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  • Toxic Epidermal Necrolysis

    Author: Dr Hector Thomson Editor: Dr Dave McCreary None of us got into emergency medicine because we love rashes. A wise FACEM once told me, “I only care if it doesn’t blanch, involves their mucous membranes, has massive vesicles or their skin is falling off.” I actually find this quite a nice list of red flags. Another way to think about this is a rash in a patient with: Systemic symptoms Fever or abnormal vital signs Intra-oral or mucous membrane lesions Blistering Bruising New medications There are just some rashes that you come across and go… what the $&@% is that? The Case At a recent MET call on the ward, I stumbled across a bloke in absolute misery. Having started Alopurinol for his gout a month prior he had come out in a rash a few days earlier. At his first ED visit, he was diagnosed with "urticaria, possibly allergic", and started on antihistamines and prednisolone. He had a slight cough so maybe a viral trigger. He had represented a few days later with it worsening. Now day 5, his whole body was covered. It looked like this with almost 90% erythroderma. Source: Thompson & Thompson Genetics in Medicine, 8th Edition He could barely swallow, his eyes were red and weeping and he was starting to having trouble passing urine. He was absolutely miserable and the MET call had been called for pain, despite enough opioids to put down an elephant in the last 4 hours. So, what is this? This is Toxic Epidermal Necrolysis (TEN). Wait, isn’t it called Steven Johnson Syndrome? Well, no… they are the same disease, on a spectrum. TENS is when the total body surface area is >30%. Source: Adapted from Fig 21.9 Bolognia and Bastuji-Garin S. et al. Arch Derm 129: 92, 1993 Pathophysiology The mechanism still isn’t fully understood but the result is a Type IV hypersensitivity reaction where cytotoxic lymphocytes apoptose kerinaocytes causing blistering, bullae formation and sloughing of detached skin. This results in full-thickness epidermal necrosis which can be confirmed on skin biopsy. Source: Wikipedia 🚨Primary Flashback: Type IV is the cytotoxic, cell mediated delayed hypersensitivity reaction 🚨 SJS/TENS is extremely rare (1-2 per million/year with a slight female predominance). This disease has a high mortality. The majority of SJS/TENS is medication-related.  More than 200 medications have been reported as a trigger. The most common can be remembered by "SATAN": Sulphonamides Allopurinol Tetracyclines Anticonvulsants (Phenytoin/Carbamazepine/Phenobarb) NSAID. Often this is within 1 week of antibiotics and 1 month of anticonvulsants. In a paediatric population think of Mycoplasma pneumoniae and Herpes simplex. In adults think of HIV, Leukaemia and lymphoma. Presentation SJS/TENS usually develops within the first week of antibiotic therapy but up to 2 months after starting an anticonvulsant. There is often a prodromal illness resembling an URTI with fever, sore throat, runny nose, conjunctivitis, malaise, arthralgia and dysuria. Diagnostic hint: Dysuria is present in the majority of cases. Rash with dysuria should raise concern for SJS with associated urethritis. Then a tender/painful red rash develops on the trunk and extending over hours to days onto the face and limbs usually reaching its maximum by four days. The blisters merge to form sheets of skin detachment, exposing red, oozing dermis. Nikolsky sign is positive –blisters and erosions form when the skin is rubbed gently. Source: Dermnet Source: Mucosal involvement is prominent and severe including: Eyes: conjunctivitis Lips/mouth: painful ulcers/red crusted hips Pharynx/oesophagus: restricted oral intake Genital area and urinary tract: erosions, ulcers, urinary retention Upper respiratory tract: cough and respiratory distress Gastrointesinal tract: diarrhoea Complications SJS/TEN can be fatal with a mortality rate of 10% for SJS and 30% for TEN  from: Dehydration Infection and sepsis ARDS GI perforation Acute renal failure DIC Thromboembolism Scoring SJS/TENS can be scored on the SCORTEN or ABCD-10 score – look this one up when you need to use it. Treatment Stop the offending agent! Then our job is supportive care. Think of this as a severe burn. Give them multimodal analgesia, fluids aiming for 1ml/kg/hr of urine output, dressings, keep them warm and isolate them to prevent secondary infection. These patients should all be transferred to a burns unit as they will need plastics, ophthalmology, intensive care and pain input. Avoid silver sulphadiazine as this can exacerbate things. Steroids, Monoclonal antibodies, IVIG, plasmapheresis are all options but controversial. ☝️Pro tip: Early IDC – the mucosal irritation can make later attempts painful! Case Conclusion After sending some photos off to our local friendly plastics surgeons and dermatologists I received some very excited return calls. The patient was whisked across to the tertiary burns centre where he stayed for over a week where he needed to get extensive input from the pain team as his rash slowly resolved. Key Points SJS/TENS are different ends of the same spectrum of your skin falling off usually after a new medication Rash + Dysuria – think TENS/SJS Nikolsky sign = epidermis detaches from dermis with rubbing Medication triggers are numerous but for exams remember: SATAN Treat as a severe burn References Dermnet: FOAM: Gerull R, Nelle M, Schaible T.  Toxic epidermal necrolysis and Stevens-Johnson syndrome: A review.  Crit Care Med.  2011; 39:1521-1532. Dodiuk-Gad RP, Chung WH, Valeyrie-Allanore L, Shear NH. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: An Update. Am J Clin Dermatol. 2015;16(6):475-493. doi:10.1007/s40257-015-0158-0 More Info Lerch M, Mainetti C, Terziroli Beretta-Piccoli B, Harr T. Current Perspectives on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis. Clin Rev Allergy Immunol. 2018;54(1):147-76. Han F, Zhang J, Guo Q, et al. Successful treatment of toxic epidermal necrolysis using plasmapheresis: A prospective observational study. J Crit Care. 2017;42:65-68. doi:10.1016/j.jcrc.2017.07.002 More Info 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.

