthalmol. 115(9), 1106-1112.

Author information

Paul Young

Paul Young

R1 Family Medicine at the University of Calgary

The post Medical Concept: Hyphema appeared first on BoringEM and was written by Paul Young.

Medical Concept: ECGs in Syncope

Editor’s Note: This absolutely fantastic piece on ECG findings in syncope has many ECGs. To get a better image click on the picture to to access the full size image at  the LIFTL ECG library. A huge shout out and thanks to the folks at LITFL for compiling such a great library!

The Case

You are a medical student working in the emergency department when a 31-year-old man presents following a syncopal episode.  

The patient had been working outdoors on a hot day. He sat for a rest, and when he stood up to return to work, he felt nauseated and clammy. A co-worker told him he ‘didn’t look so good’. A few seconds later, he lost his vision. He then passed out. After a few seconds, the patient returned to consciousness. He was alert and oriented, but still felt nauseated and “not quite right”.

When you see him in the emergency department, the patient says he feels entirely well. Your attending hands you the ECG and asks what you think.


Syncope is a common presenting complaint in the emergency department, comprising almost 1% of all visits [1]. In many cases, the goal of ED management is to rule out a life-threatening cause for syncope rather than find a definitive diagnosis. The ECG is the workhorse of ED syncope work-up. Often, we don’t see any specific findings, but the syncope ECG is a place where sharp analytic skills can detect life-threatening conditions and make a big difference in patient outcomes. It’s important to know what to look for.

Rate and Rhythm

Commonly, we approach the ECG starting with the rate and rhythm. Suppose your attending hands you an ECG that looks like this:


(Image courtesy of LITFL ECG library)

There are any number of ways to determine the rate. Here, we have five beats over a five second strip, giving a heart rate of 60 bpm. The first thing we notice about the rhythm is the mismatch between P waves and QRS complexes. In a normal ECG, we see one QRS for every P and vice versa; here, that is not the case.

Here, we see regularly-spaced P waves, so we know the atria is contracting in a regular manner. We have three narrow QRS complexes following three P waves, with a constant PR interval each time. Then we have a dropped QRS complex. Because these QRS complexes are narrow and follow associated P waves we know that these are atrial beats conducting down the AV node to the ventricles. If we had a longer rhythm strip, we’d see a regular pattern of 3 normally conducted QRS complexes each following a P wave, and then a fourth P wave with a missing QRS complex. This pattern of a dropped QRS complex tells us that we are dealing with 2nd degree AV block, which comes in two subtypes: Mobitz type 1 and Mobitz type 2.

In Mobitz type 1, the PR interval becomes longer with each conducted beat, until a beat is not conducted at all, and then the cycle repeats. Mobitztype 2, in contrast, displays a constant PR interval for all conducted beats. We’re focusing on type 2 here because it has a worse prognosis and is more likely to progress to complete AV block [1, 2]. If and when it does, the ECG may look like this:



Image courtesy of LITFL ECG Library

Image courtesy of LITFL ECG library

Image courtesy of LITFL ECG library


Image courtesy of LITFL ECG library

Image courtesy of LITFL ECG library

In each of these examples, we see the hallmark of complete AV block: regular P waves marching straight through regular QRS complexes. This makes the PR intervals variable. Complete heart block can cause syncope if the escape rhythm does not provide enough cardiac output, and it should always be considered in a case of syncope. Usually, the resulting ventricular rate is bradycardic. Complete heart block can be intermittent, typically on a background of Mobitz type 2 second degree heart block. If it is intermittent, the patient may only be symptomatic when they are in complete heart block.

Keep in mind other varieties of conduction system disease as well. High-grade AV block (having 3 or more P waves for every conducted QRS) and 2:1 AV block can both be caused by either second-degreeMobitz type 1 or second-degree Mobitztype 2 rhythms. In second-degree type 1 block the disease is in or above the AV node,and usually has a narrow QRS. In second-degree type 2 block, the disease is below the AV node in the distal conducting system, and so typically has a wide QRS. An old ECG can be useful to tell the difference between type 1 and type 2 in high-grade or 2:1 block. If the patient previously had type 1, then proximal conduction system disease (Mobitz type 1) is more likely the cause of their 2:1 or high grade AV block. Similarly, a long rhythm strip may show intermittent runs of lower grade AV block which may be more clearly type 1 or type 2., Response to atropine (AV node disease gets better, infranodal disease doesn’t) is another recommended trick to differentiate the two [1, 3].

In the case of extensive conduction disease, the term “trifascicular block” is sometimes used when there is evidence of disease in the right bundle branch, the left anterior and the left posterior branches of the His-Purkinje system. Most commonly, this means a right bundle branch block with a left anterior hemiblock, and a prolonged PR interval suggesting disease in the left posterior fascicle [4]. In the example below, we’ve got the typical right bundle branch block morphology in the anterior leads, the left axis deviation suggestive left anterior fascicular block, and first degree AV block.

