• Levitan RM, Heitz JW, Sweeney M, Cooper RM. The complexities of tracheal intubation with direct laryngoscopy and alternative intubation devices. Ann Emerg Med. 2011 Mar;57(3):240-7. Epub 2010 Jul 31. Review. PubMed PMID: 20674088

Levitan et al get into some great technical aspects of video and alternative devices for laryngoscopy. The point here is that while VL may make laryngoscopy easier, tube delivery and placement may paradoxically become more difficult, primarily because of the sharper angle between the blade and the trachea. Porn for airway enthusiasts.

Recommended by Seth Trueger

• Segal N, Yannopoulos D, Mahoney BD, Frascone RJ, Matsuura T, Cowles CG, McKnite SH, Chase DG. Impairment of carotid artery blood flow by supraglottic airway use in a swine model of cardiac arrest. Resuscitation. 2012 Mar 28. [Epub ahead of print] PubMed PMID: 22465807.

Supraglottic devices (SGDs) have been all the rage in emergency settings lately. For lots of good reasons. But this tiny study questions the use of SGDs in cardiac arrest. Without any blood pressure, SGDs compress the carotids and restrict cerebral blood flow. And the flow measurements are convincing. But – it’s on pigs. Still, this will be talked about.

Recommended by Thomas Dolven
Learn more: ScanCrit.com — Supraglottic airway devices in the critically ill

• Green RS Reflections from a Canadian visiting South Africa: Advancing sepsis care in Africa with the development of local sepsis guidelines. African Journal of Emergency Medicine (2012), http://dx.doi.org/10.1016/j.afjem.2012.03.004

Sepsis is a killer worldwide… but needs champions to pioneer it’s death. An excellent overview from Dr Green who is a world Guru on the topic.

Recommended by Sa’ad Lahri
Fulltext

• Homma S, et al; the WARCEF Investigators. Warfarin and Aspirin in Patients with Heart Failure and Sinus Rhythm. N Engl J Med. 2012 May 2. [Epub ahead of print] PubMed PMID: 22551105.

WARCEF trial – For patients with severe heart failure (LVEF < 25%), Warfarin was no better than Aspirin for the combined outcome of any stroke or death. There was a significant reduction in the incidence of ischaemic stroke, but at the expense of major haemorrhage. Patients with pre-existing AF were excluded.

Recommended by Matthew Mac Partlin
Fulltext

• Matthaiou DK, Ntani G, Kontogiorgi M, Poulakou G, Armaganidis A, Dimopoulos G. An ESICM systematic review and meta-analysis of procalcitonin-guided antibiotic therapy algorithms in adult critically ill patients. Intensive Care Med. 2012 Apr 27. [Epub ahead of print] PubMed PMID: 22538461.

Procalcitonin levels – not much good for diagnosing bacterial sepsis, but handy for shortening duration of therapy without increasing 28-day negative outcome rates.

Recommended by Matthew Mac Partlin
Fulltext

• Needham DM, Colantuoni E, Mendez-Tellez PA, Dinglas VD, Sevransky JE, Dennison Himmelfarb CR, Desai SV, Shanholtz C, Brower RG, Pronovost PJ. Lung protective mechanical ventilation and two year survival in patients with acute lung injury: prospective cohort study. BMJ. 2012 Apr 5;344:e2124. doi: 10.1136/bmj.e2124. PubMed PMID: 22491953; PubMed Central PMCID: PMC3320566.

Our ARDS-Net guided lung-protective ventilation strategy seems to work long term as well. ARDS-Net demonstrated a short term mortality benefit. This US 4 academic centre (13 ICUs – medical, surgical, trauma) prospective observational trial demonstrated an absolute 4% and 8% drop in 2 year mortality with adherence to one or both of the ARDS-Net lung-protective ventilation parameters respectively, compared to no adherence at all. No report on morbidity outcomes though.

Recommended by Matthew Mac Partlin
Fulltext

• Nomura, Jason T, Genes N, Bollinger HR, Bollinger M, and  Reed JF. “Twitter Use During Emergency Medicine Conferences.” The American Journal of Emergency Medicine (March 16, 2012). PMID 22424992

I’ve always been jealous watching my timeline on twitter fill with hashtags from folk at big conferences. @takeokun pulled the tweets from one conference to get an idea of what people were saying. I look forward to filling your timeline when I’m at ICEM2012!

