Journal Club Podcast for October 2021 Prof Peter Cameron Dr Divya Karna Dr Eanna Mac Suibhne Editor: Dr David McCreary Welcome to the Journal Club Podcast for October 2021. You can listen to the podcast above and have a read at our summary below, courtesy of our senior registrar for research, Dr Eanna Mac Suibhne. PAPER 1: DIRECT TO ANGIOGRAPHY SUITE WITHOUT STOPPING FOR COMPUTED TOMOGRAPHY IMAGING FOR PATIENTS WITH ACUTE STROKE 10.1001/jamaneurol.2021.2385 CLINICAL QUESTION: Should we bypass the CT scanner and head directly to the angio suite in patients suspected of large vessel occlusion within 6 hours of symptom onset? The researchers looked for any difference in functional outcomes between two groups of patients as measured by the Modified Rankin Scale at 90 days. FINDINGS In this randomized clinical trial, 147 patients were randomised. 74 entered the interventional group and went directly to the angiography suite and 73 into the control group and underwent conventional workflow. The primary outcome analysis showed an adjusted common odds ratio of improvement of 1 point on the Modified Rankin Scale of 2.2 favouring direct to angiography. AUTHORS' CONCLUSIONS For patients with LVO admitted within 6 hours after symptom onset, this randomized clinical trial found that, compared with conventional workflow, taking patients directly to the Angio suite increased the odds of patients undergoing EVT, decreased hospital workflow time, and improved clinical outcome. JOURNAL CLUB THOUGHTS We are always looking for ways to reduce the time to get our Stroke patients the appropriate imaging and correct treatment, so this paper looks at a very important topic and this paper certainly challenges us and what we can aspire to. Unfortunately, not all hospitals have the infrastructure or equipment to introduce a similar pathway as the team in Barcelona have so ably managed to do [insert business case proposal for a Flat panelled CT here]. The study was well constructed but a few issues were raised, one of which we looked at was how virtually 100%, got clot retrieval in the interventional arm and whether this possibly opened the study to bias. Secondly, early termination of the trial made it unpowered to detect differences between groups regarding safety variables, and an interim analysis may have overestimated the real treatment effect. Finally, in this paper, we are also dealing with small numbers from a single centre and basing a whole stroke pathway on this might be problematic. Larger studies with more patients would be needed before recommending it for every stroke centre. PAPER 2: EFFECT OF INTRAVENOUS FLUID TREATMENT WITH A BALANCED SOLUTION VS 0.9% SALINE SOLUTION ON MORTALITY IN CRITICALLY ILL PATIENTS 10.1001/jama.2021.11684 (balanced vs saline paper) 10.1001/jama.2021.11444 (slower vs bolus rate fluids) CLINICAL QUESTION: This trial posed two questions, which were reported in two separate papers. In critically ill adult ICU patients requiring IV fluids, does a balanced solution provide benefits over 0.9% Na Cl in terms of 90-day all-cause mortality?  Secondly, does a slow infusion rate compared to a fast infusion rate of a fluid bolus provide improvement in the same terms? FINDINGS Double-blind, factorial, randomized clinical trial conducted at 75 ICUs in Brazil.The population studied included any patient admitted to the ICU with a need for fluid resuscitation, were note expected to be discharged the day after admission and had at least one risk factor for AKI. Among 10 520 patients in intensive care units, intravenous fluid bolus treatment with a balanced solution vs saline solution resulted in 90-day mortality of 26.4% vs 27.2%, respectively, a difference that was not statistically significant. In the second outcome, rapid vs slow administration, there was no significant difference in 90 -day mortality, again a difference which was not statistically significant. AUTHORS' CONCLUSION Among critically ill patients requiring fluid challenges, use of a balanced solution compared with 0.9% saline solution did not significantly reduce 90-day mortality. The findings do not support the use of this balanced solution. JOURNAL CLUB THOUGHTS A large trial and a controversy that just doesn’t go away. There were some issues, albeit a study with great internal validity. For an EM audience, a large portion of the patients involved in this study were not of the calibre that we would be sending to the ICU from Resus, around 40% were planned surgical admissions. Fluids which were given pre- ICU were not accounted for and the amount of fluid given while in ICU was relatively low so you would wonder if the type and volume of fluid could have made more of an impact on sicker patients. But it’s reassuring that small amounts of 0.9% NaCl may not be harmful, the initial phase of resuscitation Also, a hypothesis generating question arose with patients fluid administration in patients with traumatic brain injury in the subgroup analysis. Watch this space. PAPER 3: DIAGNOSTIC ACCURACY OF LUNG POINT-OF-CARE ULTRASONOGRAPHY FOR ACUTE HEART FAILURE COMPARED WITH CHEST X-RAY STUDY AMONG DYSPNEIC OLDER PATIENTS IN THE EMERGENCY DEPARTMENT 10.1016/j.jemermed.2021.02.019 CLINICAL QUESTION: Among patients presenting to the ED with undifferentiated dyspnoea, does POCUS provide additional diagnostic capacity over clinical assessment and chest X-ray? FINDINGS This was a cohort study with additional health records review. The reference standard was discharged diagnosis, ED diagnosis and confirmation by another physician or diagnosis made by health record reviews. The results revealed a sensitivity and specificity of 92.5% and 85.7% respectively in the POCUS group which was superior to the 63.3% sensitivity and 92.9% specificity of radiology reading of Chest X-ray. AUTHORS' CONCLUSIONS Lung POCUS performed by emergency physicians in a real clinical setting was highly sensitive and specific in identifying acute heart failure and had higher sensitivity than chest x-ray among older patients with suspected AHF or COPD in their ED stay. JOURNAL CLUB THOUGHTS The main issue with study is what the gold standard is. If the standard being used is having the emergency physicians both do the test and say what the diagnosis is it weakens the internal validity of the study. Ideally, if the diagnosis was made independently by a separate physician and the US was being conducted by a separate, independent user, this would strengthen the methodology. In the undifferentiated dyspnoeic patient, making the most accurate diagnosis is important in order to implement appropriate treatment in a timely manner, and there are many other studies out there which detail the advantages of POCUS in this patient cohort. PAPER 4: ONE VERSUS 3-WEEK IMMOBILISATION PERIOD FOR NONOPERATIVELY TREATED PROXIMAL HUMERAL FRACTURES. A PROSPECTIVE RANDOMIZED TRIAL. 10.2106/JBJS.20.02137 CLINICAL QUESTION: Among patients with proximal humeral fractures discharged from the ED, how long should the arm be immobilised? FINDINGS The researchers conducted a prospective randomised trial to determine whether a one week or a three-week immobilisation period would be more effective if it came to pain and functional outcome. Overall, 111 patients were enrolled in the final analysis. There was no significant differences found between the 2 groups when it came to pain, neither was there any significant difference in the constant score or the simple shoulder test scores between the 2 groups. Complication rates were also similar. AUTHORS' CONCLUSIONS Short and long immobilisation periods yielded similar results for non-operatively treated proximal humeral fractures, independent of fracture pattern. These fractures can be successfully managed with a short immobilization period of1 week in order to not compromise patients’ independence for an extended period. JOURNAL CLUB THOUGHTS An interesting study, quite big numbers for this type of trial. One of the main limitations is the lack of consensus between centres in how these types of fractures are managed as the group of patients which the Orthopaedic surgeons chose not to operate on may affect generalisability. This was an important patient centred study as the majority of these patients are elderly ( as displayed by the studies baseline characteristics) who really could do with use of their upper limbs to conduct their ADL’s. There was lack of difference between the groups in terms of complication rates was somewhat reassuring however, 20 % of patients were lost to follow up here which does affect the interpretation of the results. It was noted in the Journal Club there is that signal of increased secondary displacement in the early mobilisation group – the study wasn’t powered to assess the significance of this, but it’s worthy of consideration. Making sure your patients get appropriate and timely follow up will probably affect you decision in terms of duration of immobilisation, so have a look at what your hospital offers! REFERENCES Requena M, Olivé-Gadea M, Muchada M, Hernández D, Rubiera M, Boned S, et al. Direct to Angiography Suite Without Stopping for Computed Tomography Imaging for Patients With Acute Stroke. Jama Neurol. 2021;78(9):1099–107. Zampieri FG, Machado FR, Biondi RS, Freitas FGR, Veiga VC, Figueiredo RC, et al. Effect of Intravenous Fluid Treatment With a Balanced Solution vs 0.9% Saline Solution on Mortality in Critically Ill Patients. Jama. 2021;326(9):818–29. Nakao S, Vaillancourt C, Taljaard M, Nemnom M-J, Woo MY, Stiell IG. Diagnostic Accuracy of Lung Point-Of-Care Ultrasonography for Acute Heart Failure Compared With Chest X-Ray Study Among Dyspneic Older Patients in the Emergency Department. J Emerg Medicine. 2021;61(2):161–8. Martínez R, Santana F, Pardo A, Torrens C. One Versus 3-Week Immobilization Period for Nonoperatively Treated Proximal Humeral Fractures: A Prospective Randomized Trial. J Bone Joint Surg. 2021;103(16):1491–8.

Dr Conor McDermott Emergency Registrar Editor/Peer Review: Dr David McCreary THE CASE A 70-year-old, normally fit and well lady presents to the ED following a fall in her garden. It was a simple trip over uneven paving, she fully recalls the event and aside from a painful left wrist, you don't find any other signs of injury. You prescribe her some simple analgesia and request an X-ray. WHAT DOES THE X-RAY SHOW? There are AP and lateral views of the left wrist. These show a displaced left distal radial fracture with dorsal and lateral displacement with associated dislocation of the ulnocarpal joint. WHAT NEXT? The most relevant question for an ED patient with a fracture of the distal radius is does it actually need a reduction? INDICATIONS FOR REDUCTION These are dependent on the patient: a 10-year-old is not the same as a 30-year-old is not the same as a 90-year-old. CHILDREN Indication for reduction changes with age Younger children will remodel more and can accept greater degrees of deformity without jumping in for a reduction Angulations over 20 degrees in the 0-5 group need reduced and this acceptable angulation decreases by 5 degrees in subsequent age groups (Image courtesy of the RCH Clinical Guidelines) Bayonet Fractures Named for the position of the distal fracture segment relative to the bone looking like this nasty piece of equipment: It looks as if it shouldn’t be allowed but in younger children it’s acceptable to leave the fracture in a bayonet position that will remodel and grow to length. Acceptable if <6 years old with acceptable angulation and <1cm overlap ADULTS Based off 3 measurements (remember 11, 11, 22) Radial inclination – normal 22° Radial height (shortening) – normal 11mm Volar angulation – normal 11° (Images courtesy of the OrthoFlow App, with permission) 🤓 Editor's Comment: while there are quoted acceptable deviations from normal, any deviation from 11, 11, 22 is probably worthy of a pull (if for no other reason than it’s easy to remember). These quoted criteria (all the 5s: 5mm shortening, <5o change in inclination & <5o change in angulation) are really for the final resting position of the fracture. Taking into account that it is likely to slip a little post your reduction, you may as well give it the best numbers from the outset. NEXT QUESTION IS HOW ARE WE GOING TO DO IT? Patients will need either local or systemic analgesia and/or anaesthetic. The choice of which is again down to the patient, as well as your abilities and the department work-load. Below is a quick overview of the different options with the pitfalls of each. PROCEDURAL SEDATION The choice of which sedation depends on the patient, the fracture and the resources however the details of each should be the subject of a blog themselves. The main choices are: Nitrous oxide +/- fentanyl Propofol & fentanyl Ketamine BIER'S BLOCK Great overview here RCEM guidelines Or here RCH guidelines Useful for compliant children and adults and especially useful for those you can’t sedate. Not useful in patients who are severely anxious or unable to tolerate the cuff. Other contraindications include: SBP > 200mmhg, PVD, bilateral fractures, morbid obesity as well as in rarer conditions such as Raynaud’s, scleroderma, sickle cell, methhaemoglobinaemia. DRUGS/DOSES Prilocaine (preferred): 0.6mls/kg of 5% (3mg/kg) Lignocaine: 0.6mls/kg of 5% (3mg/kg) 🤓 ED: THE QUESTION I ASK EVERYONE WHEN TEACHING BIER’S BLOCK IS – WHY DO WE HAVE TWO CUFFS? NO, IT’S NOT JUST BECAUSE WE’RE SO SCARED THAT ONE OF THE CUFFS WILL FAIL…HAVE A THINK THEN CLICK FOR THE ANSWER… To have the option of cuff rotation! Tourniquets can be pretty painful, particularly after the 20-25 minute mark, and some patients will find it worse than others. An option is to: inflate the proximal (A) cuff first, leaving the distal (B) cuff deflated inject the LA once LA is working, inflate the distal (B) cuff if patient experiences a lot of pain from the inflated cuff, the proximal (A) cuff can be deflated – leaving the (B) cuff inflated over anaesthetised limb in the unlikely event of anaesthetic leak you still have the option of inflating the (A) cuff as a backup (Image courtesy of RCEM Best Practice Guideline) HAEMATOMA BLOCK An overview - WikiEM Good for patients you can’t sedate, with relatively fresh fractures and who you can’t use a bier’s and if there are limited staffing resources, however some old evidence here showing that better analgesia gained by Bier’s. If you’re an ultrasound whizz this can be used to ensure you’re going in the right spot (the right spot being below the periosteum and into the fracture haematoma) Make sure you leave enough time for the anaesthetic to work, 5-10mins Patient’s may have some residual pain – useful to add some fentanyl Doesn’t give as good a reduction as a bier’s ULTRASOUND GUIDED BLOCKS The future for the Ultrasound buffs Different approaches are proposed, some which require single injection, others that require multiple The RAPTIR approach is a single injection with further explanation of the anatomy here by NYSORA While blocks of individual nerves further distal require 1 or more injections and are described here, here and again by NYSORA at this link (Images courtesy of NYSORA.com) Above: the RAPTIR approach and distribution of analgesia showing the needle entering the skin superiorly, passing posteriorly  to the clavicle and then injecting local anasthetic into the axillary sheath. This method does not require identification of the nerves just identification of the artery. THE REDUCTION You’ve decided it needs reduced, and chosen your mode of analgesia. Next question is how to effectively pull? The fracture is likely impacted, with intact periosteum acting as a barrier to your reduction, but will also prevent over correction if you are apprehensive. (Image courtesy of musculoskeletalkey.com) THE KEY TO AN EASY REDUCTION IS FOCUS ON THE DIS-IMPACTION. Perform prolonged traction on the distal fragment Then hyperextend the distal fragment Before flexing it back into position PULLING PEARLS It will feel funny making the fracture worse, but this will make it easier to push back into the correct position When you think you’ve dis-impacted enough, keep going for an extra minute Make sure to manipulate the distal fracture fragment and not the carpals, the hand itself should be flopping around in a neutral position with gravity. A trick is to try identify the radial styloid and work proximal from that. 🤓 Ed: you can also feel for the ulnar styloid to get a feel for how your length and position is going by comparing relative position of the two styloids. You can also get a repeat X-Ray if you’re in doubt (and leaded-up), or use US. Don’t be afraid to put all your might into the flexion, the dorsal periosteum will stop you from going too far FITTING THE PLASTER Now it’s time to plaster using what your department has (plaster of paris/dynacast or equivalent) What type, again, depends on the patient: Minor fractures in children can be treated with a simple below-elbow backslabs Almost all others can be treated with a Charnley slab shown below If this plaster is going to be definitive management e.g. nursing home patient then reasonable to place a full POP These can be split along the ulnar edge once set if you are worried about swelling RCH also have this great resource for teaching casting Again, make sure to put pressure on the distal fracture fragment, and not the carpals CHECK YOUR WORK Once you’re done, take a repeat X-ray in cast to check your position and celebrate when the report uses the words “near anatomical positioning”. Hopefully with these tips you will be able to get the same result. REFERENCES / WANT TO READ MORE? The Royal Children’s Hospital guideline for distal radial / ulna fractures Feeling like an ultrasound Jedi? Read about ultrasound guided supra-condylar blocks here The NYSORA regional anaesthesia guide for elbow blocks The Royal College of Emergency Medicine’s Best Practice Guideline for Bier’s Block RCH’s Bier’s Block guideline WikiEM on haematoma block US guided brachial plexus blocks from NYSORA The OrthoFlow App – iOS& Android CONOR MCDERMOTT Emergency Registrar, Alfred Health Conor, originally from Ireland, has been an Emergency Registrar at The Alfred since February 2021, having first started working in ED in 2015 in Brisbane as part of a planned 1 year working holiday that was extended long term. His medical interests include POCUS as well as reducing unnecessary resource waste in hospitals. Outside of work he can be found tasting wine, training for a triathlon and occasionally painting.