  • Stemetil Stiffness

    Dr Gavin Ng Emergency Physician Editor: Dr Hector Thomson THE CASE You receive an ambulance notification on Saturday morning. “We are coming to you in 10 minutes. We attended a 70-year-old gentleman with positional vertigo symptoms and gave him 12.5mg IM procholorperazine (Stemetil). His initial GCS was 14 – it is now 3. He has also desaturated to 76% on room air.” The patient arrives shortly thereafter. There are two striking features on the clinical examination – he has widespread generalised erythema over his entire body, and he is noted to have significant rigidity in his lower limbs bilaterally. His other vital signs are as follows: HR 100 BP 160/110   RR 24 SpO2 100% 15L non-rebreather   T 35.7   GCS 3 He is noted to have trismus, and bilateral peri-orbital oedema as well. A wheeze is noted on auscultation. References Caplan, L.R. (2022). Posterior Circulation Cerebrovascular Syndromes. In J. F. Dashe (Ed.), UpToDate. Retrieved March 5, 2023 from Din, L., & Preuss, C. V. (2022). Prochlorperazine - StatPearls - NCBI Bookshelf. Retrieved March 4, 2023, from Lavonas, E.J. (2021). First-generation (typical) antipsychotic medication poisoning. In M.Ganetsky (Ed.), UpToDate. Retrieved March 5, 2023 from Campbell D. The management of acute dystonic reactions [Internet]. NPS MedicineWise. 2001 Retrieved march 5, 2023 from Eskow Jaunarajs KL, Bonsi P, Chesselet MF, Standaert DG, Pisani A. Striatal cholinergic dysfunction as a unifying theme in the pathophysiology of dystonia [Internet]. Progress in neurobiology. U.S. National Library of Medicine; 2015. Retried march 5, 2023 from Gavin Ng Emergency Physician Gavin Ng is an Emergency Physician and Co-Director of Emergency Medicine training at The Alfred. 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.

  • Snakes, why did it have to be snakes?

    Dr Nick Erskine Emergency Registrar Peer review / Editor: Dr Hector Thomson | Dr David McCreary I grew up in New Zealand and therefore snakebites were never something that particularly crossed my mind. I was far more afraid of falling into quicksand or tripping a yellow barrel of radioactive green sludge than I was of creepy crawlies. However, since migrating across the ditch, my need to fear and understand venom-induced consumptive coagulopathies has grown. In fact, diving into toxinology study may have well driven me back to the safety of New Zealand if not for the discovery of a cannibalistic New Zealand sea-slug that’s riddled with tetrodotoxin. Let’s talk about Snakes, baby Despite Australia’s reputation for being fraught with deadly animals, snake bites are a relatively rare event here. Exact estimates vary, but the incidence is in the ballpark of 3 envenomations per 100,000 people per year.[1, 2] Importantly, most snakebites in Australia do not result in envenomation [3]. This may either be from a non-venomous snakebite, or from a “dry bite” by a venomous snake where insufficient venom is injected to cause envenomation in a person. Whilst there are dozens (and dozens and dozens!) of different snakes in Australia the big ones we are concerned about when it comes to envenomation are Black Snake Group (Pseudochis) Brown Snake (Pseudonaja) Death Adder (Acanthophis) Sea Snake (Hydrophiliadae) Taipan Snake (Oxyuranus) Tiger Snake Group (Notechis) It is rare that someone can reliably tell you which snake bit them (snake handlers undergoing workplace accidents excepted). We all know of cases where malicious sticks on the ground have stabbed someone in the ankle whilst an innocent snake happened to be nearby. Rather than relying on the patient’s blurred description of colours and patterns, take guidance from the environment around you and the toxidrome before you. Wherefore art my snake? Every state has different endemic snake populations, and you’ll likely be able to tell which snakes are around by which types of snake antivenom you keep in stock in your ED. In broad strokes for those planning an interstate vacation Black Snake Group – Most of Australia except Tasmania and the South Coast Brown Snake Group – Most of Australia except Tasmania Death Adder – Most of Australia except Tasmania, Victoria, and the southern parts of Western Australia Sea Snake – In the sea (again, excepting some of Tasmania and a good chunk of the South Coast) Taipan – Northern and Central Australia Tiger – Southern Australia and Tasmania However, with the exception of the Bass Strait, borders are largely just guidelines for snakes so it’s not impossible to find snakes outside their home turfs. Additionally, snake wranglers and handlers can bring different species all over Australia so it’s worth understanding the toxidromes you may come across irrespective of which AFL team you support. What to expect when you’re expecting (an envenomated patient) After the initial snakebite, the patient may notice localised symptoms at the bite site (E.g. pain, muscle tenderness). As the venom spreads through the lymphatic system people may develop non-specific systemic features (E.g. nausea, vomiting, abdominal pain, diarrhoea, diaphoresis, headache) before proceeding to specific systemic envenomation. To mitigate the spread of venom through the lymphatics (and therefore reduce the risk of systemic envenomation) a pressure bandage immobiliser (PBI) should be placed within the first four hours of the bite. This should not be removed until certain criteria are met (stay tuned for that later in the post) (From Despite the early application of a PIB, people can still progress to specific snake envenomation syndromes. The features of which can be grouped into 1)      Cardiovascular Collapse -          Syncope (often within one hour of the bite) -          Hypotension (that may spontaneously resolve before medical contact) -          Rarely (<5%) cardiac arrest 2)      Coagulopathy 3)      Myotoxicity -          Localised or systemic myalgias or muscle tenderness -          Biochemical evidence of Rhabdomyolysis (rising CK) can lag by up to 24 hours -          Hyperkalaemia and renal impairment in severe cases 4)      Neurotoxicity -          Descending flaccid paralysis -          Eyes (Ophthalmoplegia, ptosis) -> Bulbar Palsy -> Respiratory -> Limb paralysis But which envenomation goes with which snake? This is one of those situations where ultimately you just have to rote learn some patterns. Perhaps one day there’ll be a SnakeGPT app that uses AI to determine things for you, but in the meantime, we rely on that gigantic medical brain you’ve spent years developing. The most important trio of snakes to learn about are the ones that cause VICC, as they’re responsible for nearly 90% of our need for antivenom across Australian EDs.