Recommended by Andy Neill

• Ranchord AM, Argyle R, Beynon R, Perrin K, Sharma V, Weatherall M, Simmonds M, Heatlie G, Brooks N, Beasley R. High-concentration versus titrated oxygen therapy in ST-elevation myocardial infarction: a pilot randomized controlled trial. Am Heart J. 2012 Feb;163(2):168-75.

No difference in this pilot study of titrated oxygen therapy for STEMIs – but wide confidence intervals… more studies needed.

Recommended by Andy Brainard

• Smith SW, Khalil A, Henry TD, Rosas M, Chang RJ, Heller K, Scharrer E, Ghorashi M, Pearce LA. Electrocardiographic Differentiation of Early Repolarization From Subtle Anterior ST-Segment Elevation Myocardial Infarction. Ann Emerg Med. 2012 Apr 18. [Epub ahead of print] PubMed PMID: 22520989.

This is Steve Smith’s (yes that guy) big idea about distinguishing BER from STEMI on ECG criteria. This type of thing is really important as the classic STEMI criteria just aren’t cutting the mustard. It’s a dense enough paper to follow and even if you don’t understand the calculation the concept is priceless.

Recommended by Andy Neill

• Chiang HK, Zhou Q, Mandell MS, Tsou MY, Lin SP, Shung KK, Ting CK. Eyes in the needle: novel epidural needle with embedded high-frequency ultrasound transducer–epidural access in porcine model. Anesthesiology. 2011 Jun;114(6):1320-4. PubMed PMID: 21519228; PubMed Central PMCID: PMC3104409.

Tech porn. One-crystal ultrasound transducer placed on the tip of a stylette that fits in the lumbar needle! Never miss an epidural again. And when they get smaller, they will fit in a spinal needle. Maybe.

Recommended by Thomas Dolven

• Walter S, Kostopoulos P, Haass A, et al. Diagnosis and treatment of patients with stroke in a mobile stroke unit versus in hospital: a randomised controlled trial. Lancet Neurol. 2012 May;11(5):397-404. Epub 2012 Apr 11. PubMed PMID: 22497929

Taking the crazy on the road – mobile stroke response units with an MD and a scanner in order to save a few minutes for TPA administration. Not sure this is the best resource outlay….

Recommended by Ryan Radecki
Learn more: EM Literature of Note — Mobile Stroke units – Probably Not Helpful

Amitriptyline is one of the most commonly used (and sometimes misused) tricyclic antidepressants. Amitriptyline is indicated for the treatment of major depression and as well as nocturnal enuresis (where organic pathology has been excluded). Their main therapeutic effect is thought to be due to inhibition of both noradrenaline and serotonin reuptake and is thought to lead to increased activity at their specific post-synaptic receptors. Amitriptyline is available in 10, 25 and 50mg tablets in Australia.

However, tricyclics also block inactivated fast sodium channels. Tricyclics are also similar in structure to phenothiazines and thus share many of their properties (serotonin and noradrenaline reuptake inhibition, alpha-2-adrenoreceptor blockade, muscarinic receptor blockade etc.).

These aspects of tricyclic pharmacology have significant implications with regards to their toxicology.

—

Return of the ADME:

• Absorption:
  — Rapidly absorbed following oral administration. Time to peak levels is 2 hours
• Distribution:
  — Large volume of distribution (5-20L/kg).
  — Highly bound to plasma and tissue proteins
• Metabolism:
  — Undergoes hepatic metabolism by oxidation via Cytochrome p450 to active metabolites such as nortriptyline
• Excretion:
  — Mainly in the urine as metabolites. Very little is excreted unchanged

—

As mentioned earlier, amitriptyline (like other tricyclic antidepressants) have multiple potential toxicological properties due to their structure, these are:

• CNS effects
  — Delirium/confusion/agitation, sedation, seizures, coma (often precedes cardiovascular signs)
• Cardiovascular effects
  — Sinus tachycardia, hypertension, hypotension (due to alpha2-adrenoreceptor blockade), broad complex tachycardia (can develop bradycardia pre-arrest)
• Anticholinergic effects
  — Can occur at time or presentation or be delayed and prolonged
  — Agitation, restlessness, delirium, mydriasis (big pupil), dry, warm skin, tachycardia, ileus, urinary retention
• Metabolic acidosis
  (remember she was tachypnoeic at presentation… trying to compensate for this!)