Image courtesy of LITFL ECG library

Image courtesy of LITFL ECG library

In cases like these, extensive conducting system disease can be present despite a one-to-one correlation between P waves and QRS complexes. These patients are at risk of deteriorating into third degree AV block.

ECG Segments

After the rate and the rhythm, let’s take a look at individual segments of the ECG. We’ve already discussed prolonged PR intervals, but shortened PR intervals are important as well, especially in the setting of syncope. The big things to consider here are Wolf-Parkinson-White and Lown-Ganong-Levine syndromes, both of which can cause re-entrant tachycardia and cardiac syncope.

In Wolf-Parkinson-White, an abnormal branch of conducting tissue connects one atrium to the corresponding ventricle. The accessory pathway bypasses the relatively slow AV node and triggers a slower-spreading myocardially-conducted ventricular depolarization, which typically runs into the ventricular depolarization coming through the regular conduction system. Thisgives the ECG its trademark pattern – because the AV node is bypassed by the accessory pathway, the PR interval is shortened. Then the initial ventricular depolarization is slow, with a sluggish uptick, before it is eclipsed by the regularly conducted depolarization. The result is the delta wave, seen below [3].

Image courtesy of LITFL ECG library

Image courtesy of LITFL ECG library

Lown-Ganong-Levine is similar, to WPW, except that the accessory bundle is next to, or even within, the AV node [3,5]. Electrical activity bypasses the AV node, resulting in a short PR interval, but there is no slow ventricular depolarization to cause a delta wave because the depolarization continues down the normal His-Purkinje system.

Image courtesy of LITFL ECG library

Image courtesy of LITFL ECG library

Both of these syndromes create ideal conditions for a re-entrant tachycardia, where a feedback loop conducts a signal inappropriately quickly in a constant circuit between the atria and ventricles. In the case of WPW, where the accessory pathway is outside the AV node, it is called atrio-ventricular re-entrant tachycardia (AVRT), whereas if the AV node itself contains the accessory pathway (as in LGL), it is termed atrio-ventricular nodal re-entrant tachycardia (AVNRT). Occasionally, an ECG might capture the AVRT/AVNRT itself, which shows as a rapid regular tachycardia, usually consisting of narrow beats conducting anterograde down the AV node. Sometimes, it can appear as wide beats conducting retrograde up the AV node.

QRS Morphology

There are a few arrythmogenic conditions that present with abnormal QRS morphology. Of these, the Brugada syndrome is one of the most common [1]. Brugada is the result of abnormal cardiac sodium channel function, which can cause patients to spontaneously go into runs of ventricular tachycardia and fibrillation. If self-terminating, this may present as syncope. If not self-terminating, this may present as sudden cardiac death. There are a couple subtypes, and each has its own QRS morphology. Type 1 has the classic “coved” shape to the ST segment and inverted T wave, usually seen best in leads V1-V3. This type has a poor prognosis and is more likely to cause sudden cardiac death [6]. Type 2 has the “saddleback” ST segment elevation followed by a normal, inverted, or flattened T wave, and can confused with a normal variant ECG. Brugada is an important syndrome to check for on a syncope ECG, as catching it early allows for a lifesaving implantable cardioverter-defibrillator to be placed.

Image courtesy of LITFL ECG library

Image courtesy of LITFL ECG library

In the above, note the downsloping, biphasic ST stegment typical of Brugada Type 1. 

QT Interval

After looking at the QRS complex, consider the QT interval. There can only really be two things wrong with the QT interval: too long, and too short. Too long, and the patient runs the risk of having the dreaded R-on-T phenomenon: a PVC occurs during the preceding T wave, setting off a run of polymorphic ventricular tachycardia called Torsades des Pointes. This can be self-terminating, causing a clinical presentation of syncope.

Long QT is defined by a corrected QT of greater than 450 ms for men, or 470 ms for women. There are a few formulas for calculating the corrected QT (“QTc”) from the observed QT and the heart rate, but a good rule of thumb (which only applies at normal heart rates) is that a QT interval longer than half a cardiac cycle is too long. Long QT can be either congenital, or acquired. Acquired is more common [3],  and the culprits to keep in mind are antiarrythmic drugs (especially class I and 3), antipsychotics, antiemetics, antihistamines, and antibiotics – the “anti” drugs. Also consider whether your patient has low levels of potassium, calcium, and magnesium, or ischemic and hemorrhagic stroke, all of which can precipitate prolonged QT [1, 3].

Like Long QT syndrome, Short QT syndrome can be caused by genetic mutations, medications (especially digoxin, sympathomimetics) and electrolyte disturbances (hyperkalemia and hypercalcemia – again, the opposite of Long QT Syndrome) [3]. People with this are at much higher risk for atrial fibrillation, ventricular tachycardia/fibrillation, and sudden cardiac death than the general population [3].If these patients have a self-limited run of ventricular tachycardia, they may end up in the emergency department after a syncopal episode, where a sharp analysis of their ECG may save a life by leading to treatment of the underlying cause and/or implantable cardioverter. Short QT syndrome has a QTc of < 330 ms, and typically has tall peaked T waves immediately after the QRS with no ST segment [3]. See the example below:

Image courtesy of LITFL ECG Library

Image courtesy of LITFL ECG Library

ST Segment

After we have examined the QT segment, we focus in on the ST segment. While myocardial infarction and pulmonary embolism are less common causes of syncope, particularly in the absence of other symptoms, they are potentially fatal and must not be missed. Look for ST segment elevations or depressions that might clue you in to an MI. Also look for ECG findings suggestive of PE. Some of the more common findings are sometimes called the “right ventricular strain pattern” and include tachycardia, T wave inversions in V1-V3 and inferior leads, and RBBB morphology [1, 7].

