The LITFL Review 149

LITFL review

The LITFL Review is your regular and reliable source for the highest highlights, sneakiest sneak peeks and loudest shout-outs from the webbed world of emergency medicine and critical care. Each week the LITFL team casts the spotlight on the blogosphere’s best and brightest and deliver a bite-sized chuck of FOAM.

Welcome to the 149th edition, brought to you by:

The Most Fair Dinkum Ripper Beaut of the Week

resizerMRI when applied to patients with cervical spine tenderness and negative CT scans finds abnormalities but it’s unclear if these findings are clinically significant. Rory Spiegel delves into the issue in his latest post A Secondary Analysis of the Adventure of the Crooked Man. [AS]From SMACC Gold, “Punk Rock, Top Gun, and the Resus Room” discusses the parallels between music, combat aviation, and emergency medicine. (direct) [MG]

The Best of #FOAMed Emergency Medicine

The Best of #FOAMcc Critical Care

#FOAMTox Toxicology

  • Obsessed by spiders, snakes and sharks??  Don’t forget the lowly scorpion.  The Poison Review discuss a recent review article on Scorpion Envenomation, with an unforgettable video showing the effects of neuromuscular toxicity.  [CC]

News from the Fast Lane

Reference Sources and Reading List

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Research and Reviews in the Fastlane 044

Research and Reviews in the Fastlane
Welcome to the 44th edition of Research and Reviews in the Fastlane. R&R in the Fastlane is a free resource that harnesses the power of social media to allow some of the best and brightest emergency medicine and critical care clinicians from all over the world tell us what they think is worth reading from the published literature.
This edition contains 10 recommended reads. The R&R Editorial Team includes Jeremy Fried, Nudrat Rashid, Soren Rudolph, Anand Swaminathan and, of course, Chris Nickson. Find more R&R in the Fastlane reviews in the R&R Archive, read more about the R&R project or check out the full list of R&R contributors

This Edition’s R&R Hall of Famer

Emergency Medicine, Cardiology
R&R Hall of Famer - You simply MUST READ this!
Nuotio I, Hartikainen JE, Grönberg T, Biancari F, Airaksinen KE. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. JAMA. 2014 Aug 13;312(6):647-9. PMID: 25117135

  • This is an interesting research letter suggesting that we might be a little bit “button happy” with our defibs in the case of new onset AF. I’ve always been a big fan of DCC for new AF and assumed that the “within 48hrs” was a useful protection against stroke. This small research letter (with 5000 cardioversions) suggests the rate of thromboembolism might be as high as 1% in the first 30 days following unanticoagulated DCC. As it’s only a research letter there’s not much details in the way of methods but gives pause to think before you charge. Especially considering that rate control and anticoagulation seems to produce the same outcomes. Hat tip to @drjohnm for the link
  • This retrospective review challenges the widely accepted concept that patients with recent onset atrial fibrillation of less than 48 hours duration are safe for cardioversion without preceding anticoagulation. The authors report a 1.1% risk of thromboembolism after symptoms have been going for greater than 12 hours (vs 0.3% in the < 12 hour group). Before practice is completely changed, though, it should be noted that the rate of CVA after cardioversion in anticoagulated patients (3 weeks of therapeutic anticoagulation) may be as high as 0.8%. Additionally, this study suffers from the standard flaws of all retrospective studies. More research is needed to help answer this question and guide management.
  • Recommended by: Andy Neill, Anand Swaminathan
  • Read More: Shocking AF — What’s the rush? (Dr John M), Should the 48-hour Cardioversion Window Be Revised? (EM Literature of Note)

The Best of the Rest

Emergency Medicine
R&R Hot Stuff - Everyone’s going to be talking about this
Courtney DM et al. Prospective multicenter assessment of interobserver agreement for radiologist interpretation of multidetector computerized tomographic angiography for pulmonary embolism. J Thromb Haem 2010; 8: 533-9. PMID 20015156