—

This patient has taken a life-threatening overdose and is predictably demonstrating many of the aforementioned clinical features associated with amitriptyline toxicity.

Murray et al (2011) states that ingestion of greater that 10mg/kg is thought to be considered potentially life-threatening and onset of severe toxicity often occurs within two hours of ingestion (how’s that for timing?). However the dose is less than 30 mg/kg, which is the dose expected to result in severe toxicity with pH-dependent cardiotoxicity and coma lasting >24 hours.

Nevertheless she is at significant risk of developing seizures, broad complex tachycardias, coma and ultimately cardiac arrest.

As always, co-ingestion should forever be sitting in the back of your mind as a possibility and management should be accompanied with appropriate investigations to exclude other potential toxins. Given her acute decrease in conscious state, drugs such as alcohol, opiates and other anti-depressants warrant consideration as possible co-ingestants.

—

Regardless of what you would do, this is what was actually done!

In this case, the patient was fortunately in the right place (resuscitation bay) and the decision was made to promptly sedate and intubate the patient with ongoing sedation via propafol infusion. Whilst the patient was initially given boluses of sodium bicarbonate along with crystalloid, this was later changed to a sodium bicarbonate infusion (100mmol in 1L N/Saline at 250ml/hr) that was continued during the patient’s ICU admission. Serial ECGs were utilised to monitor progress, looking for resolution of the ECG changes specific to amitriptyline toxicity.

We’ll talk some more about whether this was optimal management or not below…

Learn more:

• LITFL ECG Library — Tricyclic antidepressant overdose

—

Use the Resusi-RSI-DEAD approach as all good toxicologists do…

Resuscitation

• Amitriptyline and other tricyclic overdoses are potentially life-threatening and should be managed accordingly in an area that is able to provide appropriate monitoring, resuscitation and ventilatory support (given the high likelihood of intubation in significant overdoses)
• Intubation and hyperventilation (aim for pH 7.50-7.55) are mainstays of treatment for severe overdoses (where there is a decline in GCS) in addition to sodium bicarbonate (discussed below)
• Ventricular arrhythmias caused by amitriptyline toxicity are unlikely to respond to cardioversion or defibrillation
  — First line treatment is sodium bicarbonate (100mmol or 2mmol/kg) should be given IV every 1-2 minutes until rhythm and perfusion are restored
  — Second line treatment is lignocaine (1.5mg/kg) IV once pH is greater than 7.5
• Serial ECGs and blood gases are vital to proper and effective management
• Treat hypotension with volume- crystalloid, sodium bicarbonate or failing this, vasopressor (noradrenaline or adrenaline) infusions
• Treat seizures with benzodiazepines as per usual
• Don’t stop resuscitation until patient has been intubated, has received sodium bicarbonate and has been hyperventilated to achieve a pH of 7.50-7.55. Good neurological outcome following even hours of prolonged CPR and arrest is still possible.

Supportive care and monitoring

• Supportive care will suffice for small ingestions so it is essential that it is done properly!
• Secure appropriate IV access
• Ensure adequate hydration with IV fluids- crystalloid will suffice with small (<10mg/kg) ingestions
• Remember FASTHUGS IN BED Please especially pressure care, bladder care and DVT prophylaxis
• Cardiac monitoring should continue until toxicity is reversed if ECG changes are present

Investigations

• The ECG is one of the most vital investigations in this scenario
  — Diagnostic features include prolongation of QRS, PR intervals, dominant R wave in aVR, and QT prolongation
  — QRS widening reflects the degree of fast sodium channel blockade
  — QRS > 100ms is predictive of seizures, QRS > 160ms is predictive of ventricular tachycardia
• Paracetamol and blood glucose levels should be performed as recommended for all intentional overdoses
• Use blood gases to monitor the adequacy of alkalinisation
• Consider possible co-ingestants

Decontamination

• Activated charcoal can be useful for large ingestions >10mg/kg but should not be given without a definitive airway (i.e. a tube) being established prior
• Charcoal not indicated for smaller ingestions as supportive care is often enough

Enhanced elimination

• Not useful

Antidotes

• Sodium Bicarbonate is a key treatment in amitriptyline and other tricyclic antidepressant toxicity.
• This is discussed in great detail in another case of amitriptyiline toxicity in Toxicology Conundrum 022.