Dr Hector Thomson Emergency Registrar Peer review: Dr Luke Phillips Editor: Dr David McCreary THE CASE A 37-year-old man has been ejected from his car after crashing at high speed. He was initially mildly confused but then rapidly dropped his GCS to 8. The ambulance crew on scene have intubated him and whisk him into your emergency department. During your primary survey you noticed his left pupil is dilated and non-reactive. WHAT IS HAPPENING INSIDE THIS PATIENT'S HEAD? In this post, we will discuss some concepts of intracerebral pressure regulation and outline some brain herniation syndromes. THE BASICS OF THE MONRO-KELLIE DOCTRINE You'll have seen this a few times at medical school, in primary exams and on the ATLS/EMST courses, but let's refresh ourselves on it. A couple of 18th century Scottish surgeons Alexander Monro and George Kellie noted that the brain is enclosed in non-expandable bone and is nearly incompressible. “ it does not appear very conceivable how any portion of the circulating fluid can ever be withdrawn from the cranium, without its place being simultaneously occupied by some equivalent; or how any thing new or exuberant can be intruded, without an equivalent displacement” – Kellie 1924. The sum of the volumes of the brain (1400ml), cerebrospinal fluid (150ml) and intracerebral blood (150ml) is constant. An increase in one should cause a reciprocal decrease in either one or both of the remaining two. Aside from being primary examination fodder this principle explains why small changes in volume can have marked changes in intracranial pressure. Image source(1) The Monro-Kellie model for the contents of the intracranial compartment. 'Brain tissue' includes neurons, glia, extracellular fluid and cerebral microvasculature. 'Venous' and 'Arterial blood' represents the intracranial blood volume in macro-vasculature and cerebral venous sinuses. 'CSF' includes ventricular and cisternal CSF. If into this fixed box we have a haemorrhage such as an extradural haematoma, swelling from an infarct, a tumour or an abscess then CSF and venous blood will be pushed out with an initial small increase in pressure. Extra CSF production or blockage of CSF drainage can also raise the intracranial pressure (ICP). Beyond a certain point, the pressure will rapidly increase. Squeezing brain tissue into another compartment like the last bit of toothpaste in the tube. As the pressure rises the ability of the cerebral vascular to regulate cerebral blood flow reaches a critical point, resulting in decreased compliance as cerebral ischemia. Image: Pressure Volume Curve for ICP(1) WHAT ARE THE COMMON EXAMINATION FINDINGS OF RAISED ICP? Initial signs of raised ICP are nonspecific including headache, nausea, vomiting, agitation or conversely increased drowsiness then obtundation. Examination findings of brain herniation can include: Dilated and nonreactive pupils Asymmetric pupils Extensor posturing or not response to painful stimuli Progressive decline in neurologic condition (decrease in GCS > 2 points) that are not associated with non-TBI causes Cushing reflex (hypertension, bradycardia, irregular respirations) WHAT CAUSES THESE EXAMINATION FINDINGS AND WHAT ARE THE IMPORTANT HERNIATION SYNDROMES I NEED TO KNOW? It depends on which bit of the brain is being squished. While you can also herniate upwards (reverse coning - yes, that's a thing) or out a hole in your skull (trans-calvarial), these are both extremely rare, so let’s focus on the three most common and important herniation syndromes: Subfalcine Transtentorial Tonsillar Image: Types of herniation syndromes - courtesy of Dr Matt Skalski, Radiopaedia.org, rID: 45683 1. SUBFALCINE HERNIATION The two cerebral hemispheres are separated by a sheet of dura called the falx cerebri. If there is a unilateral mass on one side the cingulate gyrus can be pushed down and under. Image: Anatomy of the falx cerebri and tentorium cerebelli(2) WHAT DO I LOOK FOR ON CT? The CT brain will have midline shift. Draw a line between the anterior and posterior attachments of the falx to the inner table of the skull and measure at the level of the foramen of Monroe as seen on the CT below. The degree of shift has prognostic implications (<5 mm has a good prognosis while >15mm generally do very poorly.) Image: Case courtesy of Assoc Prof Frank Gaillard, Radiopaedia.org. From a case rID: 15823 These axial slices show a huge acute subdural overlying the right cerebral hemisphere as well as filling the floor of the middle cranial fossa and tracking along the posterior aspect of the falx (blue arrow), resulting in marked mass effect and midline shift (red). There is marked uncal herniation (yellow) with significant distortion of the midbrain (blue dotted line). Following the craniectomy (orange arrow) and evacuation of the haematoma, an anterior cerebral artery infarct has developed on the right (green *). WHAT EXAMINATION FINDINGS MANIFEST FROM THIS SYNDROME? This shift can cause compression of the anterior cerebral artery resulting in a stroke syndrome with the most common manifestation being contralateral leg weakness. Hydrocephalus can also develop as the foramen of Monro is compressed (yep same bloke as the doctrine). 2. TRANSTENTORIAL/UNCAL HERNIATION The tentorium cerebelli covers over the posterior cranium. Descending transtentorial herniation can occur in two patterns: lateral and central. We will discuss the more common lateral pattern. With increasing pressure, the uncinate process of the temporal lobe can herniate into the anterior part of the opening, placing pressure on the midbrain. The brainstem will squeeze down through the opening in the tentorium cerebelli as shown below. Image: Anatomy of the tentorium cerebelli – Emergency Medicine Ireland HOW DO I LOOK FOR THIS ON CT? Shift of brainstem and distortion of adjacent cisterns Dilatation of the contralateral temporal horn PCA territory infarct due to compression of the posterior cerebral artery as it crosses the tentorium Image: Transtenorial Herniation(2) The axial CT slice below shows an acute left subdural causing transtentorial hernation. There is widening of the left basal cistern (arrow) with effacement of the right basal cistener (dashed line). There is also dilatation of the temporal horn of the right lateral ventricle (*). WHAT EXAMINATION FINDINGS MANIFEST FROM THIS SYNDROME? The classical presentation is: Blown pupil + Coma + Contralateral hemiparesis As the brain squeezes down this places pressure on the oculomotor nerve as shown below. This results in an ipsilateral non-reactive, dilated pupil. As the parasympathetic fibres are on the outside there will be dilatation before the motor effects causing a down and out pupil. This is the earliest and most reliable sign. Image: Anterior view of transtentorial uncal herniation caused by a large haematoma under a skull fracture. Coma develops due to compression of the reticular activating system in the brainstem. The descending corticospinal tracts will also be compressed as shown in the MRI below. This usually results in contralateral hemiparesis. Confusingly this can also be ipsilateral (false lateralising sign) in 25% if lateral displacement compresses the opposite cerebral peduncle (Kernohan’s phenomena). If untreated, this may eventually compress the midbrain (causing bilateral fixed & dilated pupils, with decorticate or decerebrate posturing). Image: Descending corticospinal tracts when compressed will cause contralateral hemiparesis – Emergency Medicine Ireland 3. TONSILLAR HERNIATION Tonsillar herniation involves the inferior descent of the cerebellar tonsils below the foramen magnum. Any mass effect on the brain can displace the posterior cranial fossa structures inferiorly. This then leads to the brain stem compression against the clivus (the surface of the skull base anterior to the foramen magnum – thanks Radiopaedia). Squeezing the brainstem impairs the function of the pons and the medulla (labelled below), which are pretty important for, you know, keeping you alive. Obstructive supratentorial hydrocephalus may result from fourth ventricle compression. HOW DO I LOOK FOR THIS ON CT? Draw a line on the sagittal slice across the foremen magnum (yellow dash) then measure the inferior descent of the cerebellar tonsils (red arrow). The radiographic definition is >3mm. Normal can vary with age and definitions vary. Image: Emergency Medicine Ireland WHAT ARE THE EXAMINATION FINDINGS? Tonsillar herniation can manifest initially as headache and irritability. The posterior fossa is a tight place and this places pressure on cardiac and respiratory centres. As the pressure increases this results in the Cushing reflex which is comprised of: Irregular breathing Bradycardia Hypertension Hypertension is the brainstem’s response to decreased cerebral blood flow, and its attempt to restore cerebral blood flow. Unfortunately, hypertension can cause a vicious cycle of increased blood volume and worsening cerebral oedema, which in turn can worsen cerebral blood flow. Finally, the patient will fall into a deep coma with low blood pressure and tachycardia before apnea and death. WITH THE PATHOPHYSIOLOGY NOW COVERED, IN PART 2 WE WILL COVER THE PRACTICAL ASPECTS OF HOW TO MANAGE THIS AT THE BEDSIDE. REFERENCES / RESOURCES FOAM RESOURCES Internet Book of Critical Care: Raised ICP – detailed notes on all things raised ICP by Josh Forkas Anatomy for Emergency Medicine: Brain Herniation – if you do nothing else, watch Andy Neill’s video on the anatomy of brain herniation (and all of his other videos while you’re there) Life in the Fast Lane: Brain Herniation Radiopedia: Brain Herniation PAPERS Harary M, Dolmans RGF, Gormley WB. Intracranial Pressure Monitoring—Review and Avenues for Development. Sensors Basel Switz. 2018;18(2):465. doi: 3390/s18020465 Berta Riveros Gilardi, José Ignacio Muñoz López, Antonio Carlos Hernández Villegas, Juan Alberto Garay Mora, Oralia Cristina Rico Rodríguez, Roberto Chávez Appendini, Marianne De la Mora Malváez, Jesús Antonio Higuera Calleja. Types of Cerebral Herniation and Their Imaging Features. (2019) RadioGraphics. 39 (6): 1598-1610. doi:10.1148/rg.2019190018- Pubmed Demetriades, D., & Benjamin, E. (2021). Head Injury. In D. Demetriades, C. Chudnofsky, & E. Benjamin (Eds.), Color Atlas of Emergency Trauma (pp. 1-23). Cambridge: Cambridge University Press. doi:10.1017/9781108776622.003Hector (the one on the left) is an Emergency Medicine Advanced Trainee at The Alfred. He's still clinging to the basic science knowledge he gained during primary exam prep and enjoys shoulder dislocations, trauma, rugby union, fresh pasta and good gin. He doesn't like vague allergies or cats. HECTOR THOMSON Emergency Registrar Hector (the one on the left) is an Emergency Medicine Advanced Trainee at The Alfred. He’s still clinging to the basic science knowledge he gained during primary exam prep and enjoys shoulder dislocations, trauma, rugby union, fresh pasta and good gin. He doesn’t like vague allergies or cats.