  • This study looks at the agreement between radiologists in reading CTPAs for pulmonary embolism. They found that more than 10% of studies initially read as positive were later read as either negative or indeterminate. Many of the change in read occurred in subsegmental embolisms. This study throws further doubt on starting patients on long term anticoagulation based on the presence of a subsegmental pulmonary embolism.
  • Recommended by: Anand Swaminathan


Raemer DB. Ignaz semmelweis redux? Simul Healthc. 2014 Jun;9(3):153-5. PMID: 24401925

  • As a rabid in situ simulationist it is good to be tempered now an then by a brilliant article. Dan Raemer, one of the many sim gurus from the Center for Medical Simulation and Harvard Medical School, writes about the pros and cons of in situ simulation. The cons provide food for thought.
  • Recommended by: Chris Nickson

Critical Care

R&R Hot Stuff - Everyone’s going to be talking about this

Marik PE. Iatrogenic salt water drowning and the hazards of a high central venous pressure. Ann Intensive Care. 2014 PMID: 25110606

  • If the author doesn’t make you want to read this, then the title will. Paul Marik’s talk on EMCrit took the FOAMiverse by storm – this article is really the distillation of his ideas about over-resuscitation, chloride toxicity and the uselessness of the CVP for assessing euvolaemia. IT is typically iconoclastic and persuasive. A word of caution, ideas like chloride being toxic are far from proven and though they may well turn out to be true we should guard against creating new dogma before the truth is really known.
  • Recommended by: Chris Nickson
  • Listen to more: Fluids in Sepsis, A New Paradigm – Paul Marik (EMCrit)


R&R Hot Stuff - Everyone’s going to be talking about this

Driver BE, Debaty G, Plummer DW, Smith SW. Use of esmolol after failure of standard cardiopulmonary resuscitation to treat patients with refractory ventricular fibrillation. Resuscitation. 2014 PMID: 25033747

Critical Care, Cardiology

Antonucci E, et al. Myocardial depression in sepsis: from pathogenesis to clinical manifestations and treatment. J Crit Care. 2014 Aug;29(4):500-11. PMID 24794044

  • An awesome bench to bedside review, summarizing the basics of the pathogenesis, diagnosis, and treatment of myocardial depression in sepsis.
  • Recommended by: Sa’ad Lahri


Heradstveit BE, Heltne JK. PQRST – A unique aide-memoire for capnography interpretation during cardiac arrest. Resuscitation 2014 PMID 25063372

  • End tidal CO2 monitoring has become a mainstay in resuscitation. This article gives a mnemonic device for applying capnography during resuscitation. This tool can help bridge the gap from theory to application for many practitioners.
    P – Position of the tube
    Q – Quality of compressions
    R – Return of spontaneous circulation
    S – Strategy for further treatment
    T – Termination of resuscitation
  • Recommended by: Anand Swaminathan

Critical Care, Haematology, Infectious Disease

Rohde JM, et al. Health care-associated infection after red blood cell transfusion: a systematic review and meta-analysis. JAMA. 2014 PMID: 24691607

  • A meta analyses providing further evidence for a restrictive PRBC transfusion policy as those patients in liberal groups were more likely to acquire hospital associated infections. A goal of Hb <7 provided a NNT of 20 to reduce infection.
  • Recommended by: Jeremy Fried


Sezik S, Aksay E, Kılıç TY. The Effect of Fresh Frozen Plasma Transfusion on International Normalized Ratio in Emergency Department Patients.  J Emerg Med. 2014 Jul 26. pii: S0736-4679(14)00636-2. doi: 10.1016/j.jemermed.2014.04.042. [Epub ahead of print] PMID 25074780

  • Fresh frozen plasma (FFP) is commonly used to reverse elevated international normalized ratios (INRs) in patients with coagulopathy and trauma or anticipated procedures.  While prior studies and recommendations have demonstrated that FFP does not reduce the iNR below 1.7, FFP is often given to patients with minimally elevated INRs.  This cross-sectional retrospective study of 87 patients who received FFP and had their INR re-checked within 6 hours found that the degree of improvement in INR is greatest in those with the most elevated INRs. They found the following reductions in INR per unit of FFP:
    INR <2:  0.03
    INR 2-5: 0.77
    INR 5-9: 2.14
    INR 9-12: 4.63
    The study has limitations and correcting numbers isn’t the same as fixing patients, but it’s good to know the gains of an intervention, especially as transfusions have associated risks.
  • Recommended by: Lauren Westafer