[3] The Brown, Tiger, and Taipan snakes are the three groups that cause VICC. I listed them non-alphabetically to save the best for last. The Taipan snake not only causes VICC but also causes neurotoxicity. A two-for-one deal for our colleagues in Northern and Central Australia. Continuing with the Neurotoxicity theme is the Death Adder. Death Adders don’t cause any form of coagulopathy but (alongside the Taipan) will cause a neurotoxic descending paralysis. Jumping over to the Myotoxicity category you’ll find the Sea Snakes and the Black Snake Groups. Sea Snakes are probably the one time where a patient’s description of the snake does help determine which one bit them (“It was in the ocean, doc”). Helpfully, the black snake group are the only Australian snakes to commonly give you the heparin-like “Anticoagulant Coagulopathy”. So, if it comes from the sea or prolongs your APTT, think myotoxicity. And finally, the snake that makes you collapse – the brown snake. We touched on this cheeky fella in the VICC category already. I flag it separately within Cardiovascular because it can be the early clue that a brown snake has been involved. Nearly a third of Brown Snake envenomed patients have a syncope early in the envenomation process, significantly higher than any of the other ones on the list. (Adapted from Ibister GK, Brown SGA, Page CB et al Snakebite in Australia: a practical approach to diagnosis and treatment Med J Aust 2013; 199 (11): 763-768) Envenomation kits – or how to occupy a distracting Intern’s time “Ah, but what about our department’s Snake Venom Detection Kit?” I hear you ask. “Wouldn’t that tell me which snake was carrying the smoking gun?” The cynic in me would say that getting someone to use one of those kits is just a good way to get noisy and chaotic person out of a noisy and chaotic resuscitation. Perhaps the more diplomatic way to say that is to say that its clinical use is limited and the reliance on an SVDK can distract from resuscitation efforts. First and most importantly, the kits do not tell you if a patient is envenomated. That is not their role, and they cannot and must not be used at such. They can be used as a guide to which monovalent antivenom to use for an envenomated patient, however, there are a number of caveats to their use. For starters, they have a lot of false positives and false negatives. And I mean a lot. One Australian Snakebite Project (ASP) study showed an incorrectly identified positive result in nearly 15% of cases[4], with another ASP study reporting up to 25% of envenomated patients showed no venom detected.[5] This inaccuracy is not helped by the relative inexperience of clinicians or laboratory staff using them (when’s the last time you picked one up and read the instructions?) Additionally – the geographic distribution of snakes and clinical envenomation syndromes means identification of the snake group is usually possible without using a detection kit. Especially in the more snakeless areas such as Tasmania, Victoria, and the Southern Coast. Even when exact identification is not clinically possible, it is often safer or more practical to administer two vials of different monovalent antivenoms based on the species endemic to an area (E.g. a vial of Tiger and Brown snake antivenom for a patient with VICC in Victoria), than it is to rely on an SVDK. And finally, there’s always Polyvalent antivenom Polyvalent Antivenom So, if we have an antivenom for all of the snakes, why don’t we just use that? The primary reason being a significantly greater risk of anaphylaxis when the polyvalent is used.[6] Up to 1% of patients getting a Monovalent Antivenom may experience anaphylactic symptoms, which climbs to 5% of those getting Polyvalent. Most often this reaction will resolve with just stopping the antivenom infusion, and usually it can be restarted at a lower rate without incident. If the anaphylactic reaction is non-responsive to this simple measure, then proceed along standard anaphylaxis pathways – lie the patient down, apply 15L/min O2 via Hudson Mask or Non-Rebreather, bolus crystalloid for hypotension, and give IM Adrenaline 0.5mg as required. Caution should be taken if commencing IV Adrenaline – as most patients receiving antivenom will be profoundly coagulopathic (~90% of patients getting antivenom have VICC) so a sudden surge in blood pressure may precipitate intracranial haemorrhage. Note: the risk: benefit and cost:benefit ratios to stocking certain monovalent antivenoms changes with different locations and different snake populations. It would be impractical to carry multiple monovalent antivenoms for snakes that are rarely seen or treated, so sometimes polyvalent antivenom is a necessary evil. Woah woah woah, you’ve jumped ahead there Nick. Why am I giving antivenom? A fine question my hypothetical friend. Absolute indications Immediate life threat: Cardiac arrest Imminent life threat: Descending paralysis, or seizure Expected life threat: VICC Relative indications: Rhabdomyolysis Coagulopathic states other than VICC Protracted, treatment-resistant systemic symptoms (GI etc) A single vial of antivenom is sufficient, and no pre-medication is required. Remember to warn any patient that receives any form of snake antivenom that one-third of people may get serum sickness (fevers, myalgias, rash) 5-14 days after administration and if that occurs they should seek immediate medical attention and steroid prescription. Let's be fair, my patient was "bitten" by a stick. When can I take off their pressure bandage and let them go home? Ah yes, the far less exciting but far more common scenario. The patient without evidence of systemic envenomation and without the need for antivenom heroics. The overarching