ECG 10

Image courtesy of LITFL ECG library

The “classic”appearance of the ECG in pulmonary embolism is sometimes called S1Q3T3 – a pronounced S wave in lead I, with Q waves and T wave inversions in lead III. Be warned, however: it is not sensitive, so the absence of S1Q3T3 means nothing at all, and while it is reasonably specific, the ECG alone can’t make the diagnosis of PE [1, 8, 9, 10].

Image courtesy of LIFTL ECG library

Image courtesy of LIFTL ECG library

The Case Revisited

So what about this case? Returning to the patients ECG, you take a thorough, systematic approach, looking for:

  • Rate and rhythm, looking for AV block particularly
  • Axis, looking particularly for any deviations suggestive of RBBB or hemiblocks
  • QRS and ST segment morphology, looking for delta waves, ST segment and T wave changes suggestive of Brugada, MI, or PE, and checking again for bundle branch morphologies
  • Intervals, including PR intervals and QT intervals.

In this otherwise healthy young man, you find a normal ECG. Unexciting, but common. Since his physical exam and other investigations are also normal, he is discharged home with a diagnosis of vaso-vagal syncope.

Take home points

  • The ECG is a key part of a syncope work-up.
  • Always consider life-threatening causes of syncope, including MI and PE
  • Have a systemic approach to syncope ECGs that includes:
    1. Bradyarrythmias and conduction system disease
    2. QRS and ST segment morphologies
    3. PR and QT segments


  1. Marx, John A., Robert S. Hockberger, and Ron M. Walls. Rosen’s Emergency Medicine, 8th Ed. Philadelphia: Saunders Elsevier, 2014.
  2. Burns, Ed. Life in the Fast Lane – “AV Block: 2nd Degree, Mobitz II”. (accessed April 2, 2015).
  3. Das, Mithilesh K. , and Douglas P. Zipes. Electrocardiography of Arrythmias: A Comprehensive Review. Philadelphia: Saunders Elsevier, 2012.
  4. Burns, Ed. Life in the Fast Lane ECG Library – “Trifascicular Block”.2014. (accessed April 02, 2015).
  5. Life in the Fast Lane ECG Library: Pre-Excitation Syndromes. (accessed April 03, 2015).
  6. Marine, Joseph E. “ECG Features that suggest a potentially life-threatening arrythmia as the cause for syncope.” Journal of Electrocardiology, 2013:46(6): 561-568.
  7. Oullette, David W, and Patocka, Catherine. 2012. Pulmonary Embolism.  Emergency Medicine Clinics; 30(2): 329-375. Link
  8. Marchick, Michael R., et al. 2010. 12-Lead ECG findings of pulmonary hypertension occur more frequently in emergency department patients with pulmonary embolism than in patients without pulmonary embolism. Annals of Emergency Medicine; 55 (4): 331-335. PMID:19766353
  9. Rodger, M, et al. 2000. Diagnostic value of the ECG in pulmonary embolism. Diagnostic value of the electrocardiogram in suspected pulmonary embolism.American Journal of Cardiology; 86(7): 807.PMID: 11018210
  10. Witting, Michael, AmalMattu, Robert Rogers, and Christian Halvorson. 2012. Simultaneous T-Wave Inversions in Anterior and Inferior Leads: An Uncommon Sign of Pulmonary Embolism. Journal of Emergency Medicine; 43(2) : 228-235. PMID:22142671

Author information

David Wonnacott

David Wonnacott

Resident physician

The post Medical Concept: ECGs in Syncope appeared first on BoringEM and was written by David Wonnacott.

Phone a Friend: the proficient paramedic

Editor’s Note: This series was created by third year medical student Gerhard Dashi and will highlight the important work that our interprofessional colleagues do.  Keep your eye open for more “Phone a Friend” articles and if you would like to be featured or know a colleague that should be highlighted follow this link to complete the questions on a google form. 

Background on the “Phone a Friend” Series

This is the second interview in the “Phone a Friend” series. This series aims to give our interprofessional colleagues another chance to remind their Emergency Medicine peers, especially the juniors ones, what they do and how we can most effectively work together.

For our first interview with pharmacist Dr. Bryan Hayes, click here.

Although we have sent requests to some of our favorite healthcare professionals, we would love to hear from you or someone you know. Please send us the questions you would like answered or your own answers to the following questions. We hope to feature your heroes and your responses on upcoming posts.