Emergency Medicine, Imaging

Carpenter CR, et al. Adult scaphoid fracture. Acad Emerg Med 2014; 21: 102-121. PMID 24673666

  • In this systematic review, only the absence of snuff box tenderness to palpation had an adequate negative likelihood ratio (- LR = 0.15) to affect management. MRI was found to be better than bone scan, CT or ultrasound for the diagnosis. This is in stark contrast with traditional teaching that only MRI can rule out occult scaphoid fractures in the acute setting.
  • Recommended by: Anand Swaminathan

The R&R iconoclastic sneak peek icon key

Research and Reviews The list of contributors R&R in the FASTLANE 009 RR Vault 64 The R&R ARCHIVE
R&R in the FASTLANE Hall of Famer R&R Hall of famer You simply MUST READ this! R&R Hot Stuff 64 R&R Hot stuff! Everyone’s going to be talking about this
R&R in the FASTLANELandmark Paper R&R Landmark paper A paper that made a difference R&R Game Changer 64 R&R Game Changer? Might change your clinical practice
R&R Eureka 64 R&R Eureka! Revolutionary idea or concept R&R in the FASTLANE RR Mona Lisa R&R Mona Lisa Brilliant writing or explanation
R&R in the FASTLANE RR Boffin 64 R&R Boffintastic High quality research R&R in the FASTLANE RR Trash 64 R&R Trash Must read, because it is so wrong!
R&R in the FASTLANE 009 RR WTF 64 R&R WTF! Weird, transcendent or funtabulous!

That’s it for this week…

That should keep you busy for a week at least! Thanks to our wonderful group of editors and contributors Leave a comment below if you have any queries, suggestions, or comments about this week’s R&R in the FASTLANE or if you want to tell us what you think is worth reading.

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Tension Pneumothorax – an alternative view

Ever since I was a junior medical officer and I was faced with a spontaneous tension pneumothorax at sea on a dived submarine…I have had an interest in managing pneumothorax.

A tension pneumothorax is the presence of intrapleural air that is under positive pressure throughout the entire respiratory cycle. It occurs when air enters the thorax through a pleural defect but can not leave (a one way cat flap). We have all been taught that we should never see a chest x-ray of a tension pneumothorax, with good reason. It is a diagnosis that should be made on clinical grounds only and certainly never have a chest x-ray performed to confirm your suspicion (although here is one… well, these things happen).

Tension Pneumothorax

Of all of the clinical signs that we have been taught to recognise – it is the rapidity of deterioration of a patients’ clinical condition, in the context of known, or clinical signs of a pneumothorax that should make you think of the presence of a tension. Learned texts speak of distended neck veins, tracheal deviation and a displaced apex beat (very difficult to ascertain); these are late signs and clinicians should have considered and be acting upon the diagnosis before these are present.

Prompt recognition and treatment is key – traditionally we have been taught needle decompression in the second intercostal space, mid-clavicular line. Whilst this does facilitate timely access to the pleural space for some – it may not be the best anatomical choice for all – but more of that (and ideal needle length) another time…

So, if we are agreed that we should not be seeing chest x-rays of tension pneumothoraces – what about a CT scan of tension pneumothorax?

What features can been seen on this CT?

  • Increased thoracic volume R side
  • Displaced mediastinum
  • Collapse and occlusion of the right main bronchus. Just distal to the carina it forms a crescent shape and then occludes. The whole of the right lung is collapsed as a result.
  • Collapse of left lower lobe
  • A large bore chest tube in situ in the right thoracic cavity with no apparent occlusion of the tube

It is worthwhile stopping and considering for a moment some of these features present on the scan. We are used to hearing about a displaced mediastinum which, as it worsens, we understand to gradually occlude the vena cava causing eventual reduction and cessation of venous return to the right ventricle. But what about complete collapse of the right main bronchus? Anatomically, there are intact concentric rings of cartilage at this point in the bronchial tree. To cause collapse and occlusion of these rings there must be a very considerable positive intrathoracic pressure acting upon them.