Disposition

• As in this case, patients with severe ingestions require HDU/ICU support (or alternatively transport to a more appropriate centre if warranted) until medically stable
• Patients with non-life-threatening overdoses (<10mg/kg) can be managed in an appropriate ward setting until clinically well
• Psychiatric review is mandatory.

—

The retrospectoscope is an amazing tool but never around until after its too late… funny that.

A few thoughts:

• Following intubation and establishment of a secure airway the patient could have been administered activated charcoal. There are few downsides in this setting and the activated charcoal might decrease any ongoing drug absorption from the gut.
• Whilst an infusion of sodium bicarbonate was used due to ongoing prolongation of the patient’s QRS and for practical reasons, boluses of sodium bicarbonate are thought to be more effective as they lead to rapid shifts in concentration of free drug due to the effect on binding to plasma and tissue proteins. Also infusions may lead to renal compensation and thus reduce the effectiveness of the antidote… throwing the baby (bicarbonate) out with the bath water (well… you know).
• Hyperventilation of intubated patients is an effective means of alkalinisation and could have been used may have achieved the same aim as a sodium bicarbonate infusion

In any event, the patient went on to do well. She was extubated the following day following reversal of her ECG changes and once medically cleared was admitted to an inpatient psychiatric unit for further management.

—

The key finding is:

Extensive pneumomediastinum

There is gas within the supra-aortic, sub-aortic and para-cardiac mediastinum, particularly in the posterior compartment of the mediastinum.

Other findings:

• endotracheal tube
• nasogastric tube
• bilateral lung opacities and altered lung architecture consistent with resolving ARDS

_

Possible causes include:

• Complication of tracheostomy resulting in a small tracheal tear
• Complication of mechanical ventilation due to ARDS and need for high pressures
• Esophageal rupture post NG tube placement
  — pleural effusion would be expected
• Mediastinitis
  — fluid or a collection would be expected

—

There may be very few clinical findings!

If present they may include:

•  subcutaneous emphysema of the neck
• Hamman’s sign (aka Hammond’s crunch)
  — a rarely heard rasping, crunching sound synchronous with the heart beat that is best heard over the precordium in the left lateral position
  — caused by the heart beating against air-filled tissues
• hemoptysis
• partial or complete airway obstruction
• respiratory distress and/or need for increased respiratory support.

If tension pneumomediastium develops the patient will become tachycardic and hypotensive due to impaired venous return mimicking cardiac tamponade. Neck vein distention will not be seen in the presence of subcutaneous emphysema of the neck.

—

Key priorities are supportive care of the patient and identification and treatment of possible tracheobronchial injury.

• ensure adequate oxygenation
• provide ventilatory support while minimising tidal volumes and airway pressures to limit exacerbation of the air leak
• fiberoptic endoscopic evaluation of the tracheobronchial tree to assess for presence, location, depth and length of tears (best performed in an operating theatre)
• tracheobronchial tears may be amenable to bypass by bronchoscopy-assisted endotracheal tube advancement, or even endobronchial intubation for tracheobronchial injury near the carina
• the indications for conservative versus surgical repair of iatrogenic tracheobronchial injury are poorly defined and remain controversial
  — surgery may be performed via thoracotomy and/or a cervical approach
  — surgery should be performed  if there is progressive pneumomediastinum, increasing subcutaneous emphysema, evidence of oesophageal injury or mediastinitis
• broad spectrum antibiotics are often used to prevent mediastinitis

Learn more:

• Esophageal rupture is considered in Pulmonary Puzzle 003.

—

True tension pneumomediastinum is rare, and requires emergency decompression by bedside mediastinotomy.