time-based rules to remember are 1)      At least 12 hours of observation 2)      Never at night It is worth telling this to your patient upfront. The moment the word “snake” left their lips, they were committed to the long haul in ED. First, the pressure bandage immobilisation It should only be taken off if: There are no clinical or laboratory signs of envenomation (cardiovascular collapse, coagulopathy, myotoxicity, neurotoxicity) There are appropriate staff to manage envenomation if it occurs (emergency/critical care staff, laboratory staff) There is immediate access to antivenom should envenomation occur OR Antivenom has been administered (because you don't want to keep the venom and antivenom separated now, do you?) This means if you’re working somewhere without the required clinical and laboratory staff, the PBI stays on until they’ve been transferred somewhere else. Next, the observation period Irrespective of how well the patient is and how not-snakey the wound appears, all patients with a potential snakebite need a clinical and laboratory assessment for envenomation at: Time of arrival 1-hour post PBI removal 6 hours post-bite 12 hours after bite Neurotoxicity can be subtle and clinician accuracy dips overnight, so being confident that there are no toxinological findings is significantly harder after hours. Additionally, community response teams (E.g. ambulance) availability overnight are lower should the patient deteriorate after discharge – so snakebite discharges should only ever occur when they’re safe and well-lit. From Toxicology and Wilderness Expert Group. Summary management of snake bite (Figure 17.3) [revised 2012 June]. In: eTG complete [internet]. Melbourne: Therapeutic Guidelines Limited, Jul 2013. If your patient is bored during their observation period, they can always watch Snakes on a Plane...13 times. References & Resources [1] Australian Institute of Health and Welfare Injury in Australia: Contact with living things Report July 2023 [2] Kasturiratne A, Wickremasinghe AR, de Silva N, et al. The global burden of snakebite: a literature analysis and modelling based on regional estimates of envenoming and deaths. PLoS Med. 2008;5(11):e218. [3] Ibister GK, Brown SG, Page CB et al Snakebite in Australia: a practical approach to diagnosis and treatment Med J Aust 2013; 199 (11): 763-768 [4] Isbister GK, Brown SG. Bites in Australian snake handlers — Australian snakebite project (ASP-15). QJM 2012; 105: 1089-1095. [5] 12. Isbister GK, O’Leary MA, Elliott M, Brown SG. Tiger snake (Notechis spp) envenoming: Australian Snakebite Project (ASP-13). Med J Aust 2012; 197: 173-177. [6] Isbister GK. Antivenom efficacy or effectiveness: the Australian experience. Toxicology. 2010;268(3):148-154. doi:10.1016/j.tox.2009.09.013 [7] General thanks to LITFL (,, DR NICK ERSKINE Emergency Registrar Nick is an Advanced Trainee working at Alfred Hospital. At work, he is moderately obsessed with point-of-care ultrasound and can usually be seen skulking the halls of the department with a Sonosite. Outside of work he lives in fear of needing a FAST himself after coming off his mountain bike on a downhill course too advanced for him. So far he’s always made it to post-ride beers with all his limbs and solid viscera intact, although will never live down the AC joint disruption he sustained when attempting to show off to the Orthopod he was riding with.


    JOURNAL CLUB PODCAST DECEMBER 2022 DR DANNY MARHABA DR JIUN KAE PUI PROFESSOR PETER CAMERON Welcome to the December Journal Club Podcast. We are again joined by Professor Peter Cameron, Academic Director for the Alfred Emergency and Trauma Centre and Dr Jiun Kae Pui, Emergency Consultant at Alfred Emergency and Trauma Centre. This month we discuss the benefit of reduced FiO2 for patients following cardiac arrest and the use of double-sequetial-external-defibrillation vs vector change in VF. EFFECT OF LOWER VS HIGHER OXYGEN SATURATION TARGETS ON SURVIVAL TO HOSPITAL DISCHARGE AMONG PATIENTS RESUSCITATED AFTER OUT-OF-HOSPITAL CARDIAC ARREST. THE EXACT RANDOMIZED CLINICAL TRIAL READ IT HERE CLINCIAL QUESTION: Does reducing FiO2 after cardiac arrest to target SpO2 90-94% in the out of hospital setting improve survival at hospital discharge? BACKGROUND Hyperoxia after OOHCA has been implicated in worse outcomes, leading to advocacy against hyperoxia (1). Does this evidence extend to the early post-arrest environment, or should early hyperoxia be tolerated for the initial resuscitation, transport and investigations? STUDY DESIGN & PICO DESIGN Open Label Randomized Controlled Trial. POPULATION Unconscious adults ≥ 18 years of age, with ROSC following OOHCA with SpO2 ≥95% while receiving oxygen of 10L/min or 100% FiO2 if intubated. INTERVENTION Oxygen reduced initially to 4LPM to achieve peripheral SpO2 of 90-94%. COMPARISON Higher flow oxygen to achieve peripheral SpO2 of 98-100%. OUTCOME Primary: Survival to hospital discharge Secondary Outcomes A collection of findings including rearrest, hypoxia out-of-ICU, survival to ICU discharge, and hospital LOS. FINDINGS Survival to discharge was not improved in the arm with reduced oxygen targets (90-94%). AUTHORS' CONCLUSIONS Among patients achieving ROSC after out-of-hospital cardiac arrest, targeting an oxygen saturation of 90% to 94%, compared with 98% to 100%, until admission to the ICU did not significantly improve survival to hospital discharge. JOURNAL CLUB THOUGHTS The lower target of SpO2 90-94% did not improve survival. In fact, there was a signal to harm with an absolute survival difference of 9.6%, and an odds ratio of 0.68 reaching P = 0.05 in favour of the early hyperoxia arm (the actual number was 0.0496 however JAMA requires this be rounded up to 0.05. When looking at the secondary outcome of hypoxia, there was a clear increased likelihood of hypoxia when targeting the lower SpO2. Intuitively this makes sense, hypoxia is more likely with lower initial oxygen targets, and early hypoxia after OOHCA can cause worse outcomes. Though we know that hyperoxia is harmful, hypoxia is probably worse. In the undifferentiated patient after OOHCA, who is undergoing transport and initial investigations – it is prudent to provide a