Experimental physiological data on this subject are sparse to give reliable estimates, but it is known that a pressure of 6Kpa (~60cm/H20) will cause the posterior membrane of human trachea to invaginate with surface contact between the membrane and lateral walls. The likelihood of collapse is greater when there is longitudinal tension or flexion on the trachea. In this case with right main bronchus collapse, the concentric cartilagenous rings should (in theory) be able to withstand more pressure before deformation or collapse than the incomplete ‘C’ shaped rings in the trachea. Perhaps in this case the additional longitudinal tension and/or flexion on the bronchial tree as the mediastinum was deviated modified that likelihood.

This individual already had a 28F chest tube in place following penetrating thoracic trauma and a haemopneumothorax – this was subsequent ‘traumagram’ CT. He was clinically stable going in – says he felt dreadful in the scanner, and quickly better when the gantry moved back out again. Considering the patient had a patent chest tube at the beginning of the investigation and a patent tube as we rushed in straight after the investigation – what could have happened?

So what happened?

We think that the chest drain tubing got snagged in the gantry as the patient moved into the scanner. This occluded the tube, stopping egress of air from the thoracic cavity, resulting in increasing intrathoracic pressure and ultimately a tension on the affected side.

Either way, this case allows you to appreciate the gross cardiopulmonary insult a tension pneumothorax can induce in a short space of time.

Take home message

Transfer of the traumatised and/or critically ill patient requires careful handing and planning ahead – particularly when moving parts are involved. Tubes, lines and monitoring wires may all be sitting safely before the scan starts – but think ahead to where all these items will be when the patient has moved into the scanner!


  1. Brims F. Primary spontaneous tension pneumothorax in a submariner at sea. Emergency medicine journal: EMJ 2004;21:394. [Full Text]
  2. Begis D, Delpuech C, Le Tallec P, Loth L, Thiriet M, Vidrascu M. A finite-element model of tracheal collapse. Journal of applied physiology 1988;64:1359-68. [Abstract]
  3. Leigh-Smith S, Harris T. Tension pneumothorax–time for a re-think? Emergency medicine journal : EMJ 2005;22:8-16. [Full Text]

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Changes in systolic and diastolic pressure

BSCC Physiology 016


Draw a diagram of the changes in systolic and diastolic pressure as blood flows through the systemic circulation

Examiner explanation:

Changes in systolic and diastolic pressure


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Changes in systolic and diastolic pressure

BSCC Physiology 016


Draw a diagram of the changes in systolic and diastolic pressure as blood flows through the systemic circulation

Examiner explanation:

Changes in systolic and diastolic pressure


The post Changes in systolic and diastolic pressure appeared first on LITFL.

ECG waves and hyperkalaemia

BSCC Physiology 015


Draw a normal ECG tracing showing the durations of the major intervals

Examinee response


How does the ECG tracing change in hyperkalaemia

Examinee response

ECG waves and hyperkalaemia

There are a number of intervals on an ECG that are important:PR = 0.12-0.2 sec
QRS = 0.08 – 0.1 sec
QT = 0.4 – 0.43 sec
ST = 0.32 sec

Changes with Hyperkalaemia and Hypokalaemia:

Initially peak T waves are present (T waves you would not want to sit on)
As the hyperkalaemia progresses there is flattening of the P wave and PR prolongation with a peaked T wave.
At higher levels no atrial activity is seen and QRS widening develops
Severe hyperkalaemia causes idoventicular rhythms, sine wave and VF arrest.

Initially the PR interval is prolonged but the QRS remains unchanged and a U wave develops
As the hypokalaemia progresses there is still PR prolongation but ST depression, T wave inversions and a more prominent U wave can develop

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