Journal Club Podcast for January 2022 Prof Peter Cameron Dr Divya Karna Dr Eanna Mac Suibhne Editor: Dr David McCreary Welcome to the Journal Club Podcast for January 2022. You can listen to the podcast above and have a read at our summary below, courtesy of our senior registrar for research, Dr Eanna Mac Suibhne. This month I was joined by Professor Peter Cameron, Academic Director for the Alfred Emergency and Trauma Centre and Emergency Physician Dr Divya Karna. This month in our Journal Club we reviewed a couple of papers from the COVID-sphere. The first reviews cardiac side-effects of COVID infection & vaccination and the second the use of fluvoxamine for the treatment of COVID infection (spoiler alert, it’s probably not that helpful, despite what the authors say). Fear not, we also looked at two non-COVID papers: we discuss a paper assessing closed reduction vs open fixation of distal radius fractures and then the latest iteration of the surviving sepsis guidelines. As always, have a look at the papers yourself and draw your own conclusions but, for a snap shot of what we thought, read on! PAPER 1: RISKS OF MYOCARDITIS, PERICARDITIS, AND CARDIAC ARRHYTHMIAS ASSOCIATED WITH COVID-19 VACCINATION OR SARS-COV-2 INFECTION READ IT HERE CLINICAL QUESTION: Does vaccination lead to increased rates of cardiac events, specifically myocarditis/pericarditis/cardiac arrhythmia? FINDINGS Of the 38,615,491 vaccinated individuals included in the study, 1,615 (0.004%) were admitted to hospital with, or died from, myocarditis at any time in the study period. Similarly, 0.004% were admitted to hospital with, or died from, pericarditis and 1% with cardiac arrhythmia. There was no evidence of an increase in the risk of pericarditis or cardiac arrhythmias following vaccination, except in the 1–28days following a second dose of the mRNA-1273 vaccine. In the same population, there was a greater risk of myocarditis, pericarditis and cardiac arrhythmia following SARS-CoV-2 infection. The increased risk of myocarditis after vaccination was higher in persons aged under 40 years. Extra myocarditis events were estimated to be between 1 and 10 per million persons in the month following vaccination, which was substantially lower than the 40 extra events per million persons observed following SARS-CoV-2 infection. AUTHORS' CONCLUSIONS Vaccination for SARS-CoV-2 in adults was associated with a small increase in the risk of myocarditis within a week of receiving the first dose of both adenovirus and mRNA vaccines, and after the second dose of both mRNA vaccines. By contrast, SARS-CoV-2 infection was associated with a substantial increase in the risk of hospitalization or death from myocarditis, pericarditis and cardiac arrhythmia. JOURNAL CLUB THOUGHTS This was a big study conducted in the UK which was an ideal location given that the three vaccinations were rolled out at speed and scale and the large sample size facilitated the study to be powered to investigate and detect the chosen outcomes. All this is obviously very topical and it’s useful to have this data to hand which is reassuring to the public. One of the main take-homes should be that if you don’t want to get myocarditis or pericarditis - get vaccinated. The researchers relied on hospital admission codes and death certification to define their outcome measures, as opposed to standard investigations such as imaging or biopsy and so cannot determine accurately which patients had myocarditis or pericarditis. This is problematic in interpreting the results and affects the internal validity of the study. The observation that the risk of myo- and pericarditis is much greater following Covid-19 disease than it is after Covid-19 vaccination is not new information, but this paper supports and confirms this. PAPER 2: VOLAR PLATE FIXATION VERSUS CAST IMMOBILIZATION IN ACCEPTABLY REDUCED INTRA-ARTICULAR DISTAL RADIAL FRACTURES A RANDOMIZED CONTROLLED TRIAL READ IT HERE CLINICAL QUESTION: Do functional outcomes differ between volar plate fixation and cast immobilization in a series of adult patients with displaced and acceptably reduced intra-articular distal radius fracture? FINDINGS Patients aged 18 and 75 years with a displaced, intra-articular fracture of the distal radius which had been successfully reduced were randomised to either operative fixation within 2 weeks of their injury or to nonoperative management in cast immobilisation for 4 to 5 weeks. The primary outcome here was difference in Patient-Rated Wrist Evaluation (PRWE) score at one year and this was found to favour the operative intervention group. Of note the prespecified clinically significant difference of 14 points was only found up to 6 months of followup and while there remained a statistically significant difference in the groups at 12 months, this no longer met the clinically significant criteria with a difference of 7 points favouring the operative group. Secondary outcomes included a clinical evaluation of range of motion and grip strength, superior in the operative group at 6 weeks but not at subsequent follow-ups. 13 non-operative patients (28%) had subsequent surgery due to displacement or malunion observed during the follow-up period. AUTHORS' CONCLUSIONS Adult patients with an acceptably reduced intra-articular distal radial fracture had better functional outcomes during 12 months when treated operatively instead of nonoperatively. Additionally, a subsequent surgery rate of 28% in the nonoperative group was found. Due to rising health-care costs, it has become increasingly important to provide effective care with good functional outcomes. The authors recommended surgery for patients with these fractures. JOURNAL CLUB THOUGHTS This study indicates ORIF improves early functional status without meaningful differences after a year and is logical, as ORIF allows for earlier mobilization and more rapid return to function. The 28% surgery rate in the non-operative group would indicate that early Ortho outpatient follow-up or referral at presenting episode is worthwhile to consider operative intervention. Even in less dependent patients, early ortho follow-up following initial reduction and immobilization is indicated to identify those at higher risk of malunion and re-evaluate the reduction status. PAPER 3: EFFECT OF EARLY TREATMENT WITH FLUVOXAMINE ON RISK OF EMERGENCY CARE AND HOSPITALISATION AMONG PATIENTS WITH COVID-19: THE TOGETHER RANDOMISED, PLATFORM CLINICAL TRIAL READ IT HERE CLINICAL QUESTION: Does outpatient treatment with fluvoxamine when compared to placebo prevent either extended emergency room observation or hospitalization due to COVID-19? FINDINGS This was a placebo-controlled, double-blind, randomised trial performed at 11 outpatient clinical sites in Brazil. Patients were randomly assigned to fluvoxamine at a dose of 100 mg twice a day for 10 days or corresponding placebo starting directly after randomisation. The primary outcome was a composite endpoint of admission to hospital due to COVID-19-related illness, or observation in the emergency department for more than 6 hours due to COVID-19-related illness, within 28 days of randomisation. In the fluvoxamine group, 11% of participants had a primary outcome event compared with 16% in the placebo group. Hospitalisations were not statistically different between the groups (10% vs 13%, p=0.1). There was a statistically significant difference in the number of patients who were observed in the emergency department for 6 hours (1% vs 5%, p=0.0001). There was no difference in viral clearance at day 7, mechanical ventilation, number of days ventilated, or number of days hospitalized. 84 participants stopped fluvoxamine and 64 participants stopped placebo owing to issues of tolerability. The difference was statistically significant. AUTHORS' CONCLUSIONS Treatment with fluvoxamine (100 mg twice daily for 10 days) among high-risk outpatients with early diagnosed COVID-19, reduced the need for extended emergency room observation or hospitalisation. JOURNAL CLUB THOUGHTS There were a few issues identified with this paper that limit our confidence in the results. In terms of generalisability, the study was only performed in unvaccinated patients. These results may not be generalisable to vaccinated patients. Less relevant now in countries with over 90% vaccination rates, which most countries are heading towards and limits the applicability of these results in other settings.  The composite outcome that was used also raises questions, particularly the 6-hour observation in the ED being counted as a negative outcome. Also, the difference in primary outcome was driven by ED visits, not hospitalisations. In usual cases patients deemed safe to be discharged directly from the ED would typically be counted as a positive outcome so it's unclear why the authors used this measure. The authors also made alterations to the primary outcome changing from >12hrs to >6hrs. It is unclear from the paper when this was changed (i.e. before or after data analysis). With a positive result on a RCT, the knee jerk reaction is to jump on a treatment, however replication is the key to science, and no treatment should become standard based on a single RCT. The authors' conclusions are a bit misleading. As Peter comments, you can look up this and other such COVID trials on the National COVID-19 Clinical Evidence Taskforce website. PAPER 4: SURVIVING SEPSIS CAMPAIGN: INTERNATIONAL GUIDELINES FOR MANAGEMENT OF SEPSIS AND SEPTIC SHOCK 2021. READ IT HERE The final topic we discussed this month was the recently published update to the international guidelines for the management of sepsis and septic shock from the Surviving Sepsis Campaign. The guidelines summarised the evidence from the literature up to July 2019, and are composed of 6 parts as “screening and early treatment”, “infection”, “hemodynamic management”, “ventilation”, “additional therapies” and “long-term outcomes and goals of care”. There are a total of 93 items and 99 recommendations. Sepsis care has changed significant in the last 20 years. You can find a full list of updates here. The guys over at emDOCs.net have a nice summary of the guidelines and have a few selected ED-relevant points for consideration, including discussion of the evidence behind them: For adults with septic shock, we suggest using capillary refill time to guide resuscitation as an adjunct to other measures of perfusion. Weak, low quality of evidence, NEW. The ANDROMEDA SHOCK trial evaluated resuscitation using capillary refill time and found it to be more effective than a resuscitation strategy using lactate in reducing organ dysfunction. You can hear Dave’s discussion of this study on the RCEMLearning Podcast here. For patients with sepsis-induced hypoperfusion or septic shock we suggest that at least 30 mL/kg of IV crystalloid fluid should be given within the first 3 hr of resuscitation. Weak, low quality of evidence DOWNGRADE from Strong, low quality of evidence. There are no prospective interventional studies looking at different volumes for the initial resuscitation of those with sepsis or septic shock. A retrospective study including ED adult patients with sepsis or septic shock found failure to receive 30 mL/kg of crystalloids was associated with higher mortality. For adults with sepsis or septic shock, we suggest using balanced crystalloids instead of normal saline for resuscitation. Weak, low quality of evidence, CHANGED from weak recommendation, low quality of evidence. The SMART and SALT ED trials support the use of balanced crystalloids, with a network meta-analysis demonstrating decreased mortality with balanced fluids For adults with septic shock on vasopressors, we recommend an initial target mean arterial pressure (MAP) of 65 mm Hg over higher MAP targets. Strong, moderate-quality evidence. An RCT evaluating patients in septic shock randomized to MAP targets of 65-70 mm Hg versus 80-85 mm Hg found no difference in mortality. There was reduced risk of renal replacement therapy in patients with chronic hypertension and higher rates of atrial fibrillation in the group randomized to the higher MAP target group. For adults with septic shock, we suggest starting vasopressors peripherally to restore mean arterial pressure rather than delaying initiation until central venous access is secured. Weak, very low quality of evidence, NEW. Vasopressors play an important role in treatment of septic shock. Peripheral administration of vasopressors is generally safe if infused in the antecubital fossa for a short period of time (< 6 hours). Peripheral infusion is associated with shorter time to administration and time to achieving a MAP > 65. For adults with sepsis-induced hypoxemic respiratory failure, we suggest the use of high flow nasal oxygen (also known as HFNC) over non-invasive ventilation (NIV). Weak, low quality of evidence, NEW. One RCT demonstrates improved 90-day survival with HFNC compared with NIV (OR 0.42, 95% CI 0.21-0.85), with more days from mechanical ventilation. REFERENCES Patone M, Mei XW, Handunnetthi L, Dixon S, Zaccardi F, Shankar-Hari M, et al. Risks of myocarditis, pericarditis, and cardiac arrhythmias associated with COVID-19 vaccination or SARS-CoV-2 infection. Nat Med. 2021;1–13. Selles CA, Mulders MAM, Winkelhagen J, Eerten PV van, Goslings JC, Schep NWL, et al. Volar Plate Fixation Versus Cast Immobilization in Acceptably Reduced Intra-Articular Distal Radial Fractures: A Randomized Controlled Trial. J Bone Joint Surg. 2021;103(21):1963–9. Reis G, Moreira-Silva EA dos S, Silva DCM, Thabane L, Milagres AC, Ferreira TS, et al. Effect of early treatment with fluvoxamine on risk of emergency care and hospitalisation among patients with COVID-19: the TOGETHER randomised, platform clinical trial. Lancet Global Heal. 2022;10(1):e42–51. Evans L, Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063–143.