higher oxygenation target in the early 1-2 until transport, resuscitation and initial investigations are attained. Typically, researchers will exert a great degree of effort to avoid stopping a trial early. One reason is because the results often vary in both directions as the trial progresses, this is why a pre-determined stop point is optimal – so that the trial is not stopped as soon as a 0.05 limit is reached (in either direction). Recruitment in this trial was challenged by varying ethics requirements across states, which changed during the course of recruitment – as well as the COVID pandemic due to changes of protocols in oxygen provision. SHOULD PREHOSPITAL CLINICIANS INCORPORATE DOUBLE-SEQUENTIAL-EXTERNAL-DEFIBRILLATION OR A VECTOR CHANGE IN REFRACTORY VFIB ARREST? READ IT HERE CLINCIAL QUESTION: Should prehospital clinicians incorporate double-sequential-external-defibrillation or a vector change in refractory VFib arrest? BACKGROUND Double-Sequential-External-Defibrillation (DSED) has been proposed as an intervention to improve the likelihood of achieving return of spontaneous circulation (ROSC) from refractory ventricular fibrillation (VF) (2), without damaging the involved defibrillators (3). Reducing time to ROSC, is one component of the pursuit to increase neurologically intact survival in patients with out-of-hospital-cardiac-arrest (OOHCA). STUDY DESIGN & PICO DESIGN Open-label cluster randomised controlled trial. POPULATION (TARGET) Patients ≥18 years of age who suffered an OOHCA in VF or VT, which persisted despite 3 standard anterolateral defibrillations with 2-minute intervals. INTERVENTION 6 prehospital cohorts, crossing over to vector change antero-posterior defibrillation, or to one-person DSED. COMPARISON Standard ALS including standard anterolateral defibrillation. OUTCOME Primary outcome Survival to Hospital Discharge Secondary outcomes Termination of VF ROSC Modified Rankin Scale Score ≤2 WHAT WERE THE FINDINGS? Primary Outcome 38/125 (30.4% of) patients in the DSED arm survived, compared with 31/143 (21.7%) in the Vector Change arm, and 18/135 (13.3%) in the standard treatment arm. The adjusted relative risk (aRR) of both DSED and Vector Change arms demonstrated a statistically significant increase in survival when compared to standard treatment. Secondary Outcomes All secondary outcomes in the DSED arm reached statistically significance, from termination of VF (aRR 1.25, CI 1.09 – 1.44) to likelihood of ROSC (aRR 1.72, CI 1.22 – 2.42), to proportion of MRS ≤ 2 at discharge (aRR 2.21, CI 1.26 – 3.88). Only likelihood of termination of VF in the vector change arm reached statistical significance (aRR 1.18, CI 1.03 – 1.36). AUTHORS' CONCLLUSIONS Among patients with refractory ventricular fibrillation, survival to hospital discharge occurred more frequently among those who received DSED or VC defibrillation than among those who received standard defibrillation. JOURNAL CLUB THOUGHTS A 30% survival under any intervention for patients with a refractory VF arrest is a high survival percentage. CLINICAL BOTTOM LINE This is a practice-changing trial - in patients with a refractory VF or VT arrest, who fail to respond to standard defibrillation where other interventions (such as E-CPR) are unavailable, it would be prudent to make use of a vector change or DSED to improve patient outcomes. DR DANNNY MARHABA Emergency Registrar Danny is an Emergency Medicine Registrar at the Emergency and Trauma Centre and the current Senior Registrar for research. He trained in regional NSW before moving back to Melbourne to complete his training at the Alfred.


    Journal Club Podcast February 2023 Dr Danny Marhaba Dr David McCreary Professor Peter Cameron Welcome to the second Journal Club Podcast of 2023. We are joined by Professor Peter Cameron, Academic Director for the Alfred Emergency and Trauma Centre and Dr David McCreary, Emergency Consultant at Alfred Emergency and Trauma Centre. BACKGROUND - A Primer on the history of Sepsis Literature Wholistic discussions around sepsis can begin from 1991, when the ACCP (American College of Chest Physicians) and the SCCM (Society of Critical Care Medicine) convened a “Consensus Conference,” which as other conferences to follow implied, might be referred to as – Sepsis 1 {1}. This consensus defined sepsis as a response to infection manifested by ≥2 SIRS criteria. In 2001, this group expanded to include the ESICM (European Society of Intensive Care Medicine), the ATS (American Thoracic Society), and the SIS (Surgical Infection Society); their new definition – colloquially referred to as Sepsis 2 – largely maintained the definitions and divisions of sepsis, severe sepsis and septic shock {2). In parallel the now infamous Rivers Trial, where a bundle of interventions termed EGDT (Early Goal Directed Therapy), showed that this bundle when applied to the 130 out of 263 patients with severe sepsis or septic shock who were randomised to its arm, dramatically reduced in hospital mortality from 44.4% to 29.2% {3}. This single centre trial with a relatively high control-group mortality led to the now well-known Surviving Sepsis campaign recommended the interventions of EGDT and continued doing so for the decade that followed {4, 5} – specifically, this was an era that can be differentiated by relatively liberal blood transfusions, continuous central venous co-oximetry, and dobutamine. The differences in actual interventions received such as transfusions, pulmonary artery catheterisation and intubation are shown in the original study’s Table 4 {3}, shown here as figure 1. Though they took took over 10 years to plan and carry out, the three collaborative and harmonised international trials of ARISE (1600 patients in 51 oceanic hospitals, 2014), PROCESS (1351 patients in 31 American hospitals, 2014) and PROMISE (1260 patients in 56 UK hospitals, 2015) did not replicate the findings of the original Rivers trial – and the use of EGDT slowly waned {6 – 8}. In fact, today our practice can be characterised by avoidance where possible, of transfusions, central venous lines and invasive ventilation – the emphasis then became on early recognition, early intravenous fluids, and timely antibiotics. In 