The Proficient Paramedic

Ian Drennan PhD(c), BScHK, ACP (@IanR_Drennan) completed his undergraduate degree training at the University of Guelph and his Primary Care Paramedic diploma from Humber College. He has been a paramedic in southern Ontario for six years, obtaining his Advanced Care Paramedic diploma from Durham College. Ian also holds part-time faculty positions in the health sciences department at both Georgian College and Centennial College. Ian

Furthermore, Ian is a PhD candidate at the Institute of Medical Science, University of Toronto and Rescus at St. Michael’s Hospital. His thesis is focused on the development of clinical prediction rules and the treatment of out-of-hospital cardiac arrest patients early in the post-arrest period as well as other aspects of cardiac arrest care. Ian is also involved in the development and implementation of initiatives aimed to examine the impact of community paramedic interventions.

In addition to his PhD work, Ian is a member of a number of committees related to EMS practice and research including the steering committee for the Canadian Paramedic Research Network, a peer reviewer for a number of medical journals, and a writing group member for the 2015 American Heart Association Guidelines for CPR and ECC.

Profession/current job title: Paramedic/Clinical Researcher

Years of practice: 7

Country of practice: Canada

Practice setting: Pre-hospital medicine

How does your work impact patient care? 

As pre-hospital providers, we have unique interactions with our patients in that we have limited time and diagnostics, but can in some instances have a critical role in outcomes. The biggest impact I have on patient care is by always acting as a patient advocate. This involves treating patients to the best of my abilities; respecting their wishes, and treating them medically when I can and is appropriate. I need to be an advocate for my patients and provide them with the best treatment I can, even if the hospital is just a short distance away. For me, I always go the extra distance and put in the extra effort to treat my patients the way I feel is best. Furthermore, advocacy for my patients in the hospital can have an enormous impact on their care by pushing for a bed when I feel my patient is acutely ill.

What is the most common misperception about your role in the the treatment of the acutely ill? 

The misconception that still follows paramedics is that we are all still very technician-based. Paramedics today have higher and higher levels of training, enabling them to think critically and fulfill the role of a clinician. My hope is that paramedics will continue to become more valued members of a healthcare team.

How can the ED utilize your skills more effectively? 

Paramedics do not play a large role in ED care in most centres. I think the relationships that we have with all levels of ED staff are improving and are for the most part professional. The interaction between paramedics and ED staff when medics first arrive in hospital and during patient transfer of care can make a large difference in patient care. This is where I think other health care professionals can use the paramedic’s skills effectively, by listening to the report and treatment provided so far.

What is your favourite part about working in an interprofessional environment? 

Working in an interprofessional environment allows for professional growth and development by working and learning from others around you that have experience and expertise in different areas. Each profession brings different strengths and weaknesses that can accelerate learning and promote excellence.

What is the most difficult aspect of working in the ED? 

Most difficult part of working in an interprofessional environment is working among the complex relationships with different individuals and different providers.

What can be done to improve interprofessional practice in the ED?

Again, our interprofessional interactions are limited in the ED, however I think that ensuring appropriate communication during patient handoffs is important to ensuring good patient care. As paramedics we often have pieces of the story/history that were gathered in the pre-hospital setting that are important for patient care. We also have experience dealing with acutely ill patients and make sound clinical judgements in these situations.Something what I think would also be beneficial in improving interprofessional relationships is to train as we practice. Incorporating more training, rounds, simulation that used paramedics with the ED staff would help to overcome some barriers that currently exist.

What is your biggest pet peeve when you are working in the ED? 

My biggest pet peeve inside and outside the ED is not being listened to. Spending time gathering information, treating a patient, and building a rapport with the patient only to not be listened to when transferring care to the ED really hurts interprofessional relationships. I make sure that I make an effort in my practice to listen to others whom I interact with in this same respect.

What is the aspect of your job that you are most proud of?

The thing I am most proud of in my career is my continued work to increase the level of care provided by all paramedics in the pre-hospital setting. This includes, increasing the skillset of medics, increasing fundamental knowledge and clinical decision making, increasing the education and research capacity of paramedics and finally improving the interprofessional interactions that occur between paramedics and other healthcare providers as we become more respected members of the healthcare community.

Can you provide an example of an optimal patient interaction (e.g. one in which you used all of your training to positively impact the outcome for a patient)?

For me, optimal patient interactions are ones in which I have helped patients to make decisions regarding their healthcare. In the prehospital setting, this often involves decisions around whether or not to go to the hospital – for example, a patient with new onset rapid atrial fibrillation, chest pain, and mild shortness of breath who refuses to go and get examined at the hospital. Being able to sit with these patients, to discuss their situation and what might happen if they don’t get treated, and to help them come to the right conclusion is extremely rewarding.

Author information

Gerhard Dashi

Gerhard Dashi

Gerhard Dashi is a second year medical student at Queen’s University with growing interests in Emergency Medicine, mentorship, interprofessional teamwork, and #FOAMed.

The post Phone a Friend: the proficient paramedic appeared first on BoringEM and was written by Gerhard Dashi.