Dr Eanna Mac Suibhne Emergency Registrar Peer review: Dr David McCreary THE CASE Gerard is a 55-year-old gentleman who has presented to your ED with a collapse episode while at home. It was an unwitnessed event but he reports it to be like a fainting episode. He slowly picked himself up and called an ambulance because he didn’t feel right. Recently, he reports having some chest pain and has become more short of breath on exertion in the past week. Gerard thought he was getting back to his old self after he underwent an ORIF of his tibia 5 weeks ago having fallen off some scaffolding at work. As you sit there with Gerard, you note that he is quite pale and sweaty, not entirely comfortable. His blood pressure reads a systolic of 95mmhg and has had a persistent tachycardia of 115 bpm since arriving in the department. The nurse hands you an ECG which shows a RBBB, which is new for Gerard since his pre-op ECG 5 weeks previously. An i-Stat troponin has come back elevated above the reference range. NO MARKS FOR GUESSING THE DIAGNOSIS HERE…BUT WHAT ARE WE GOING TO DO ABOUT IT? DO YOU ANTICOAGULATE OR DO YOU PULL OUT THE BIG-GUNS AND THROMBOLYSE THIS CHAP? WHEN DO YOU PUSH THE BUTTON FOR THROMBOLYSIS IN PE? If you were to go with current literature basically it would suggest you should thrombolyse a massive PE and after that, well, the evidence is sketchy. About 10% of patients diagnosed with acute PE die within the first three months of diagnosis<1>, so getting the correct treatment to the correct patient is important. The difficult decision relates to a particular subset of patients who have maintained hemodynamic stability yet have signs of RV dysfunction and who could potentially deteriorate. What to do? When it comes to this topic it all seems to hinge on definitions and so let’s start with the question: WHAT’S THE DIFFERENCE BETWEEN A MASSIVE AND A SUBMASSIVE PE? MASSIVE PE Let’s first talk about massive PE, as there is little argument in the literature that thrombolysis is the appropriate treatment here. To be labelled with this ominous tag, a PE must satisfy certain criteria, which vary depending on where you are looking. The definition had originally relied on anatomical criteria, those being occlusion of two or more lobar arteries or more than 50% occlusion of pulmonary vasculature. This view, however, has evolved to incorporate a patient’s hemodynamic status. A succinct definition is provided by the AHA: An acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock). ‘Shock secondary to another cause’; this point should not be skimmed over. Are you sure your patient is not hypotensive for another reason that you haven’t considered, e.g. sepsis, hypovolemia, arrhythmia, LV dysfunction etc?<2> Approaches to help you consider this would be: Assess the clot burden on CT. For a PE to be the perpetrator of a patient’s compromised hemodynamics, there should be at least moderate to large clot burden on the CT. Patients who are hemodynamically unstable with a small amount of clot - it’s probably not going to be the PE that is causing the instability. Get your probe out. If the IVC and RV aren’t dilated, consider reassessing if it’s the PE that is causing the shock. In patients with massive PE, systemic thrombolytic therapy has been shown to reduce mortality<3>, decrease the risk of developing chronic thromboembolic pulmonary hypertension and improve quality of life<4> <5>. The Alfred guideline, summarised in the flow chart below, supports thrombolysis in the massive PE patient cohort in the context of no contraindications for its administration. SUBMASSIVE PE For submassive PE, the definition again varies. Sticking with the AHA, they proposed the following definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis. RV dysfunction means the presence of at least 1 of the following: RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT Elevation of BNP (>90 pg/mL) or N-terminal pro-BNP (>500 pg/mL); or Electrocardiographic changes: new RBBB (complete/incomplete) anteroseptal ST elevation or depression anteroseptal T-wave inversion) Myocardial necrosis is defined as either of the following: Elevation of troponin I (>0.4 ng/mL) or Elevation of troponin T (>0.1 ng/mL) Thrombolysis in this group is more controversial and the evidence is far from definitive in helping the clinician come to a decision. It is challenging to look for guidance here when the international organisations can’t agree on recommendations. Unfortunately there is no large, multi-centre RCT which has unequivocally proven the benefit of thrombolysis in submassive PE. Yet a recent meta-analysis suggests that systemic thrombolytic therapy reduces mortality in this patient group (OR 0.48; 95% CI 0.25 - 0.92)<6>.  The trade-off is a significantly increased risk of major bleeding<7> . The decision to initiate thrombolysis is often taken in terms of the individual risk-to-benefit analysis. WHAT CAN THROMBOYSIS DO FOR SUBMASSIVE PE? The primary reason to give thrombolytics in submassive PE is to reduce the risk of cardiac arrest, yet the goal isn’t to normalise pulmonary pressure, but to cut back pressure sufficiently to prevent cardiac death. This allows for an improvement in right ventricular function, thus reducing the risk of acute RV failure. We have trials, MAPPET and PEITHO which demonstrate that thrombolysis decreases the risk of hemodynamic deterioration, but at the expense of increase major bleeding (11.5% vs 2.4%; NNH = 20) and ICH (2.4% vs 0.2%; NNH = 46)<8>. So, is there any way we can achieve our goal of unburdening the RV and reduce the likelihood of major haemorrhage? How about a reduced dose to offset the risk? We administer heparin on a weight-based dose, so why should it be a one dose for all comers when it comes to tpA dose. Let’s look at this. Again, evidence is sparse here. Wang et al<9> in 2010 conducted a prospective RCT comparing 50 mg vs. 100 mg tPA infused peripherally over two hours among 118 patients with submassive or massive PE. That study found no difference in hemodynamics between the two doses and an increased risk of haemorrhage with 100 mg tPA, particularly among patients weighing below 65 kg. Another study The OPTALYSE PE trial<10> was a prospective trial comparing different regimens of alteplase administered via catheter-directed thrombolysis.  There was no apparent difference in efficacy between doses of ~8 mg and ~24 mg. Full dose thrombolysis is traditionally considered to be 100 mg IV alteplase over 2 hours with the initial 10mg given as a push, yet there is no evidence supporting the use of this dose, as compared to a lower dose. Half-dose, 50 mg alteplase, has been shown to have identical efficacy compared to 100 mg alteplase, with fewer bleeding complications<11>. So, it would seem that half-dose thrombolytics improve surrogate outcomes (i.e. mortality; not the primary outcome in any of these studies) and the added benefit of less major bleeding or ICH. SO WHERE DOES THAT LEAVE US? In terms of take-home points, this is a murky field as Submassive PE is a spectrum of disease and not all patients will require thrombolytics. Following your own hospital’s guidelines will keep you in the green zone. The Alfred’s guideline has categorised PE’s as either massive or submassive, with submassive being subcategorised to high risk or low/ standard risk. The criteria for a patient to enter the low/ standard risk group have been determined to be haemodynamic stability and an absence of the markers of adverse prognosis that define massive of submassive PE. Thrombolysis is recommended for the 'High Risk' submassive group. See the flow chart below. There is a recommendation that patients under 65kg should not receive a dose in excess on 1.5mg/kg, thereby reducing the risk of major bleeding. Half dose thrombolytics seem to be a good option, watch this space. Clinical decision making should be guided by objective findings and any decisions made, should be made in conjunction with the patient, senior medical staff and our specialty colleagues who will be admitting the patient. 🤔 TAKE HOME – WHAT WERE THOSE DEFINITIONS AGAIN? 🤔 MASSIVE Sustained hypotension (systolic <90 x 15mins) OR needing inotropes OR sustained HR <40bpm with shock OR cardiac arrest (obvs) SUBMASSIVE - HIGH RISK RV dysfunction or myocardial injury: RV dilation (echo or CT) RV systolic dysfunction (echo) ↑BNP ECG Changes ↑Troponin SUBMASSIVE - LOW RISK None of the above REFERENCES Aujesky D et al. Weekend versus weekday admission and mortality after acute pulmonary embolism. Circulation 2009;119:962-968 Jaff MR, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011 Apr 26;123(16):1788-830. Jerjes-Sanchez C, et al. Streptokinase and heparin versus heparin alone in massive pulmonary embolism: a randomized controlled trial. J Thromb Thrombolysis 1995;2:227-9 Sharifi M, et al. "MOPETT" Investigators. Moderate pulmonary embolism treated with thrombolysis (from the "MOPETT" Trial). Am J Cardiol 2013;111:273-7 Kline JA, et al. Prospective evaluation of right ventricular function and functional status 6 months after acute submassive pulmonary embolism: frequency of persistent or subsequent elevation in estimated pulmonary artery pressure. Chest 2009;136:1202-10 Chatterjee S, et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA 2014;311:2414-21 Marti C, et al. Systemic thrombolytic therapy for acute pulmonary embolism: a systematic review and meta-analysis. Eur Heart J. 2015 Mar 7;36(10):605-14.. Meyer G, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014 Apr 10;370(15):1402-11. doi: 10.1056/NEJMoa1302097. PMID: 24716681. Wang C, et al. Efficacy and safety of low dose recombinant tissue-type plasminogen activator for the treatment of acute pulmonary thromboembolism: a randomized, multicenter, controlled trial. Chest. 2010;137(2):254-262. Tapson V, et al. A Randomized Trial of the Optimum Duration of Acoustic Pulse Thrombolysis Procedure in Acute Intermediate-Risk Pulmonary Embolism: The OPTALYSE PE Trial. JACC Cardiovasc Interv. 2018;11(14):1401-141 Wang C, et al. China Venous Thromboembolism (VTE) Study Group. Efficacy and safety of low dose recombinant tissue-type plasminogen activator for the treatment of acute pulmonary thromboembolism: a randomized, multicenter, controlled trial. Chest. 2010 Feb;137(2):254-62.Eanna is an Irish-trained Emergency physician whose interests broadly include trauma, toxicology and sports injury management. The search of experiencing working in an MTC has resulted in sticks being upped and his recent move to Melbourne. The freely available great coffee was a happy coincidence. EANNA MAC SUIBHNE Emergency Registrar Eanna is an Irish-trained Emergency physician whose interests broadly include trauma, toxicology and sports injury management. The search of experiencing working in an MTC has resulted in sticks being upped and his recent move to Melbourne. The freely available great coffee was a happy coincidence.

Dr Gavin Ng Emergency Physician Peer review: Dr David McCreary THE CASE A 23-year-old gentleman presents to your Emergency Department with the complaint of difficulty walking. He has other medical history, and takes no regular medications. He is somewhat overweight, but maintains a balanced diet. The following history is provided: Difficulty walking over the last 4 months Describes mainly losing balance and falling over once. Associated with gradual onset back pain, which the patient attributes to lifting at work. Has attended a physiotherapy session, who has recommended he present to ED for a medical opinion. Describes pins and needles in the right leg, in comparison to the left. Confirms the following: No episodes of bladder or bowel incontinence No loss of saddle sensation No history of trauma to the back. The lower limb neurological exam is detailed below: Lower limb neurological exam Otherwise, the upper limb examination, cerebellar examination and cranial nerve examination is unremarkable. He has intact saddle sensation and intact anal tone. QUESTION 1: HOW DO WE CLASSIFY NEUROLOGICAL COMPLAINTS IN THE ED? Motor neurological complaints may be classified as either upper motor neuron (UMN) syndromes or lower motor neuron (LMN) syndromes, based on their clinical findings. Lesions to UMN or LMN areas produce distinct clinical features that may help identify the location and thus assist with decision making, e.g. imaging choices. QUESTION 2: WHAT ARE UMNS AND LMNS? UMNs are neurons that are responsible for initiation and inhibition of movement. They originate in the cortex, travel to the ipsilateral medulla where they decussate to form the contralateral corticospinal tract. They terminate at the anterior horn, where they synapse with a LMN. LMNs are neurons that connect the UMN to the effector cell. Figure 1: demonstrating the location of both UMNs and LMNs (Case courtesy of OpenStax College, Radiopaedia.org, rID: 53266) QUESTION 3: WHAT EXAMINATION FINDINGS ARE ASSOCIATED WITH UMN AND LMN SYNDROMES? As the UMNs are associated with initiation and inhibition of movement, this syndrome produces both positive and negative features. LMN syndromes predominantly have negative features. The table below provides a summary of the expected examination findings: QUESTION 4: WHAT ARE THE POTENTIAL CAUSES OF UMN AND LMN SYNDROMES? As the UMN travels from the cortex through the cortico-spinal tract, any injury before the anterior horn will produce an UMN syndrome. Remember that as discussed above, as the decussation occurs at the level of the medulla, lesions above the medulla will present with contra-lateral signs and lesions below the medulla will present with ipsilateral signs. Some examples of lesions that can produce an UMN syndrome are: Brain lesions – strokes; traumatic brain injury; anoxic brain injury Spinal cord lesions – MS; transverse myelitis; amyotrophic lateral sclerosis LMN syndromes occur when there is injury to the anterior horn cells, or the peripheral nerve. A disorder at the neuromuscular junction (E.g., myasthenia gravis) may mimic a LMN syndrome as well. QUESTION 5: WHAT DO THE HISTORY AND EXAMINATION FEATURES SUGGEST? An upper motor neuron (UMN) syndrome; suggestive of a spinal cord lesion. The lesion is probably in the thoraco-lumbar region, given the absence of clinical findings in the head, neck and upper limbs. QUESTION 6: COULDN'T THIS BE CAUDA EQUINA SYNDROME (CES)? CES is worth mentioning here, as it should be on the list of differentials for all patients presenting to the ED with back pain and lower limb neurological complaints. However, remember that CES presents as a LMN syndrome, with bladder and bowel dysfunction. This is in contrast to our patient’s presentation. The key features of CES are(1): Lower back pain, with pain radiating down one or both legs. Weakness – weakness in plantar flexion suggests S1-S2 nerve root involvement Hyporeflexia – loss of ankle jerks suggests S1-S2 nerve root involvement. Bladder and rectal sphincter paralysis The most common symptom is urinary retention(2). Loss of sensation in the saddle area. OUTCOME Given the clinical findings, the patient was admitted to the neurology ward for further investigation. MRI Brain and MRI Spine was performed, which demonstrated multi-level spinal canal stenosis in the thoracic spine, secondary to osteophyte formation. There was also evidence of cord myelopathy at T1-T2 region. He was then referred on to the spinal surgery team for definitive fixation. REFERENCES Eisen A. Anatomy and localization of spinal cord disorders In: Aminoff M, editor. UpToDate. UpToDate, Waltham, MA Wiseman D. Cauda Equina Syndrome https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Cauda-Equina-Syndrome.=">https://www.aans.org/en/Patients/Neurosurgical-Conditions-and-Treatments/Cauda-Equina-Syndrome.">Gavin Ng is a Fellow of the Australasian College for Emergency Medicine, and is currently employed as an Emergency Physician at Alfred Health and Ballarat Health Services. GAVIN NG Emergency Physician Gavin Ng is a Fellow of the Australasian College for Emergency Medicine, and is currently employed as an Emergency Physician at Alfred Health and Ballarat Health Services. Gavin has completed his undergraduate medical training in 2011, graduating from the University of Melbourne. He has been training in Emergency Medicine since 2014. Gavin has worked in a variety of clinical settings, ranging from metropolitan EDs to regional areas in Victoria. His clinical interests are Critical Care Medicine and Trauma medicine, and he has previous experience working as a Trauma Fellow at Alfred Health. He is also a current ALS2 (Advanced Life Support Level 2) instructor. He also has a passion for education – he has previously been involved in teaching junior medical staff through the Northern Clinical School.