2016 the Third International Consensus Definitions for Sepsis and Septic Shock – colloquially known as Sepsis 3 – made some improvements {9}; they did away with severe sepsis – keeping only the categories of simple infection, sepsis, or shock, – they placed an emphasis on SOFA scores and de-emphasized SIRS criteria in diagnosis, and they provided a good definition for sepsis – “life threatening end-organ dysfunction that results from a dysregulated response to infection. However, what followed was the 2016 guidelines of the Surviving Sepsis Campaign and it’s now infamous 2018 update {10, 11}, which brought on an uproar by many clinicians who these guidelines applied to. Specifically, two strong recommendations were perceived as being mismatched with their supporting evidence: i) to rapidly administer 30mL/kg of crystalloid for any patient with hypotension or lactate ≥4mmol/L who was thought to be in septic shock. ii) a 1hour door-to-antibiotics times for any patient with sepsis. The first strong recommendation was challenged for the relative-lack of supporting evidence {12} as well as its potential to cause harm: titrating therapy to patient-centered parameters and clinical response is a more nuanced approach they may have better outcomes than rather large fluid boluses of pre-determined volumes {13}. The second strong recommendation was challenged for its feasibility as well as the relative-lack of supporting evidence {14}: though earlier antibiotics are associated with survival in septic shock, the link in sepsis without shock is more elusive, and differentiating sepsis from the bulk of simple infections that people acquire is a process that commonly takes longer than 1 hour, especially in access blocked and overcrowded emergency departments. Thus, we arrive at the current 2021 issue of the Surviving Sepsis Guidelines {15}, where antibiotics for possible sepsis carries a more reasonable recommendation of administration within 3 hours (timing for probable sepsis remains at <1hr), the advice for 30mL/kg of fluid was downgraded to weak strength and linked with dynamic measures to guide the fluid resuscitation, and norepinephrine (noradrenaline) was upheld as the first line vasopressor targeting a MAP of ≥66mmHg. PAPER ONE INTRODUCTION OF AN EMERGENCY MEDICINE PHARMACIST-LED SEPSIS ALERT RESPONSE SYSTEM IN THE EMERGENCY DEPARTMENT: A COHORT STUDY READ IT HERE CLINICAL QUESTION The stated aim of this study was to evaluate the impact of a sepsis performance improvement program in the ED with early involvement of an EM pharmacist. The stated key findings of the study relate to whether the above implementation reduced key performance indicators including time to antibiotics. JOURNAL Emergency Medicine Australasia, 2023 LEAD AUTHOR Christina Petronela Roman, EM Pharmacist DESIGN Single centre self-controlled prospective cohort study POPULATION 180 patients presenting to a metropolitan major referral hospital’s ED during pharmacist working hours, who were admitted to ICU with a diagnosis of sepsis. EXPOSURE Sepsis alert response system which includes an EM-pharmacist, from February 2016 to February 2018. COMPARISON Self-controlled parameters for patients admitted to ICU from ED with a diagnosis of sepsis from January 2015 to February 2016. OUTCOME Primary: Proportion of patients who received antibiotics within 60 minutes. Secondary Outcomes Proportion of patients completing the sepsis bundle within 60 minutes of arrival (fluid bolus, 2 blood cultures and serum lactate) FINDINGS Primary Outcome Proportion of patients receiving empiric antimicrobials improved from 26.3% to 81.7% (OR 12.6, 95% CI 6.2 – 25.4%, P<0.001). Secondary Outcomes Proportion receiving IV Fluids improved from 47.5% to 72.1% (P=0.002) Proportion receiving blood cultures improved from 52.5% to 85.6% (P<0.001) Proportion receiving a serum lactate improved from 50.0% to 66.9% (P<0.001) Secondary outcomes: No significant difference in pain at any measured time-point. No significant difference secondary outcomes in function questionnaires. Statistically significant difference in parent satisfaction on day 1 and analgesia use on day 1. While not statistically significant, trend for bandage group to be more likely to have used analgesia (except D1), and have missed school. AUTHORS' CONCLUSIONS The authors report that the implementation of a sepsis alert response that included early involvement of the EM pharmacist was associated with improvement in time to antimicrobials in the ED. BOTTOM LINE Due to the breadth of confounders in any time-controlled study, it is difficult to use this as evidence for a cause-effect relationship. However, it does seem that whether it was due to a sepsis alert response or whether it was due to a department continuously improving its KPIs (probably both), time to antimicrobials, fluids and serum lactate seem to have improved between 2015 and 2018. Limiting the subjects to only those admitted to ICU was wise (and probably the only feasible was to arrive at a comparator). This is because time to antibiotics is a more appropriate measure in patients with septic shock, and typically those are the patients with sepsis who require intensive care. This also then means that the conclusions of this study do not extend to patients who did not require ICU. In my anecdotal experience, the presence of EM pharmacist in this sepsis alert response is very helpful – they track previous sensitivities, help identify dose adjustments when required, can safely chart the medicines decided upon with the medical officer, and seem to act as an advocate in reducing time-to-intervention in patients with sepsis. However, this study cannot differentiate the EM pharmacist from the sepsis alert response itself – therefore even if the study design enabled us to draw a clear link between the sepsis alert response and times to intervention, drawing out the effect of the EM-pharmacist from the sepsis alert would then still need to be shown. Operational decisions cannot be limited to only that which has high quality evidence, and therefore until a feasible high-quality trial that isolates and demonstrates the effects of an EM pharmacist within a sepsis alert bundle is conducted, I