Medical Concept: Delirium tips and tools

The Case

A 65-year-old woman presents to your emergency department (ED) feeling fatigued and weak. Her history is vague, and you have to redirect her conversation many times. She appears drowsy but is easily rousable. Her blood work, ECG, chest x-ray, urine all come back normal. When you return to re-asses her, you see that she is quietly resting in your ED with her daughter at the bedside. Her daughter tells you that the patient is “just tired today”; the two want to go home to get some proper sleep.

You astutely recognize that the patient may be delirious and require further work-up. What tools are available to help you confirm this diagnosis?


Recently, a very well-written article by Dr. Woods highlighted an approach to geriatric patients in the emergency department1. As explained in the article, it is important to get a full functional assessment of the geriatric patient, and to be aware of the variety of tools available to do so. The elderly make up a large proportion of the ED population. With their many comorbidities, we focus much of our efforts on the common conditions that imminently threaten lives. The pleasantly confused quietly sleeping elderly, however, merit equal consideration and a thorough diagnostic evaluation.

Why is delirium important?

Delirium is present in approximately 7% to 10% of older ED patients, but often goes undetected2-4. In fact, studies have shown that emergency physicians identify delirium in only 16% – 35% of positive cases2-4 .Patients discharged home from the ED with unidentified delirium have 6 month mortality rates almost three times greater than those without delirium5. Delirium is an independent predictor of death among older adults seeking care in the ED6.

What is delirium?

Delirium, as defined in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), is a syndrome of acute change in mental status marked by inattention, cognitive changes, and a fluctuating course7.

Diagnostic Criteria of Delirium in DSM V

A. Disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) and awareness.
B. Change in cognition (e.g., memory deficit, disorientation, language disturbance, perceptual disturbance) that is not better accounted for by a preexisting, established, or evolving dementia.
C. The disturbance develops over a short period (usually hours to days) and fluctuates during the course of the day.
D. There is evidence from the history, physical examination, or laboratory findings that the disturbance is caused by a direct physiologic consequence of a general medical condition, an intoxicating substance, medication use, or more than one cause.

Keeping a wide differential diagnosis

The causes of delirium are complex and not fully understood. Delirium results from a wide variety of structural or physiological insults; consequently, the differential diagnosis is extensive. The mnemonic I WATCH DEATH is a useful memory aid8. In the current era of extensive polypharmacy, drugs are a common cause and it is helpful to have a good understanding of the most common culprits9.

Differential Diagnosis for Delirium

IInfectionsUTI, pneumonia, encephalitis
WWithdrawalAlcohol, benzodiazepines, sedatives-hypnotics
AAcute metabolicHypo/hyperglycemia, renal failure, hypo/hypernatremia, hyper calcemia etc.
TToxinsAlcohol, benzodiazepines, sedatives-hypnotics
Opiates, salicylates, indomethacin, lidocaine, dilantin, steroids, other drugs like digoxin, cardiac medications, anticholinergics, psychotropics
CCNS pathologyStroke, tumor, seizures, hemorrhage, infection, vascular
HHypoxiaAnemia, pulmonary/cardiac failure, hypotension
DDeficiencesThiamine (with ETOH abuse), B12
EEndocrineThyroid, hypo/hyperglycemia, adrenal insufficiency, hyperparathyroid
AAcute vascularSchock, hypertensive encephalopathy
TTraumaHead injury, post-op fall, subdural
HHeavy metalsLead etc.

An important concept to understand is that delirium itself has a spectrum of clinical presentations, each with their own implications. Hyperactive delirium is the type we most commonly associate with the diagnosis. Patients are loud and agitated, basically signaling to you that they have delirium (“Hey, I’m delirious over here!”). These patients have a good prognosis because they are diagnosed early. On the other hand, hypoactive delirium is associated with the quiet, sleeping, elderly patient who does not bother anyone; as a result, the diagnosis of delirium is often missed. There is also a mixed subtype, which includes characteristics of both.10

Agitated, loud, sympathetic nervous system changesLethargic, quite, withdrawn, mute, decreased LOC
Recognized earlierMore common and easier to miss
Better prognosisWorse prognosis
Prototype: alcohol withdrawal deliriumPrototype: hepatic encephalopathy

*delerium can be mixed with aspects of both hyper and hypoactive states

What tools are available to help diagnose delirium?

As always, it is important to look at the vital signs, check a capillary glucose, and complete a careful history and physical.  Once the patient is stabilized, and any easily reversible causes are fixed, obtain a collateral history from family, allied health professionals, or nursing home staff to establish the acuity of the change in cognition. Establishing the patient’s baseline status is essential in diagnosing delirium8, 11.

Diagnosing delirium based on the DSM-5 criteria listed above is labour-intensive and requires psychiatric expertise. In a noisy, time pressured environment it can be difficult to do.