Journal Club Podcast for February 2022 Prof Peter Cameron Dr Myles Sri Ganeshan Dr Eanna Mac Suibhne Editor: Dr David McCreary Welcome to the Journal Club Podcast for February 2022 (yes, published in March...sometimes it takes a while for our timetables to sync!). You can listen to the podcast above and have a read at our summary below, courtesy of our senior registrar for research, Dr Eanna Mac Suibhne. In February, I was joined by Professor Peter Cameron, Academic Director for the Alfred Emergency and Trauma Centre, and our new Research Fellow, Dr Myles Sri Ganeshan. We reviewed 2 more COVID-related papers, the first regarding Molnupiravir as an option for outpatient management of COVID and another concerning rapid antigen tests. We also reviewed papers exploring ketamine nebulisation for pain, and the risks of not anticoagulating patients with subsegmental PEs. As always, have a read of the papers for yourselves and draw your own conclusions. But read on to get a snapshot of what we discussed. PAPER 1: MOLNUPIRAVIR FOR ORAL TREATMENT OF COVID-19 IN NON-HOSPITALIZED PATIENTS READ IT HERE CLINICAL QUESTION: Is Molnupiravir superior to placebo in preventing hospitalisation and death through day 29 in patients with mild to moderate COVID-19? FINDINGS In the interim analysis, the Molnupiravir group had a lower risk of hospitalisation or death through day 29, 7.3% (28/385) compared to 14.1% (53/377) in the placebo group. There was a statistically significant treatment difference of 6.8%. However, the treatment difference was much lower in the full trial. In the full trial, the Molnupiravir group noted that 6.8% (48/709) of participants were hospitalised or died through day 29. The Placebo group noted that 9.7% (68/699) participants were hospitalised or died through day 29. There was a statistically significant treatment difference of 2.9% in favour of the intervention. AUTHORS' CONCLUSIONS In this trial, oral Molnupiravir was found to be effective for the treatment of COVID-19, without evident safety concerns, when initiated within 5 days after the onset of signs or symptoms in this population of non-hospitalised, unvaccinated adults who were at risk for progression to severe disease. JOURNAL CLUB THOUGHTS Some strengths of this study were that the primary outcome was both clinically relevant and patient-oriented. It was a double-blind, parallel-group, randomised, placebo-controlled trial that minimised bias. This was also an international study with enrolment at more than 100 sites in 20 countries which increased the external validity. However, the trial is markedly underpowered, and some benefits may be due to gender differences in the experimental and placebo groups. The primary outcome is a composite, and the two components (hospitalisation and death) do not have equal importance. An independent review board opted to stop the trial early for benefit, in the absence of predetermined stop criteria. It is also notable that vaccinated patients were excluded; this limits the generalisability of the results in a population where the vast majority is vaccinated. Finally, based on animal models, Molnupiravir may be teratogenic and is not recommended during pregnancy. Potential teratogenicity is a major issue and compliance with contraceptive methods may be difficult to attain particularly for men. PAPER 2: COMPARISON OF NEBULIZED KETAMINE AT THREE DIFFERENT DOSING REGIMENS FOR TREATING PAINFUL CONDITIONS IN THE EMERGENCY DEPARTMENT: A PROSPECTIVE, RANDOMIZED, DOUBLE-BLIND CLINICAL TRIAL READ IT HERE CLINICAL QUESTION: Which dose of nebulised ketamine is most effective for pain relief? FINDINGS This was a prospective, randomised, double-blinded trial comparing 3 doses of nebulised ketamine (0.75 mg/kg, 1 mg/ kg, and 1.5 mg/kg) administered through breath-actuated nebulisation to patients with moderate to severe acute and chronic pain in an adult emergency department. The primary outcome was the difference in pain scores on an 11-point numeric rating scale at 30 minutes in each group. 120 subjects (40 per group) were enrolled. All doses demonstrated clinically significant pain reduction. However, there was no additional benefit to higher doses of ketamine. To add context to the chosen secondary outcomes (adverse events and need for rescue analgesia), the authors compared their results to previous studies done on IV ketamine and morphine. Clinical pain reductions were on par with the degree of pain relief seen with IV ketamine and morphine. AUTHORS' CONCLUSIONS The authors concluded that they found no difference between the 3 doses of ketamine administered through breath-actuated nebuliser for short term treatment of moderate to severe pain in the emergency department. JOURNAL CLUB THOUGHTS It is always useful to have another option when it comes to analgesia in the ED. However, in terms of generalisability, access to breath actuated nebulised ketamine devices is limited. The study had numerous limitations including convenience sampling and a small sample size. In addition, the authors did not provide a breakdown of the conditions being treated while analgesia was provided. Finally, it would have been interesting to see this study done in a paediatric population, as the non-invasive aspect of treatment is especially appealing. Paper 3: Risk for Recurrent Venous Thromboembolism in Patients With Subsegmental Pulmonary Embolism Managed Without Anticoagulation Read it here CLINICAL QUESTION: Are patients with subsegmental pulmonary embolism (SSPE) at low risk for recurrent venous thromboembolism (VTE) and need clinical surveillance, or is anticoagulation indicated? FINDINGS In the study, patients with isolated subsegmental PE but no DVT on ultrasound were managed without anticoagulation. The primary outcome was recurrent VTE during 90-day follow-up which occurred in 8 patients with a cumulative incidence of 3.1%. Study recruitment ended early because the predefined stopping rule was met when 292 of the projected 300 patients were enrolled. Overall, 266 patients were included in the study. Other notable results were that patients with multiple isolated SSPE had a higher incidence of recurrent VTE compared to those with single isolated SSPE (5.7% vs 2.1%, respectively), and patients over 65 years of age had a higher rate of recurrent VTE compared to those 65 years or under (5.5% vs 1.8%). In total, 4 patients had recurrent proximal PE and 4 patients had DVT. No patients had a fatal recurrent PE. AUTHORS' CONCLUSIONS Patients with isolated single or multiple SSPE, who did not have proximal DVT, had higher than expected rates of recurrent VTE. This has implications for the treatment of these patients with anticoagulation in clinical practice. JOURNAL CLUB THOUGHTS Despite the small numbers included in this study, the results would make you think twice before skipping anticoagulation in the management of patients with isolated single or multiple SSPE. This study addressed a clinically important question and adds to the existing research which has been retrospective until this point. The background rates of SSPEs in the community are unknown, and with more and more CTPAs being performed, there are increased rates of SSPEs being diagnosed of questionable clinical significance. The subgroup analysis, which is to be interpreted with caution, suggests that the rate of recurrent VTE may be greater in older versus younger patients and in those with multiple versus single isolated SSPE. These factors, if present, could assist when considering anticoagulation. Guidelines from the American College of Chest Physicians suggest clinical surveillance over anticoagulation in a select group of patients with SSPE but there is only low-level evidence to guide this recommendation. The opinion at the journal club swayed towards anticoagulating this patient group and involving our haem/thrombosis colleagues in the discussion. PAPER 4: SARS-COV-2 RAPID ANTIGEN TESTING IN THE HEALTHCARE SECTOR: A CLINICAL PREDICTION MODEL FOR IDENTIFYING FALSE NEGATIVE RESULTS READ IT HERE CLINICAL QUESTION: What parameters can be used to identify false-negative rapid antigen tests, and could these facilitate the development of a clinical prediction model? FINDINGS In this multicentre trial, patients with documented paired results of rapid antigen tests (RAT) and RT-PCR were retrospectively analysed in respect to clinical findings. Variables included demographics, laboratory values, and specific symptoms. Three different models were evaluated using Bayesian logistic regression. The initial dataset included 4,076 patients. Overall, the sensitivity and specificity of RAT was 62.3% and 97.6%, respectively. 2,997 cases with negative RAT results (false negative (FN): 120; true negative: 2,877) were evaluated further. The best-performing model for predicting FN RAT results containing 10 variables yielded an area under the curve of 0.971. The most important variables for model performance with respect to Bayesian factor were leucocyte count, fever, respiratory rate, dyspnoea, and musculoskeletal symptoms. AUTHORS' CONCLUSION FN RAT results can be accurately identified through ten routinely available variables. In addition to RAT testing in the clinical setting, implementation of a prediction model can provide useful information to guide decision making when initiating appropriate hygiene measures and therefore helps avoiding nosocomial infections. JOURNAL CLUB THOUGHTS The rapidly changing face of COVID and the development of new variants means that the utility of these results may shortly expire. The study predates the evolution of the omicron variant which, at the time of writing, is the predominant variant and, as such, questions the effectiveness of the proposed model. There were a few issues with the methodology including the data being collected retrospectively which limits data quality, especially regarding symptom assessment. There was also a significant number of missing values and data in the final results. Additionally, the reference standard of PCR testing isn't itself 100% sensitive. REFERENCES 1. Bernal AJ, Silva MMG da, Musungaie DB, Kovalchuk E, Gonzalez A, Reyes VD, et al. Molnupiravir for Oral Treatment of Covid-19 in Nonhospitalized Patients. New Engl J Med. 2021;386(6):509–20. 2. Dove D, Fassassi C, Davis A, Drapkin J, Butt M, Hossain R, et al. Comparison of Nebulized Ketamine at Three Different Dosing Regimens for Treating Painful Conditions in the Emergency Department: A Prospective, Randomized, Double-Blind Clinical Trial. Ann Emerg Med. 2021;78(6):779–87. 3. Gal GL, Kovacs MJ, Bertoletti L, Couturaud F, Dennie C, Hirsch AM, et al. Risk for Recurrent Venous Thromboembolism in Patients With Subsegmental Pulmonary Embolism Managed Without Anticoagulation: A Multicenter Prospective Cohort Study. Ann Intern Med. 2022;175(1):29–35. 4. Leiner J, Pellissier V, Nitsche A, König S, Hohenstein S, Nachtigall I, et al. SARS-CoV-2 rapid antigen testing in the healthcare sector: A clinical prediction model for identifying false negative results. Int J Infect Dis. 2021;112:117–23.