Bedside cervical mediastinotomy can be performed by making an incision in the jugular notch. If air is trapped in posterior spaces then this approach may not be effective. A subxiphoid approach can be attempted, and an approach through the esophageal hiatus via a mini-laparotomy has been described.

—

It is argued that complications following PDT are rare and that new abnormalities on chest x-ray are rarely seen. However, if difficulties are encountered during the procedure, or if the patient deteriorates afterward, a chest x-ray should be performed.

—

• Popat M, Mitchell V, Dravid R, Patel A, Swampillai C, Higgs A. Difficult Airway Society Guidelines for the management of tracheal extubation. Anaesthesia. 2012 Mar;67(3):318-40. PMID: 22321104

The Difficult Airway Society has published these guidelines for tracheal extubation. The focus is on the peri-operative patient but it provides an overview and framework for a procedure rarely undertaken in the ED. It’s also healthy reminder that what goes in must come out.

Recommended by John Larkin, Cliff Reid
Learn more: Extubation guidelines
Fulltext

• Moyer VA. What we don’t know can hurt our patients: physician innumeracy and overuse of screening tests. Ann Intern Med. 2012 Mar 6;156(5):392-3. PubMed PMID: 22393136.

Clear evidence that physicians need education on what our tests are telling us.

Recommended by Mike Jasumback

• Reiter DA, Lakoff DJ, Trueger NS, Shah KH. Individual Interactive Instruction: An Innovative Enhancement to Resident Education. Ann Emerg Med. Elsevier Inc.; 2012 Apr. 18;:1–4. PMID 22520994

A useful discussion of how web2.0 and ‘asynchronous learning’ has an important role in educating trainees and getting it recognised as valid learning. This is really important I think but my one concern is that if we show how much we can learn in our own time via free resources then they’ll take away our protected training time.

Recommended by Andy Neill, Chris Nickson, Mike Cadogan

• Corrado D, Pelliccia A, Heidbüchel H, Sharma S, Link M, Basso C, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. European Heart Journal. 2010 Jan.;31(2):243–259. PMID: 19933514

Linked to by someone on twitter (as usual I can’t remember). This is by the Italian folk famous for ECG screening of ALL athletes. Seeing as 50% of athletes will have “abnormal” ECGs this is a great paper to pick out which “abnormal” bits matter and which are actually normal.

Recommended by Andy Neill

• Dumas F, Manzo-Silberman S, Fichet J, Mami Z, Zuber B, Vivien B, Chenevier-Gobeaux C, Varenne O, Empana JP, Pène F, Spaulding C, Cariou A. Can early cardiac troponin I measurement help to predict recent coronary occlusion in out-of-hospital cardiac arrest survivors? Crit Care Med. 2012 Apr 6. [Epub ahead of print] PubMed PMID: 22488008.

Some cardiac arrest patients will do better going to the cath lab – but your bedside troponin measurement doesn’t accurately predict who.

Recommended by Ryan Radecki
Learn more: Post-arrest troponin measurements predict little

• Le Cong M, Gynther B, Hunter E, Schuller P. Ketamine sedation for patients with acute agitation and psychiatric illness requiring aeromedical retrieval. Emergency Medicine Journal. 2011 May 12. PMID: 21565879

We all know Minh Le Cong is a retrieval legend but now we have publications to prove it. This describes a series of psychotic patients who got ketamine to get them on a plane (I suspect he stole the idea from the A-team) and transferred safely. I suspect ketamine would be useful to get control in the ED too.

Recommended by Andy Neill

• Brancati FL. The art of pimping. JAMA. 1989 Jul 7;262(1):89-90. PubMed PMID: 2733128.

The classic, original work on the art of pimping in medicine.

Recommended by Chris Nickson
Learn more: Pimping in perspective

• Ding W, Shen Y, Yang J, He X, Zhang M. Diagnosis of pneumothorax by radiography and ultrasonography: a meta-analysis. Chest. 2011 Oct;140(4):859-66. Epub 2011 May 5. Review. PubMed PMID: 21546439.

Ultrasound for pneumothorax is more frequently useful than FAST for free fluid. This should really be standard EM practice.

Recommended by Andrew Brainard