A recent systematic review by Lemantia and colleagues (2014)12 took a look at delirium screening tools in the ED, compared to the old DSM IV criteria and identified the Confusion Assessment Method (CAM) as the only tool validated in the ED setting (Sensitivity 0.94, Specificity 0.96),  although the quality of evidence was admittedly weak. The CAM tool takes less than 5 minutes to apply and correlates well with both the mini mental status exam and the DSM IV criteria (the criteria for delirium have been updated in the DSM 5 based on current available evidence but the change has little clinical impact). 13

There are many variations of the CAM that have been studied within the ED including the CAM-ICU, which has been recently validated within the ED. In older ED patients (age >65), the CAM-ICU is highly specific; sensitivity is modest14.

A recent variation of the CAM, called the modified Confusion Assessment Method for the ED (mCAM ED) is currently being evaluated in studies. This tool screens all patients greater than 65 years of age with a quick inattention screen; if positive, the tool then uses a modified CAM to determine delirium15. Unfortunately, the initial study was small and not able to determine sensitivity or specificity compared to the old DSM IV criteria.

Han and colleagues16 recently proposed a delirium screening strategy. Their strategy uses a highly-sensitive quick screen at triage to rule-out delirium. This is called the Delirium Triage Screen (DTS), and incorporates the patient’s level of consciousness and attention. If no concerning features are identified on initial screen, the assessment is concluded. On the other hand, if the screen is positive, the physician then performs the brief Confusion Assessment Method (bCAM), a further variation of the CAM-ICU. Compared to using DSM-IV-TR criteria, the sensitivity and specificity of this method when performed by an ER physician were 82% and 95.8% respectively16. This tool needs further testing and validation in larger ED settings.

While both Rosen’s17 and Tintinalli11 describe the use of the Mini Mental Status Exam (LR+  6.3 and LR 0.19) 11 and the Quick Confusion Scale18 in the diagnosis of delirium, these tools were not studied to look for delirium specifically and therefore confounded by other diagnosis such as dementia and depression which is left to the physician to determine (Table 3)8.

Bottom Line

Delirium is an important clinical entity to recognize due to its association with mortality rate and the high miss rate within the ED. Delirium exists as a spectrum from hypoactive to hyperactive presentations, which makes it difficult to diagnose. The differential diagnoses for delirium is extensive, and we must have a good knowledge of a wide variety of causes. In terms of diagnosis, have a high clinical suspicion for delirium in all elderly who present to the ED. There are multiple tools available to help you diagnose delirium. Although no one tool currently exists which has been extensively validated, the CAM and the CAM-ICU may be the most helpful tools to include in your diagnostic toolbox for delirium.

Delirium Diagnostic Tools


Sens 94.0%, Spec 96.0%
+LR= 23.5 and –LR= 0.06
-Well studied
-Validated within the ED for delirium
-Correlates well with MMSE
-<5 min to complete
Good sensitivity
-Not well validated for novice learners

Sens 72.0%, Spec 98.6%
+LR= 51.3 and -LR= 0.28
-Well studied and validated within the ICU and ED for delirium
-Does not require verbal communication or use of hands
-High specificity
-Low sensitivity

no reported LR
-Designed specifically for delirium screening
-< 5 minutes to complete
-Easy to use
-Not well studied, no sensitivity/specificity reported
-Not validated

Sens 82.0%, Spec 95.8%
+LR= 19.52 and -LR=0.18
-Designed specifically for delirium screening
-<5 minutes to complete
-Easy to use
-High specificity
-Needs further studies

+LR= 6.3 and -LR= 0.19
-Well studied,
-Validated within the ED
-Time consuming >7 mins
-Requires use of drawing and completion of tasks with hands
-Designed to screen for cognitive impairment; not specific for delirium