Journal Club Podcast for March 2022 Dr Bertha Wu Prof Peter Cameron Dr Myles Sri Ganeshan Editor: Dr David McCreary Welcome to this month’s journal club podcast. We are joined by Professor Peter Cameron, Academic Director for the Alfred Emergency and Trauma Centre, and Dr Myles Ganeshan, Alfred Research Fellow. This month we reviewed three papers, covering a range of topics that are finally, not COVID related! The first paper we reviewed looked at the effect of early intra-arrest transport and extracorporeal cardiopulmonary resuscitation on functional neurological outcome in refractory out of hospital cardiac arrests. This was a single centre, randomized control trial published in JAMA just last month in February 2022 by Belohlavek et al. The second paper we reviewed looked at whether delivering low-intensity mental health outreach programs online prevents self-harm in adult outpatients who have suicidal ideation. It was also published in JAMA in February 2022 by Simon GE et al. Yes it’s a bit of a left-field study to cover in our journal club! But was an interesting read. The last paper we reviewed looked at the effect of using bougie versus endotracheal tube with stylet on first pass successful tracheal intubation. It was published in JAMA in December 2021 by Driver BE et al. PAPER 1: EFFECT OF INTRA-ARREST TRANSPORT, EXTRACORPOREAL CARDIOPULMONARY RESUSCITATION, AND IMMEDIATE INVASIVE ASSESSMENT AND TREATMENT ON FUNCTIONAL NEUROLOGICAL OUTCOME IN REFRACTORY OUT-OF-HOSPITAL CARDIAC ARREST READ IT HERE CLINICAL QUESTION: In patients with witnessed refractory out-of-hospital cardiac arrest, does early intra-arrest transport, ECPR and invasive assessment and treatment improve outcomes compared with standard resuscitation? DESIGN Single centre, randomized clinical trial in Prague over 8 years – March 2013- October 2020. POPULATION Adults aged 18-25yrs receiving ongoing resus for witnessed OHCA of presumed cardiac etiology + received a minimum of 5 min of ACLS without ROSC + ECPR team was available at cardiac centre. Planned sample size 285 → 256 participants enrolled. INTERVENTION Invasive strategy group (n=124) – mechanical compression initiated followed by intra-arrest transport to a cardiac centre for ECPR and immediate invasive assessment and treatment. COMPARISON Regular advanced cardiac life support continued on-site in the standard strategy group (n=132). OUTCOMES Participants were observed until death or day 180. Primary outcome: survival with a good neurological outcome (using Cerebral Performance Scale CPC  - defined as CPC 1-2 at 180 days Secondary outcomes: neurological recovery at 30 days – no need for pharmacological or mechanical cardiac support for at least 24 hours FINDINGS 256 patients were enrolled with all participants completing the trial. 31.5% in the invasive strategy group and 22% in the standard strategy group surviving to 180 days with good neurologic outcome. The difference of 9.5% was not found to be significant with p value of 0.09. At 30 days, neurologic recovery had occurred in 30.6% in the invasive strategy group, and in 18.2% in the standard strategy group; a statistically significant difference of 12.4% (p 0.02). Cardiac recovery had occurred in 43.5% and 34.1% respectively; again not a significant difference. Bleeding occurred more frequently in the invasive strategy group, occurring in 31% of the invasive strategy group vs 15% of the standard strategy group. AUTHORS' CONCLUSIONS Among patients with refractory OHCA, the bundle of early intra-arrest transport, ECPR, and invasive assessment and treatment did not significantly improve survival with neurologically favourable outcome at 180 days compared with standard resuscitation. However, they also concluded that the trial was possibly underpowered to detect a clinically relevant difference. JOURNAL THOUGHTS CLUB Previous studies like the ARREST study have shown that ECPR does improve survival. It was unfortunate that this study was underpowered to find a statistically significant difference in survival and neurologic outcome between the study groups. The power calculation required a 15% absolute difference between the groups – this is a big number to achieve with any intervention! Other factors like the crossover from intervention group to standard group having all survived, and having more patients with VF in the standard group vs more with asystole in the study group could have potentially confounded and skewed the data in favour of the standard group. BOTTOM LINE This paper will unlikely change our practice of offering ECPR to eligible patients at the Alfred. PAPER 2: EFFECT OF OFFERING CARE MANAGEMENT OR ONLINE DIALECTICAL BEHAVIOUR THERAPY SKILLS TRAINING VS USUAL CARE ON SELF-HARM AMONG ADULT OUTPATIENTS WITH SUICIDAL IDEATION READ IT HERE CLINICAL QUESTION: Can low-intensity outreach programs, based on effective clinical interventions but delivered primarily online, prevent self-harm or suicidal behaviour among outpatients reporting frequent suicidal ideation? DESIGN Pragmatic randomized clinical trial conducted at 4 US integrated health systems conducted from March 2015 to September 2018 POPULATION Included outpatients reporting frequent suicidal thoughts identified using routine Patient Health Questionnaire depression screening at the 4 US integrated health systems. Total of 18,882 patients were randomized over the course of 3 years when the trial was conducted. INTERVENTION Care management intervention (n=6230) that included systematic outreach and care Skills training intervention (n=6227) which introduced 4 dialectical behaviour therapy skills (mindfulness, mindfulness or current emotion, opposite action, paced breathing) Interventions were delivered Intervention up to 12mo, primarily through EMR online messaging to supplement ongoing mental health care. COMPARISON Usual care (n=6187) OUTCOMES Primary outcome: Time to first nonfatal or fatal self-harm; with non-fatal self-harm ascertained from health system records, and fatal self-harm ascertained from state mortality data. Secondary outcome: included more severe self-harm (leading to death or hospitalization) and broader definition of self-harm (selected injuries and poisonings not originally coded as self-harm). FINDINGS Of the 18,644 patients recruited, only 31% of participants offered care management and 39% of those offered skills training actively engaged in intervention programs. Over the 18 months following randomization, a total of 540 participants had a self-harm event, with 45 deaths attributed to self-harm and 495 to non-fatal self-harm events. These self-harm events were contributed by 3.27% in care management and 3.92% in skills training and 3.27% in usual care. Therefore the risk of fatal or non-fatal self-harm over 18 months was found not to differ significantly between the care management and usual care groups. However, the risk was significantly higher in the skills training group than in usual care. AUTHORS' CONCLUSIONS Among adults with frequent suicidal ideation, offering care management did not significantly reduce the risk of self-harm, and offering brief DBT skills training significantly increased the risk of self-harm compared with usual care. These findings do not support the implementation of the programs tested in this study. JOURNAL CLUB THOUGHTS This was a well-designed study in an area where research is scarce. In the COVID era where many things including healthcare are becoming virtual, this study does ask an important question of whether providing mental health care online works. The paper shows that it’s not a good idea, at least for the study population amongst patients with significant disorders of self. This group of patients rely on the human connection to heal – virtual medicine is more impersonal than face-to-face care and likely did not provide the human connection that they needed. This may explain why there was low engagement by participants in both groups. Furthermore, the short-term skills training provided in the study didn’t provide the full course of evidenced-based dialectical behavioural therapy. This probably explains why the skills training group in fact did worse in the study! BOTTOM LINE The study population poorly represents the patient population that presents to our ED. The study will not change our current practice. PAPER 3: EFFECT OF USE OF A BOUGIE VS ENDOTRACHEAL TUBE WITH STYLET ON SUCCESSFUL INTUBATION ON THE FIRST ATTEMPT AMONGST CRITICALLY ILL PATIENTS UNDERGOING TRACHEAL INTUBATION READ IT HERE CLINICAL QUESTION: In critically ill adult patients undergoing tracheal intubation, does the use of a tracheal tube introducer (“bougie”) increase the incidence of successful intubation on the first attempt, compared with the use of an endotracheal tube with stylet? DESIGN Multicentre, unblinded, pragmatic randomized clinical trial performed between April 2019 and February 2021. POPULATION 1102 critically ill adults undergoing tracheal intubation with sedation and standard geometry blades in 7 Emergency Departments and 8 Intensive Care Units in the US. INTERVENTION Use of a bougie (n = 556) ComparisonUse of endotracheal tube with stylet (n=546). OUTCOMES Primary outcome: single insertion of a laryngoscopy blade into the mouth and either a single insertion of a bougie followed by a single insertion of an ETT into the mouth or a single insertion of an ETT with stylet into the mouth. Secondary outcome: incidence of severe hypoxaemia (defined as sats < 80%) during the interval between induction and 2 minutes post tracheal intubation. FINDINGS Successful intubation on the first attempt occurred in 80.4% in the bougie group and in 83% in the stylet group; risk difference -26% <95%ci -73 - 2.2; p value 0.27>. Therefore, successful intubation on the first attempt did not significantly differ between groups. This finding did not change when adjusted analysis and multiple sensitivity analysis, including one defining successful intubation on the first attempt based only on the number of laryngoscope insertions, was performed. These analyses also showed that the odds of successful intubation on the first attempt did not differ significantly between any of the subgroups, including among more experienced operators, patients with difficult airway characteristics, or when video laryngoscopy was used. For the secondary outcomes, 11% in the bougie group vs 8.8% in the stylet group experienced severe hypoxaemia. Esophageal intubation, pneumothorax and injury to oral, glottic or thoracic structures had a low incidence in both study groups. AUTHORS' CONCLUSION Among critically ill adults undergoing tracheal intubation, use of a bougie did not significantly increase the incidence of successful intubation on the first attempt compared with use of an endotracheal tube with stylet. JOURNAL CLUB THOUGHTS This study showed around 80% first-pass success rates in both groups. This is much lower than what we generally expect to see in an ED population. The BEAM trial published in 2018 showed a first-pass success rate of 98% when a bougie was used – this is the number we expect and should aim for. The low success rate in the study is probably due to how they defined a successful first attempt. Previous studies have defined this as when the laryngoscope gets taken out of the mouth. In this study, it was defined as a single insertion of a laryngoscope blade into the mouth, and either a single insertion of a bougie followed by a single insertion of an ETT, or a single insertion of an ETT with stylet into the mouth. The operators in this study had a wide range of experience – from resident physicians who never performed an ETT to attending physicians with thousands of prior intubations. The study showed that overall the use of a bougie did not significantly increase the incidence of first-pass intubation success.  With effect modification analysis, this study also showed that the use of a bougie will unlikely increase the rate of successful intubation on the first attempt for operators who had performed a greater number of intubations, and those who commonly use ETT with a stylet. BOTTOM LINE Train and get comfortable with both methods. This has the best chance of getting you out of trouble when you encounter a difficult airway as there is no one-size-fits-all approach to the airway and it's good to have more options in your armamentarium. REFERENCES Belohlavek J, Smalcova J, Rob D, Franek O, Smid O, Pokorna M, et al. Effect of Intra-arrest Transport, Extracorporeal Cardiopulmonary Resuscitation, and Immediate Invasive Assessment and Treatment on Functional Neurologic Outcome in Refractory Out-of-Hospital Cardiac Arrest. Jama. 2022;327(8):737–47. Simon GE, Shortreed SM, Rossom RC, Beck A, Clarke GN, Whiteside U, et al. Effect of Offering Care Management or Online Dialectical Behavior Therapy Skills Training vs Usual Care on Self-harm Among Adult Outpatients With Suicidal Ideation. Jama. 2022;327(7):630–8. Driver BE, Semler MW, Self WH, Ginde AA, Trent SA, Gandotra S, et al. Effect of Use of a Bougie vs Endotracheal Tube With Stylet on Successful Intubation on the First Attempt Among Critically Ill Patients Undergoing Tracheal Intubation. Jama. 2021;326(24):2488–97. DR BERTHA WU Emergency Registrar MBBS, CCPU (eFAST, AAA, BELS). Emergency Medicine Advanced Trainee and Intensive Care Medicine Trainee in Melbourne, Australia. Particular interests in POCUS, medical education and health care in resource-poor settings. Twitter: @berthawu29

Dr Luke Phillips Emergency Physician Peer review: Dr Binula WickramarAchchi Welcome to Fast Fridays – a case-based, rapid review of a topic. The cases have been adapted from real patients but have been changed for anonymity and to emphasise key learning points. THE CASE An 80-year-old patient presents with an intentional overdose of Amlodipine. They state that they have taken 70 x 10mg tablets of Amlodipine (standard release) about 3 hours ago in an attempt to end their life. The patient’s family called the ambulance after a distressed phone call. On arrival to the ED the patient’s Blood Pressure is 75/40mmHg, Heart rate 66 and Oxygen Saturation 99% on room air; they are maintaining their own airway and have a GCS of 15. The patient is on regular Amlodipine for hypertension and does not take any other medications. This is a complex and massive overdose, and they are already showing signs of acute poisoning. A useful approach I like to use for managing toxicology cases in the ED (and when thinking about answering fellowship questions) can be summarised by the mnemonic Resus-RSI-Dead. WHAT ARE OUR INITIAL RESUSITATIO N PRIORITIES? We primarily have a circulation problem here. In the case of this patient: They should be managed in a resuscitation bay and attached to cardiac monitoring. 2 large-bore, 16-18G peripheral cannula should be sited with an early upgrade to central access. Initial fluid bolus 1-2L of normal saline. Placement of an arterial line for close invasive BP monitoring. Early initiation of inotropes: either initial Metaraminol boluses or begin a Noradrenaline infusion. Aim for SBP > 90mmHg of MAP > 60. Toxicology bloods including venous gas and paracetamol level should be sent. Of particular interest on the blood case will be the ionised calcium level. An ECG should be requested early in the management although I am not expecting many changes with this overdose. In this case a new first degree heart block was noted. An early phone call to a toxicology service and review of local toxicology guidelines should be made. WHAT IS YOUR RISK ASSESSMENT FOR THIS PATIENT? Agent: Amlodipine (standard release). Note that Sustained Release formulations have a slower onset of toxicity and may need to prolonged periods of observation/delayed onset. There were no co-ingestants. ☝️ Primary Pearl: Amlodipine is a dihydropyridine calcium channel blocker (same family as nifedipine, felodipine, lercanidipine) that inhibits the calcium influx through slow channels in peripheral vascular and coronary smooth muscle cells causing vasodilation in peripheral and coronary vascular beds. It has minimal effect on cardiac contractility or conduction delays when compared with verapamil/diltiazem. It is highly protein bound with high bioavailability and is metabolised primarily by the liver and eliminated renally. Dosage: 700mg – This is a massive ingestion! We are expecting a challenging resus here. Timing of Ingestion: The patient’s reported ingestion was 3 hours ago. Given how rapidly absorbed amlodipine is we already expect the drug to be at peak levels. Current Clinical Status: The patient is already demonstrating signs of severe toxicity – we are expecting severe refractory vasoplegia. In addition, there may be metabolic abnormalities such as a metabolic lactic acidosis likely due to poor perfusion. Patients may also have nausea and vomiting and may develop an ileus. Patient Factors: It is important to consider underlying co-morbidities especially cardiac disease. Co-ingestion of other cardiac agents may worsen symptom and make treatment more difficult – ACE inhibitors and Angiotensin Receptor Blockers co-ingestion can cause profound vasoplegia. WHAT ARE SOME SPECIFIC TREATMENT OPTIONS THAT CAN BE GIVEN TO THIS PATIENT? After consulting with our state-wide toxicology service and toxicology guidelines, the following treatments were suggested: Calcium gluconate 30 mL (3 grams, 6.6 mmol) bolus IV over 5-15 minutes +/- repeat boluses or infusion to achieve an ionised calcium level >1.5-2 Early commencement of a noradrenaline infusion with addition of vasopressin if rapidly increasing noradrenaline requirements High-dose insulin, euglycemic therapy (HIET) if poor contractility on a bedside echo (note that this may worsen vasodilation) WHAT ARE SOME OPTIONS FOR DECONTAMINATION/ENHANCED ELIMINATION? 50g of activated charcoal should be considered especially if ingestion < 2 hours prior or if the ingestion is an extended-release formulation. Whole bowel irrigation is an option, but this should be discussed with your Toxicology service. THE OUTCOME After the initial resuscitation as outlined above a central line was placed as our noradrenaline requirements rapidly increased. The patient demonstrated relatively good contractility on point of care echo and a vasopressin infusion was commenced. Calcium boluses were administered, and once central access was obtained an infusion was commenced. The patient was transferred to intensive care for ongoing management. REFERENCES AND FURTHER READING: Austin Toxicology Guidelines Life in the Fast Lane – Approach to Acute Poisoning LUKE PHILLIPS Emergency Physician Dr Luke Phillips is an Emergency Physician at Alfred Health in Melbourne and currently the Co-Director of Emergency Medicine Training. He is a passionate educator and has been fortunate enough to be able to combine this with his love of emergency ultrasound. Luke has a special interest in the use of focused ultrasound for critically unwell patients, in trauma management and in the use of ultrasound to guide procedures and improve patient safety in the ED. He is currently the Co-Chair of the Emergency Medicine Ultrasound Group (EMUGS.org) Board of Directors and holds a number of CCPU units through ASUM. Luke is also involved in the department’s international education program and has developed a Certificate of Emergency Medicine which is currently being run in both Germany and India. He also has interests in human factors, debriefing (particularly after clinical events), and simulation. His Twitter handle is @lukemphillips.