Links to Delirium Screening Resources


  1. Woods, R. Approach to geriatric patients: Functional assessment in the ED. Boring EM, 2015.
  2. Lewis LM, Miller DK, Morley JE, et al. Unrecognized delirium in ED geriatric patients. Am J Emerg Med 1995;13:142-5
  3. Elie M, Rousseau F, Cole M, et al. Prevalence and detection of delirium in elderly emergency department patients. CMAJ 2000;163:977-81. PMID: 7893295
  4. Hustey FM, Meldon SW. The prevalence and documentation of impaired mental status in elderly emergency department patients. Ann Emerg Med 2002;39:248-53 PMID: 11867976
  5. Kakuma R, du Fort GG, Arsenault L, et al. Delirium in older emergency department patients discharged home: effect on survival. J Am Geriatr Soc 2003;51:443-50. PMID: 12657062
  6. Han JH, Shintani A, Eden S, et al. Delirium in the emergency department: An independent predictor of death within 6 months. Ann of Emerg Med 2010; 56(3):244-52. PMID:20363527
  7. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.
  8. Smith J, Seirafi J. Delirium and dementia. In: Marx JA III, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine Concepts and Clinical Practices. 7th ed. Philadelphia, PA: Elsevier; 2010:1367–1373
  9. Agostini JV, Inouye SK. Delirium. In: Hazzard WR, Blass JP, Halter JB, et al, eds. Principles of Geriatric Medicine & Gerontology. 5th ed. New York, NY: McGraw-Hill; 2003:1503–1515
  10. Han JH, Zimmerman EE, Cutler N, et al. Delirium in older emergency department patients: recognition, risk factors, and psychomotor subtypes. Acad Emerg Med 2009;(16):193-200. PMID: 19154565
  11. Tintinalli, JE, Stapczynski SJ, Ma JO, Cline D, Cydulka R, Meckler G. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill, 2010. Print.
  12. LaMantia MA, Messina FC, Hobgood CD, Miller DK. Screening for delirium in the emergency department: a systematic review. Ann Emerg Med 2014;63(5):551–60.e2. PMID:24355431
  13. American Psychiatric Association. Highlights of changes from DSM-IV-TR to DSM-5. American Psychiatric Publishing, 2013.
  14. Han JH, Wilson A, Graves AJ, et al. Validation of the Confusion Assessment Method for the Intensive Care Unit in older emergency department patients. Acad Emerg Med Off J Soc Acad Emerg Med 2014;21(2):180–7. PMID: 24673674
  15. Grossmann FF, Hasemann W, Graber A, Bingisser R, Kressig RW, Nickel CH. 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). Scand J Trauma Resusc Emerg Med 2014;22:19. PMID: 24625212
  16. Han JH, Wilson A, Vasilevskis EE, et al. Diagnosing delirium in older emergency department patients: validity and reliability of the delirium triage screen and the brief confusion assessment method. Ann Emerg Med 2013;62(5):457–65. PMID: 23916018
  17. Marx, J. Rosen’s emergency medicine: concepts and clinical practice. 7th ed. Philadelphia, PA: Mosby/Elsevier; 2010
  18. Stair TO, Morrissey J, Jaradeh I, Zhou TX, Goldstein JN. Validation of the Quick Confusion Scale for mental status screening in the emergency department. Intern Emerg Med 2007;2(2):130–2. PMID: 17619832


Author information

Martin Badowski

Martin Badowski

PGY-2 Family Medicine, Queen's University

The post Medical Concept: Delirium tips and tools appeared first on BoringEM and was written by Martin Badowski.

Medical Concept: Nicotine toxicity, a new trend in toxicology

The Case

A 2 year old male presents to the Emergency Department with his parents immediately after ingesting an unknown amount of Pina Colada e-cigarette (electronic cigarette) refill liquid (18mg/mL of nicotine).  It is a 30mL bottle and there is still some liquid inside.  His breath smells of Pina Colada.

Topic Overview

This case is becoming more and more familiar in Emergency Departments across North America and around the world.  E-cigarettes and other nicotine replacement products have become very popular in the past several years as an alternative to cigarettes and as smoking cessation aids.  Cases of nicotine overdose and accidental ingestion are following a similar rise in popularity.  In New Zealand, the increase in calls to poison control about pediatric exposure to nicotine replacement therapy products has mimicked the increase in sales (Figure 1) [1].  Mean age of pediatric exposure was 29 months and 99.5% of exposures occurred in the patient’s own home.  In the United States, calls to Poison Control about e-cigarette exposures increased from 1 to 215 per month from February 2010 to December 2014 (Figure 2) [2].

Pediatric nicotine therapy replacement therapy (NRT) product exposures per year (left) and sales of NRT products (right).

Pediatric nicotine therapy replacement therapy (NRT) product exposures per year (left) and sales of NRT products (right). [1]

Figure 2. Calls to poison centers for e-cigarette and cigarette exposures in the United States.

Figure 2. Calls to poison centers for e-cigarette and cigarette exposures in the United States. [2]

E-cigarettes contain a variety of substances and they are not guaranteed to be accurate to what is on the label.  Ingredients include nicotine, diethylene glycol, ethylene glycol, ethanol, formaldehyde, glycerin, flavouring, colouring, and much more. [3] The alcohols are usually used as solvents and generally the amounts are within approved FDA limits. [3] One brand, however, did contain an unknown amount of Oil of Wintergreen [3], which can cause salicylate toxicity in very small doses.  E-cigarette liquid can contain anywhere from 6-72mg/mL of nicotine, depending on the brand. [3]

Figure 3

Figure 3

E-cigarettes refills are particularly attractive to children.  They smell and taste delicious and they come in a wide variety of flavours and colours.  They have vibrant labels and some have cartoons on the packaging (Figure 3).  In Canada, advertisement or sale of liquids containing nicotine is illegal, but possession or consumption of them is not and it is easy to order products online.  In the United States, there are no FDA regulations regarding liquids containing nicotine.  Across North America, there is no legislation mandating child resistant packaging and most people do not know that nicotine can be toxic in small doses.

This brings us to the next question.  What is the lethal dose of nicotine?  Textbooks, safety datasheets, and poison control tend to cite 45-60mg of nicotine as the potentially lethal dose. [4,5]  It turns out that the original data was from a single paragraph in a textbook written in 1906 by Dr. R. Kobert. [6]  Kobert obtained his data by doing self-experiments and it conflicted with other data that was available at the time.  His reputation as a leading scholar in toxicology led to universal acceptance of 60mg as the lethal dose (LD50 of 0.5-1mg/kg). [6]  A comprehensive review by Mayer in 2014 suggests an LD50 of 6.5-13mg/kg (500-1000mg for adults), which is more consistent with actual fatalities and dog studies. [6]  Considering that e-cigarette liquid may contain up to 72mg/mL of nicotine, this lethal dose may still only be a millilitre of liquid for a child.  My interpretation of this data is that the lethal dose is probably higher than most textbooks state, but information is lacking and we should still err on the side of caution.  As ingestions become more frequent, more information will become available.

Nicotine can have a wide range of clinical signs and symptoms as it activates nicotinic receptors all over the body.  It primarily effects the autonomic, neuromuscular, and central nervous systems.  It is easier to remember if it is divided into early and late symptoms.  Early in toxicity (within the first hour or so) nicotine acts as a stimulant. [4,5]  Delayed effects (after an hour) are due to nicotinic receptor blockade (See Table 1).4,5  Nicotine has a short half life of 1-4 hours.4  Vomiting is an early sign and occurs in 50% of symptomatic cases. [4]  If symptoms are not seen within the first several hours, they are unlikely to occur.  However, the half life with large overdoses is not well studied and it may take up to 72 hours for symptoms to fully clear. [4]

SystemEarly Effects (<1hr)Delayed Effects (>1hr)
CardiovascularTachycardia, hypotensionBradyarrythmia, hypotension
RespiratoryBronchorrhea, hyperpneaHypoventilation, apnea
NeurologicTremor, headache, ataxiaSeizure, coma

If you have a patient with suspected nicotine overdose, how should it be managed?  The patient should be on a cardiorespiratory monitor, have intravenous access, and be watched closely.  Symptomatic management should be initiated (ie: anti-emetics, atropine for bradycardia, respiratory support as needed, benzodiazepines for seizures, etc.) Bloodwork may be indicated if the patient is unstable, the history is unclear, it was an attempted suicide, or if the toxidrome is inconsistent.  The use of activated charcoal for tobacco ingestions is recommended, but the benefit in liquid nicotine overdoses is unclear. [4,5]  Activated Charcoal is usually recommended within the first two hours post ingestion. However, its efficacy is questionable due to rapid absorption of liquid nicotine. This needs further study.”  Multi-dose activated charcoal may be indicated in patients with significant toxicity due to the enterohepatic circulation of nicotine. [4]  As always, one must consider airway precautions when giving charcoal to a patient who is vomiting or has decreased level of consciousness.  Unfortunately, there is no antidote and dialysis is not effective.  The physician should call Poison Control in all cases of suspected nicotine overdose.  The patient should be observed in the Emergency Department.  If they are without symptoms for several hours they may be discharged without follow up.

As primary care physicians it is our job to educate patients and parents.  The general public may not be aware that nicotine is toxic.  Patients should be advised to store nicotine refill liquids away from children and in a locked area.  It should be treated as any other dangerous medication and any history of ingestion, no matter how small, should prompt an immediate visit to the Emergency Department.  Physicians should also advocate for changes that may reduce unintentional exposures, such as FDA regulations and child resistant packaging.

Back to the Case

The patient remained in the Emergency Department for 6 hours.  His vitals remained stable and he never developed any symptoms.  There were no investigations and he did not receive any treatment.  He was discharged home in the care of his parents, who were educated about the toxicity of e-cigarette liquid.

Take Home Points

  • Nicotine (in e-cigarette refill liquid) is a “one pill killer”
  • Clinical presentation is initially a stimulant, then a receptor blockade
  • The toxic dose of nicotine is unclear, but we should err on the side of caution and treat all ingestions as potentially toxic
  • Treatment is primarily symptomatic, but there may be a role for multi-dose activated charcoal
  • It is the physician’s responsibility to educate patients (and parents) about the dangers of nicotine toxicity


  1. Pediatric poisoning due to nicotine replacement therapy products: an emerging hazard.  JPCH 2014;50:164-165. PMID: 24528448
  2. Calls to poison centers for exposures to electronic cigarettes – United States, September 2010-February 2014. MMWR 2014;63(13):292-293. PMID: 24699766
  3. Toxicity assessment of refill liquids for electronic cigarettes. IJERPH 2015;12:4796-4815. PMID: 25941845
  4. Goldfrank, L. R., & Flomenbaum, N. (2006). Goldfrank’s toxicologic emergencies. New York: McGraw-Hill.
  5. Tintinalli, J. E., Kelen, G. D., & Stapczynski, J. S. (2010). Tintinalli’s emergency medicine: A comprehensive study guide. New York: McGraw-Hill, Medical Pub. Division.
  6. How much nicotine kills a human? Tracking back the generally accepted lethal dose to dubious self-experiments in the nineteenth century.  Arch Toxicol;88:5-7. PMID: 24091634

Author information

Alana Hawley

Alana Hawley

Resident Contributor at McMaster University

Resident Physician, McMaster University Royal College Emergency Medicine Program

The post Medical Concept: Nicotine toxicity, a new trend in toxicology appeared first on BoringEM and was written by Alana Hawley.