Dr Luke Phillips Emergency Physician Peer review: Dr David McCreary WELCOME TO FAST FRIDAYS – A CASE-BASED, RAPID REVIEW OF A TOPIC. THE CASES HAVE BEEN ADAPTED FROM REAL PATIENTS BUT HAVE BEEN CHANGED FOR ANONYMITY AND TO EMPHASISE KEY LEARNING POINTS. THE CASE A 18-year-old male has been brought to your rural Emergency Department suffering a mixture of mid-deep dermal burns to his face, left arm and thorax and full thickness burns to his right arm. He was lighting a campfire and poured petrol onto the fire which resulted in his burns. The paramedics report initial first aid was given at the scene. You estimate the extent of the burns to be around 35% Total Body Surface Area (TBSA). This was an isolated injury, and no other trauma was reported. There were no circumferential burns. His initial vital signs are Glasgow Coma Scale 15, Blood Pressure 150/80, Heart Rate 130, Oxygen Saturations 98% (Room Air). His estimated weight is 80kg The Alfred is a major burns centre, we receive all the adult major burns in the state; how the patient is initially assessed, resuscitated and then packaged for transfer is important in their ongoing care. This post highlights some of the key concepts that apply both at our centre but also in a non-burns centre. With the upcoming Easter Holidays (think camping trips and campfires 🏕), I thought it would be timely to remind ourselves of the key aspects of managing this patient group. ☝️ Practice Pearl: Get an APP to help you estimate TBSA. A great examples can be found on the Trauma VIC app (iPhone/Android) WHAT ARE THE KEY PRINCIPLES IN MANAGING THIS PATIENT WITH SEVERE BURNS? 1. RESUSCITATION On reception of a burns patient a systematic assessment using an A-E approach should be used with interventions as necessary. Look specifically for signs of airway burns such as hoarse voice, stridor, harsh cough, facial burns (especially mouth/lips/nose) + singed hairs, inflamed oropharynx, coughing up carbonaceous sputum and soot in mouth/oropharynx. You should also exclude associated trauma as required and if all is ok then move on to managing the burns. 2. ANALGESIA Burns are bloody painful, particularly if they are mid-deep dermal where all those nociceptors are located. Give your patient some form of intravenous opioid medication (Morphine 5-10mg q5min or Fentanyl 50-100mcg q5min). He is 18-years-old so please don’t mess about with paediatric doses and give a decent dose. You could also consider Ketamine (10-20mg IV boluses) as an adjunct and potentially commence an infusion if there are high opioid requirements.  Don’t forget your multi-modal analgesia, so load them up on paracetamol 1g QID and ibuprofen 400mg TDS. 3. FLUID MANAGEMENT A large TBSA burn (>20% in adults) means you have lost the skin barrier; these patients loose fluids via third spacing caused by capillary leak. Commence fluid resuscitation early using the modified Parkland formula: 3-4ml x TBSA% x Wt (kg) In this case, we calculated 8.4 – 11.2L. My preference is to use Hartmann’s Solution, giving 50% (4.2-5.6L) in the first 8 hours and the remainder over the next 16 hours. Physiological targets are important to monitor and in this case I would aim for normotension or a MAP >60-65mmHg, urine output > 0.5ml-1ml/kg/hr, monitor the lactate and base excess and examine the patient for signs of worsening perfusion. ☝️Practice Pearl: A rising lactate or persistent lactate > 10 along with a metabolic acidosis can be a sign of cyanide toxicity a common byproduct of burning all the plastic crap we have in our houses. If in doubt treat for this. 4. TEMPERATURE MANAGEMENT That pesky skin again – apparently losing your skin leads to problems controlling temperature. Remember to keep your patient warm and aim for normothermia. Monitor temperature centrally (IDUC catheters are ideal for this) and use warmed fluids, blankets or Bair Huggers to prevent heat loss. Don’t forget to change all those soaked sheets from the leaky capillaries too. 5. WOUND MANAGEMENT We don’t need anything fancy here. Once the patient arrives at a burns centre, we can sort this out. If contaminated, please do your best to clean the burns then after your assessment cover them in either cling film or impregnated gauze/crepe bandages. Application of dressings can help with decreasing fluid losses and pain and improving thermoregulation. You should also administer ADT (if required) and if grossly contaminated burns, then consider IV antibiotics (Antibiotics should not be given routinely). ☝️Practice Pearl: Don’t apply your cling film circumferentially or too tight as you can cause an iatrogenic compartment syndrome. Apply loosely and if able longitudinally. 6. TRANSFER Early referral to your nearest trauma centre is important for both operative management of the burns and ICU supports for large TBSA burns. Contact your local retrieval service to help coordinate this. THE OUTCOME The key principles of management were applied to this patient, and they were retrieved to a major burns centre where, after their initial reception in ED, they were transferred to ICU for ongoing supportive care. The patient underwent extensive skin grafting before being discharged to a community rehabilitation centre. REFERENCES AND FURTHER READING: Trauma Victoria – Burns Guidelines VicBurns Website – Burns Management Guidelines ACI NSW: Clinical Guideline - Escharotomy for Burns Patients ALFRED EMERGENCY EDUCATION - THE PROCEDURES COURSE The Procedures Course from Alfred Emergency Education is a cadaver based practical course where you can learn how to perform several emergent procedures including how to perform a burns escharotomy. This excellent podcast from Dr Mike Noonan discusses key principles of Escharotomy. LUKE PHILLIPS Emergency Physician Dr Luke Phillips is an Emergency Physician at Alfred Health in Melbourne and currently the Co-Director of Emergency Medicine Training. He is a passionate educator and has been fortunate enough to be able to combine this with his love of emergency ultrasound. Luke has a special interest in the use of focused ultrasound for critically unwell patients, in trauma management and in the use of ultrasound to guide procedures and improve patient safety in the ED. He is currently the Co-Chair of the Emergency Medicine Ultrasound Group (EMUGS.org) Board of Directors and holds a number of CCPU units through ASUM. Luke is also involved in the department’s international education program and has developed a Certificate of Emergency Medicine which is currently being run in both Germany and India. He also has interests in human factors, debriefing (particularly after clinical events), and simulation. His Twitter handle is @lukemphillips.

Dr Dave McCreary Emergency Physician Peer review: Dr Stephen Gilmartin Welcome to Fast Fridays – a case-based, rapid review of a topic. The cases have been adapted from real patients but have been changed for anonymity and to emphasise key learning points. A 60-year-old gentleman presents for assessment of a 2-week history of a swollen, erythematous left foot. His GP has been treating him for cellulitis with oral flucloxacillin, which has offered no improvement. He has a previous medical history of poorly-controlled type two diabetes with associated nephropathy and peripheral neuropathy. On assessment, he is afebrile, with normal observations and walked unaided from the waiting room for his assessment. The patient’s left foot is swollen compared to the right, is warm to touch, has no tracking redness, no skin breaches and looks like this: Image courtesy of the BMJ(1) WHAT ARE YOUR DIFFERENTIALS FOR THIS PRESENTATION? Non-resolving cellulitis Foreign body Osteomyelitis Charcot foot Gout DVT The following X-ray was taken: WHAT IS YOUR INTERPRETATION OF THIS X-RAY? The X-ray was interpreted in the department and formally reported as normal. WHAT WOULD YOUR DISPOSITION BE FOR THIS PATIENT? As the patient reported that the erythema was improving, he was discharged to continue the flucloxacillin his GP has prescribed and follow up with his podiatrist. 🥱 THAT’S NOT A VERY BLOGGABLE CASE, DAVE… One week later, the patient was referred back to the orthopaedic team by his podiatrist with the following X-ray: CLEARLY NO LONGER 'NORMAL'; WHAT'S YOUR INTERPRETATION OF THE X-RAY THIS TIME? “Homolateral Lisfranc’s dislocation. Widening of the joint spaces between the cuneiforms and also the cuneiform-cuboid articulation, with medial subluxation of the medial cuneiform, lateral subluxation of the lateral cuneiform.” SO, WHAT'S THE DIAGNOSIS? This was Charcot foot all along. WHAT IS CHARCOT FOOT? A non-infectious destruction of bone and joint associated with neuropathy and characterised by inflammation in the earliest phase. It was classically described by Jean-Martin Charcot (Off-of all things Charcot – he really did love to stick his name on things) in 1883. It can be caused by any condition resulting in loss of protective sensory innervation or autonomic neuropathy. Think diabetes, alcohol, spinal injury etc. WHAT'S THE PATHOPHYSIOLOGY? Neurovascular theory: Nerve damage → increased local vascularity → osteoclastic activation → osteopenia, fractures, deformity Neurotraumatic theory: Microtrauma to insensate joints → progressive bony destruction → repeated partial healing & activation of pro-inflammatory junk cytokines → increased vascularity → osteoclasts again as above They reckon hyperglycaemia makes it worse too (increased advanced glycosylation end products, if you’re interested), so it’s more common in poorly controlled diabetics. STAGES 0. Inflammatory (as in this case) Bit of warmth, swelling, redness ± pain Radiographically normal MRI helpful 1.Developmental Joint and bone destruction Joint unstable 2. Coalescence Destructive phase slows, healing starts 3. Remodelling Bones and joints healed Residual instability and deformity may occur HOW IS IT DIAGNOSED? It's largely about pattern recognition (as with so many things in medicine). Think of it in any Diabetic patient presenting with swelling, redness and (sometimes) pain in the foot and ankle of short duration (within 4-6 weeks of symptoms)(2). Bloods? Probably not helpful in the early stages as can be normal, but they can help include or exclude the differentials Imaging? The cruncher for this case. Plain films are often normal in the early stage and should not exclude Charcot foot MRI is the best option for detection of subtle, early changes and also has great sensitivity and specificity for osteomyelitis CT is better than plain film for osteomyelitis, but not reliable in early disease HOW IS IT MANAGED? Any suspected Charcot foot should be made immediately Non-Weight-Bearing and referred to orthotics for a Total Contact Cast (TCC). Off-loading can arrest disease progression by disrupting the inflammatory cycles mentioned above In the meantime, they can have a double tubigrip for swelling and pain. Urgent outpatient referral to podiatry, orthotics, and endocrinology to get their diabetes in order. 🔭 THE RETROSPECTOSCOPE – WAS THAT FIRST X-RAY REALLY NORMAL? 🔭 Let’s look at the AP view and, as I often like to do, let’s see what my Orthoflow App would say… Images courtesy of Orthoflow When assessing for midfoot injury we look (amongst other things) for disruption of the 1st metatarsal-medial cuneiform line, then for disruption of the 2nd metatarsal-middle cuneiform line. Disruption of these lines suggests disruption of the Lisfranc ligament. I would suggest there is definitely a disruption in both of those lines in this case. If you were in any doubt, weight-bearing views may help or imaging of the unaffected foot will provide comparison. 🤓 LEARNING POINTS 🤓 Not all reddness is cellulitis. Consider an exclude alternative diagnoses. Keep a high index of suspicion for Charcot foot in patients with peripheral neuropathy and diabetes in particular. Plain films aren't helpful in the early stages of Charcot foot. If it's at all a possibility, treat as Charcot foot, NWB the patient, consider advanced imaging and seek a podiatry/orthopaedic opinion. REFERENCES AND FUTURE READING Baglioni P, Malik M, Okosieme OE. Acute Charcot foot. Bmj. 2012;344(mar14 1):e1397. Doi: 1136/bmj.e1397 Yousaf S, Dawe EJC, Saleh A, Gill IR, Wee A. The acute Charcot foot in diabetics. EFORT Open Rev. 2018;3(10):568–73. Doi: 1302/2058-5241.3.180003 DAVE MCCREARY Emergency Physician Dave is an Emergency Physician and project lead for our FOAMed content. He completed training between the UK and Australia and completed an MSc in Trauma Science with QMUL. His clinical interests include trauma, critical care, orthopaedics, evidence-based medicine and human factors. Dave is a regular contributor the RCEMLearning podcast with a regular evidence-based medicine segment “New in EM” and is a FOAMed editor for RCEMLearning. He dislikes coriander, decaf coffee (“really, what’s the point?”) and dermatology.

Journal Club Podcast April 2022 Dr Bertha Wu Prof Peter Cameron Dr Divya Karna Editor: Dr David McCreary WELCOME TO THIS MONTH’S JOURNAL CLUB PODCAST. WE ARE JOINED BY PROFESSOR PETER CAMERON, ACADEMIC DIRECTOR FOR THE ALFRED EMERGENCY AND TRAUMA CENTRE, AND DR DIVYA KARNA, EMERGENCY PHYSICIAN. This month we review 4 papers covering topics of pre-hospital resuscitation of trauma patients with blood products, pad positioning for cardioverting AF, large-bore vs pigtail intercostal catheter use for traumatic haemothorax, and whether pain scores impact the prediction of patient outcome by triage scores. PAPER 1: RESUSCITATION WITH BLOOD PRODUCTS IN PATIENTS WITH TRAUMA-RELATED HAEMORRHAGIC SHOCK RECEIVING PREHOSPITAL CARE (REPHILL): A MULTICENTRE, OPEN-LABEL, RANDOMIZED CONTROLLED, PHASE 3 TRIAL READ IT HERE CLINICAL QUESTION: Is prehospital administration of packed red cells and lyophilised plasm (LyoPlas) superior to 0.9% in resuscitating patients with trauma-related haemorrhagic shock? DESIGN Multicentre, open-label, parallel group, randomized controlled trial, with allocations concealed and primary outcome accessors blinded. The study was performed over 6 years from 2016-2021. POPULATION Inclusion: Adults (>16 years) Trauma-related haemorrhagic shock and hypotension (defined as SBP<90mmHg or absent palpable radial pulse) Exclusion: Patient had already been transfused blood products prior to assessment for eligibility Known refusal to receive blood products Pregnancy (known or apparent) Isolated head injury without evidence of haemorrhage Prisoners INTERVENTION Participants receive up to two units each of PRBC and LyoPlas COMPARISON Participants receive up to 4 x 250mL bags of 0.9% NaCl For both groups, the interventions were administered until either hospital arrival, a return of systolic BP to 90mmHg or more, or when a radial pulse was palpable. If BP decreased on the way to hospital, treatment was re-instigated. OUTCOMES Composite primary outcome: (powered for 10% difference) Episodic mortality OR Impaired lactate clearance (<20% in 2 hours) OR Both Secondary outcomes: Rates of transfusion related complication sin the first 24hrs after ED arrival Serious adverse events Treatment-related deaths FINDINGS Trial recruitment was stopped before it achieved the intended sample size of 490 participants due to disruption caused by the COVID pandemic Only 432 participants were assigned to the PRBC-LyoPlas (n=209) or to the 0.9% sodium chloride group (n=223) The composite primary outcome occurred in 128 (64%) of 199 participants randomly assigned to PRBC-LyoPLas and 136 (65%) of 210 randomly assigned to 0.9% sodium chloride  adjusted risk difference -0.025% with 95% CI -9.0 to 9.0, p = 0.996 Rates of transfusion related complication in first 24hrs after ED arrival were low and similar across treatment groups (PRBC-LyoPlas 11 (7%) of 148 vs 0.9% NaCl 9 (7%) of 137, adjusted relative risk 1.05 (95% CI 0.46-2.42) One rare serious adverse events in each treatment group (Cerebral infarct in PRBC-LyoPlas vs deranged LFTs 0.9% NaCl) No treatment-related deaths AUTHORS' CONCLUSIONS The study did not show that prehospital PRBC-LyoPlas resuscitation was superior to 0.9% NaCl for adult patients with trauma related haemorrhagic shock. JOURNAL CLUB THOUGHTS The study had a robust design and an important clinical question asked. It was disappointing that a positive outcome wasn’t found and it won’t add much to our current practice. The choice of including lactate clearance in the composite outcome was interesting… It’s not very relevant to clinical practice! Notably, death within 3 hours was 16% for the PRBC-LyoPlas group and 22% for the 0.9% NaCl group, correlating to a 6% difference. It leaves one to wonder if the study would have had a different finding if it was better powered and mortality was used as the primary outcome. However, average prehospital time for participants in the study was 20-30 minutes, so it’s possible that whether we resuscitate with blood products vs crystalloids in this patient cohort with a short prehospital transport time indeed does not make a difference. This is likely much more relevant for the patients from rural and remote areas where transport times to a major trauma centre can sometimes take a few hours. BOTTOM LINE Unfortunately, this study did not have any practice-changing findings, even though it set out to be a very promising trial. Further trials with improved study power and including patient cohorts with longer prehospital transport times would add to the clinical question asked. PAPER 2: ANTERIOR-LATERAL VERSUS ANTERIOR-POSTERIOR ELECTRODE POSITION FOR CARDIOVERTING ATRIAL FIBRILLATION READ IT HERE CLINICAL QUESTION: Is either anterior-lateral or anterior-posterior electrode position superior to the other for cardioverting Atrial Fibrillation? DESIGN Multicentre, open-label, randomized controlled trial POPULATION Inclusion criteria Adult patients (>18yo) with AF Scheduled for elective cardioversion Pts had received sufficient anticoagulation or a TTE documenting the absence of intracardiac thrombi Exclusion criteria Pt with arrhythmias other than AF Untreated hyperthyroidism Known or suspected pregnancy Those previously enrolled in the trial INTERVENTION Receiving cardioversion shocks using anterior-lateral electrode positioning Shocks were delivered until sinus rhythm was restored or up to max of 4 shocks – using escalating energy shocks of 100J, 150J, 200J, 360J COMPARISON Receiving cardioversion shocks using anterior-posterior electrode positioning OUTCOMES Primary outcome: The proportion of patients in sinus rhythm 1 minute after the first shock Secondary outcome: The proportion of patients in sinus rhythm 1 minute after final shock (up to 4 shocks) Cardioversion efficacy at discharge 2 hrs after cardioversion Safety outcomes: Number of pts with arrhythmic events (asystole, AV block, transient brady, ventricular Arrhythmia) Skin redness Patient-reported periprocedural pain FINDINGS Primary outcome (return to SR after first shock) Anterior-lateral: 54% | Anterior-posterior: 33% | 22% risk difference (95% CI 13-30, p < 0.001); corresponding to NNT 5. Secondary outcome Number of patients in sinus rhythm after final shock was 93% in anterior-lateral compared to 85% in anterior-posterior positioning. Risk difference 7% (95% CI, 2-12), corresponding to NNT 14 (95%, CI 8-50). Safety outcomes similar between treatment groups. AUTHORS' CONCLUSIONS Anterior-lateral electrode positioning resulted in significantly more patients obtaining SR when compared with Anterior-posterior electrode position for cardioverting AF. JOURNAL CLUB THOUGHTS The study finding was interesting, as the traditional teaching is that anterior-posterior electrode positioning is better than anterior-lateral positioning in cardioverting AF. Unfortunately, participants included in this study were not representative of the ED patient cohort as they were all elective patients booked for cardioversion in the outpatient setting. A study in the future including patients indicated for cardioversion in the emergency department would be useful. BOTTOM LINE The study finding changes how we think about electrode positioning in cardioverting AF. I may be more inclined to use anterior-lateral electrode positioning in the future, especially for the unstable patient who requires multiple people to do a log roll for posterior pad placement in a busy department. PAPER 3: THE SMALL (14 FR) PERCUTANEOUS CATHETER (P-CAT) VERSUS LARGE (28-32 FR) OPEN CHEST TUBE FOR TRAUMATIC HEMOTHORAX: A MULTICENTRE RANDOMIZED CLINICAL TRIAL READ IT HERE CLINICAL QUESTION: Are small (14 Fr) percutaneous catheters (P-CAT) non-inferior to large (28-32 Fr) open chest tubes in the treatment of traumatic hemothorax? DESIGN Multicentre RCT performed over 6yrs from 2015-2020 POPULATION Inclusion: 18yrs or older, and Traumatic haemothorax, or Haemopneumothorax requiring drainage Exclusion: Pt in extremis e.g. haemodynamic instability that required emergent tube placement Those who refused to participate INTERVENTION Small (14 Fr) percutaneous catheter (P-CAT) insertion COMPARISON Large (28-32Fr) open chest tube insertion OUTCOMES Primary outcome: Failure rate – defined as retained haemopneumothorax requiring a second intervention Secondary outcome: Daily drainage output Tube days Intensive care unit LOS Hospital LOS Insertion perception experience (IPE score) on a scale of 1-5 (1 tolerable, 5 worst experience) FINDINGS The study was cut short due to prolonged period of enrollment and interruption by COVID outbreak. After exclusion, 119 pts participated in the trial - 56 randomized to the P-CAT arm and 63 to the chest tube arm. Baseline characteristics between two groups were similar. The failure rate for P-CATs was 11% vs 13% for chest tubes  (p = 0.74). Secondary outcomes were similar between groups, except patients in the P-CAT arm reported lower insertion perception experience IPE scores (median 1 “tolerable experience”, IQR 1-2) vs chest tubes (median 3 “it was a bd experience”, IQR 2-5 p < 0.001). AUTHORS CONCLUSION Small caliber 14 Fr P-CATs are equally as effective as 28-32 Fr chest tubes in their ability to drain traumatic haemothorax with no difference in complications. JOURNAL CLUB THOUGHTS This study has many design flaws. Patients who were hemodynamically unstable were excluded from the study – this patient cohort constitutes most of those who we would usually insert a large bore chest tube for in ED. The authors created their own institutional score termed IPE scores which was subjective and not scientifically validated. They also didn’t standardize the dosage or type of analgesia used for tube insertion. There was also significant conflict of interest – the study was partially funded by Cook Medical LLC – the company that makes pigtails. BOTTOM LINE This is not a well-designed study, performed on a population that is not generalizable to the ED patient cohort. It will not change my practice. PAPER 4: IMPACT OF PAIN ASSESSMENT ON CANADIAN TRIAGE AND ACUITY SCALE PREDICTION OF PATIENT OUTCOMES READ IT HERE CLINICAL QUESTION: How does pain as a triage factor affect the ability of CTAS to predict patient acuity? DESIGN Single centre, retrospective observational cohort study performed in a tertiary ED POPULATION All adults aged >18yrs who visited the Jewish General Hospital ED over June 2017 – Jan 2022 All patient visits prior to COVID-19 pandemic were included Data post COVID-19 pandemic was not included as this substantially altered patient population and workflow INTERVENTION A modified “pain-free” CTAS algorithm used for each visit in the cohort, assuming that pt had not reported any pain. COMPARISON Using standard CTAS algorithm which combined patient-reported pain levels with other data to generate a triage score for each visit, The standard CTAS algorithm has a minimum level of acuity that must be assigned to a patient based on the severity, location and chronicity of pain. OUTCOMES Primary outcome: Acuity of patient, defined by 3 variables Admission ICU consultation In-hospital mortality within 72 hours on arrival to ED FINDINGS A sample of 229,744 patients were analysed. Distribution of standard CTAS scores showed that most visits were assigned to the mid range CTAS – 2 (22.5%), 3 (50%), 4 (21%). The study found that removing pain scale from CTAS algorithm can lower the acuity of a case compared to the standard CTAS, but can never increase it. Higher pain was slightly negatively correlated with hospital admission, ICU consultation, and 72-hour mortality (r = - 0.008, -0.009, -0.006 respectively). AUTHORS' CONCLUSIONS The removal of pain scale from CTAS did not reduce its ability to predict hospital admission, ICU consultation or the 72-hour mortality. But this did move a large number of patients to the less acute triage categories. JOURNAL CLUB THOUGHTS We all know that patients’ reported pain score do not always correlate with the severity of the underlying pathology that caused the pain. However, these patient groups do require early medical attention for pain management. We’re not sure what this study adds. BOTTOM LINE The study is somewhat irrelevant and there will be no change to current practice. REFERENCES Crombie N, Doughty HA, Bishop JRB, Desai A, Dixon EF, Hancox JM, et al. Resuscitation with blood products in patients with trauma-related haemorrhagic shock receiving prehospital care (RePHILL): a multicentre, open-label, randomised, controlled, phase 3 trial. Lancet Haematol. 2022; Schmidt AS, Lauridsen KG, Møller DS, Christensen PD, Dodt KK, Rickers H, et al. Anterior–Lateral Versus Anterior–Posterior Electrode Position for Cardioverting Atrial Fibrillation. Circulation. 2021;144(25):1995–2003. Kulvatunyou N, Bauman ZM, Edine SBZ, Moya M de, Krause C, Mukherjee K, et al. The small (14 Fr) percutaneous catheter (P-CAT) versus large (28–32 Fr) open chest tube for traumatic hemothorax: A multicenter randomized clinical trial. J Trauma Acute Care. 2021;91(5):809–13. Davis S, Ju C, Marchandise P, Diagne M, Grant L. Impact of Pain Assessment on Canadian Triage and Acuity Scale Prediction of Patient Outcomes. Ann Emerg Med. 2022;79(5):433–40.MBBS, CCPU (eFAST, AAA, BELS). Emergency Medicine Advanced Trainee and Intensive Care Medicine Trainee in Melbourne, Australia. Particular interests in POCUS, medical education and health care in resource-poor settings. Twitter: @berthawu29 DR BERTHA WU Emergency Registrar MBBS, CCPU (eFAST, AAA, BELS). Emergency Medicine Advanced Trainee and Intensive Care Medicine Trainee in Melbourne, Australia. Particular interests in POCUS, medical education and health care in resource-poor settings. Twitter: @berthawu29