suspect that we will continue to see our pharmacist colleagues supporting us in offloading some of the pharmacological cognitive burdens that often accompany these alerts. PAPER TWO RESTRICTION OF INTRAVENOUS FLUIDS IN ICU PATIENTS WITH SEPTIC SHOCK READ IT HERE CLINICAL QUESTION: What are the effects of a restriction of IV fluids on mortality and other outcomes in adult patients with septic shock in the ICU? JOURNAL The New England Journal of Medicine, June 2022 LEAD AUTHOR Tine Sylvest Meyhoff, MD DESIGN Open Label Prospective Multicentre RCT POPULATION 1554 patients ≥18 years of age who were admitted to ICU with suspected septic shock, as defined by suspected infection with lactate ≥2mmol/L, ongoing inopressors, and having received ≥1L IV Fluids within the prior 24 hrs. EXPOSURE Restrictive IV Fluid therapy for the following indications: Severe hypoperfusion => 250 – 500mL bolus lactate ≥4mmol/L, MAP <50mmHg despite inopressors, skin mottling score of ≥2 urine output <0.1mL/kg/hr Fluid Losses => Replace the same volume Dehydration / Electrolyte derangements => Correct the derangement Total daily fluid => Top up to target total daily fluid intake of 1L COMPARISON Standard / Unlimited IV Fluid therapy for the following indication Improve haemodynamic compromise Replace expected or observed losses Correct dehydration / electrolyte derangement Maintenance fluids as per local ICU protocol ACTUAL EXPOSURE VERSUS COMPARATOR Intravenous Balance             and                  Cumulative Fluid Balance D1: 1               vs 1.7 L            and                  +0.7L   vs +1.3L D5: 2.3            vs 3.8L             and                  +1.6L   vs +2.4L OUTCOME Primary: Death within 90 days post randomisation Secondary Outcomes Number of patients with ≥1 serious adverse event (CVA, MI, Mesenteric ischemia, or Limb ischemia. Number of patients with ≥1 serious advance reaction to IV crystalloid (Seizures, Anaphylaxis, osmotic demyelination, severe hypernatremia, severe hyperchloremic acidosis, or severe metabolic alkalosis). The number of days, at 90 days, where the patient wasn’t requiring life support or was alive and out of hospital. WHAT WERE THE FINDINGS? No difference in death at 90 days (42.3 vs 42.1 %, ARR 1.0, 90% CI 0.89 – 1.13). No statistically significant difference in any of the secondary outcomes AUTHORS' CONCLUSIONS There was no significant difference in 90-day mortality or serious adverse events among patients who received restricted fluid therapy and those who received standard therapy. CLINICAL BOTTOM LINE Technically this is an ICU trial, it therefore applies to ICU patients – not to ED patients, unless those patients are spending upwards of 12 hours in the ED. Don’t treat the algorithm, treat the patient. The lessons learnt over the past 30 years emphasize the avoidance of blanket interventions for all patients, instead emphasizing patient-specific clinical parameters – even the restricted arm of this trial factors lactate, skin mottling, blood pressure and urine output into the decision-making process. In deciding whether to give more fluids in Emergency Department patients with septic shock, we target MAP ≥65mmHg, CR <2, Conscious State, Urine Output and a point of care echo. The ED is certainly capable of providing good critical care (resuscitation), but it is not an ICU. When ICU patients spend ≥12 hours in the ED, change gears and use whatever good methodology your ICU teaches, I was taught to use FAST HUGS (Feeding, Analgesia, Sedation, Thromboprophylaxis, Head Up, Ulcer Prophylaxis and Glycaemic Management). PAPER THREE PERIPHERAL VASOACTIVE ADMINISTRATION IN CRITICALLY ILL CHILDREN WITH SHOCK: – A SINGLE CENTRE RETROSPECTIVE COHORT STUDY READ IT HERE CLINICAL QUESTION What were the characteristics of critically unwell children on peripherally administered vasoactive medicines? What were the characteristics of the associated extravasation injuries? JOURNAL Journal of Pediatric Critical Care Medicine, August 2022 LEAD AUTHOR Robert A. Levy, MD DESIGN Single-centre retrospective cohort study POPULATION 231 patients with peripheral vasoactive access (PVA) and 525 patients with central vasoactive access (CVA), aged 31 days to 18 years who required adrenaline, noradrenaline or dopamine in a quaternary PICU. EXPOSURE Inotropes and vasopressors administered through a PVA. COMPARISON Inotropes and vasopressors administered through a CVA OUTCOME No primary outcome was differentiated from the basket of outcomes studied. Anthropomorphic characteristics within the two groups Percentages of Primary Diagnoses and of Invasive Interventions Proportions and doses of the various inotropes and vasopressors received Proportion of the PVA patients who ultimately required a CVA Proportion of the PVA patients who experienced extravasation injuries WHAT WERE THE FINDINGS? Patients who initially received vasoactive medicines through a PVA were: older (10.3 vs 9.4 years, p = 0.003) and heavier (30.9 vs 25.3 kg, p = 0.001). more likely to have sepsis (40.3 vs 19.8 %, p < 0.001) more likely to have had the vasoactive medicines initiated at night (64.5 vs 50.5 %, p < 0.001), less likely to have been intubated (50.7 vs 82.7 %, p < 0.001), less likely to have received CPR (3.0 vs 8.0 %, p < 0.001) Spent fewer days in PICU (2.8 vs 5.8 days, p < 0.001) Had a lower mortality (19.0 vs 10.4 %, p < 0.001) 75% of the PVAs used were 20 or 22 gauge. 4 out of 231 had an extravasation event, all in the hand. 3 of those received antidotes (phentolamine or terbutaline), none suffered from rebound hypotension. Of Patients who initially received vasoactive medicines through a PVA, the 53.7% who went on to require a CVA were: Lighter in weight (26.8 vs 37.2 kg, p = 0.04) More likely to be intubated (63.7 vs 35.5 %, n < 0.001) Spent longer in PICU (3.8 vs 1.9 days, p < 0.001) Had a higher mortality (15.3 vs 4.8 %, p = 0.009) AUTHORS' CONCLUSION Initial use of vasoactive medicines through a PVA may be an appropriate option while evaluating the need for CVA. CLINICAL BOTTOM LINE This is informative data. It is particularly informative to see the low rate of extravasation in critically unwell children with 20- or 22-gauge cannulas. The characteristics of patients on vasoactive medicines through PVAs was different, they were older, more likely to have sepsis, and were typically less unwell than those who received CVAs – this is largely intuitive. When needing to start vasoactive medicines in children, one option is to initiate them peripherally – ideally through a high-quality cannula in a proximal vessel – whilst making a decision on the need for a CVA. REFERENCES Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest. 1992 Jun;101(6):1644-55. doi: 10.1378/chest.101.6.1644. PMID: 1303622. Levy, Mitchell M. MD, FCCP; Fink, Mitchell P. MD, FCCP; Marshall, John C. MD; et al. For the International Sepsis Definitions Conference. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Critical Care Medicine 31(4):p 1250-1256, April 2003. | DOI: 10.1097/01.CCM.0000050454.01978.3B Rivers E, Nguyen B, Havstad S, et al. Early Goal-Directed Therapy Collaborative Group. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001 Nov 8;345(19):1368-77. doi: 10.1056/NEJMoa010307. PMID: 11794169. Dellinger RP, Carlet JM, Masur H, et al. Surviving Sepsis Campaign Management Guidelines Committee. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004 Mar;32(3):858-73. doi: 10.1097/01.ccm.0000117317.18092.e4. Erratum in: Crit Care Med. 2004 Jun;32(6):1448. Dosage error in article text. Erratum in: Crit Care Med. 2004 Oct;32(10):2169-70. PMID: 15090974. Dellinger RP, Levy MM, Rhodes A, et al. Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013 Feb;41(2):580-637. doi: 10.1097/CCM.0b013e31827e83af. PMID: 23353941. ARISE Investigators. Goal-directed resuscitation for patients with early septic shock. N Engl J Med 2014;371(16):1496-506 ProCESS Investigators, Yealy DM, Kellum JA, Huang DT, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med. 2014 May 1;370(18):1683-93. doi: 10.1056/NEJMoa1401602. Epub 2014 Mar 18. Mouncey PR, Osborn TM, Power GS, et al. Protocolised Management In Sepsis (ProMISe): a multicentre randomised controlled trial of the clinical effectiveness and cost-effectiveness of early, goal-directed, protocolised resuscitation for emerging septic shock. Health Technol Assess. 2015 Nov;19(97):i-xxv, 1-150. doi: 10.3310/hta19970. PMID: 26597979; PMCID: PMC4781482. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10. doi: 10.1001/jama.2016.0287. PMID: 26903338; PMCID: PMC4968574. Rhodes, Andrew MB BS, MD, Evans, Laura E. MD, MSc, FCCM, Alhazzani, Waleed MD, MSc, FRCPC, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Critical Care Medicine 45(3):p 486-552, March 2017. | DOI: 10.1097/CCM.0000000000002255 Levy, Mitchell M. MD, MCCM, Evans, Laura E. MD, MSc, FCCM, Rhodes, Andrew MBBS, FRCA, FRCP, FFICM, MD. The Surviving Sepsis Campaign Bundle: 2018 Update. Critical Care Medicine 46(6):p 997-1000, June 2018. | DOI: 10.1097/CCM.0000000000003119 Marik PE, Byrne L, van Haren F. Fluid resuscitation in sepsis: the great 30 mL per kg hoax. J Thorac Dis. 2020 Feb;12(Suppl 1):S37-S47. doi: 10.21037/jtd.2019.12.84. PMID: 32148924; PMCID: PMC7024756. Marik PE, Malbrain M. The SEP-1 quality mandate may be harmful: How to drown a patient with 30 mL per kg fluid! Anaesthesiol Intensive Ther 2017;49:323-8. 10.5603/AIT.a2017.0056 Sterling SA, Miller WR, Pryor J, et al. The Impact of Timing of Antibiotics on Outcomes in Severe Sepsis and Septic Shock: A Systematic Review and Meta-Analysis. Crit Care Med. 2015 Sep;43(9):1907-15. doi: 10.1097/CCM.0000000000001142. PMID: 26121073; PMCID: PMC4597314. Evans, Laura, Rhodes, Andrew, Alhazzani, Waleed, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Critical Care Medicine 49(11):p e1063-e1143, November 2021. | DOI: 10.1097/CCM.0000000000005337Danny is an Emergency Medicine Registrar at the Emergency and Trauma Centre and the current Senior Registrar for research. He trained in regional NSW before moving back to Melbourne to complete his training at the Alfred. DR DANNY MARHABA Emergency Registrar Danny is an Emergency Medicine Registrar at the Emergency and Trauma Centre and the current Senior Registrar for research. He trained in regional NSW before moving back to Melbourne to complete his training at the Alfred.


    Journal Club Podcast January 2023 Dr Danny Marhaba Dr Rob Melvin Professor Peter Cameron Welcome to the first Journal Club Podcast of 2023. We are joined by Professor Peter Cameron, Academic Director for the Alfred Emergency and Trauma Centre and Dr Rob Melvin, Emergency Consultant and Deputy Director at Alfred Emergency and Trauma Centre. This month has a paediatric theme with papers looking at: immobilisation of torus fractures, the mid-arm point for paediatric ICC insertion, and screen time in paediatric concussion. IMMOBILISATION OF TORUS FRACTURES OF THE WRIST IN CHILDREN (FORCE): A RANDOMISED CONTROLLED EQUIVALENCE TRIAL IN THE UK READ IT HERE CLINICAL QUESTION Is rigid immobilisation necessary in paediatric buckle fractures of the distal radius? JOURNAL The Lancet, July 2022 LEAD AUTHOR Daniel C Perry BACKGROUND Buckle Fractures of the distal radius are among the most common fractures in children {1}. Fractures of the distal radius can be classified as those affecting the growth plate (physis), those involving the metaphysis and/or those affecting the diaphysis. There has been a wide variation of practice recommendations in the management of buckle fractures of the distal radius, with some recommending rigid immobilisation and others recommending bandaging {2,3,4}. A 2018 Cochrane review into the treatment of buckle fractures concluded that they were unable to recommend a particular treatment strategy (partly due to the low quality of evidence), however, they did note that their review findings were consistent with the move away from cast immobilisation for buckle fractures {5}. DESIGN Multicentre, Randomised, Controlled, Equivalence Trial Population665 children 8 – 15 years of age, and 300 children 4 – 7 years of age, who presented to one of 23 emergency departments in the UK, with a radiologically confirmed buckle fracture of the distal radius. Excluded were children whose injuries were ≥36 hours old, children who’s clinician suspected a cortical disruption of the radius, or those deemed unable to adhere to trial procedures (insufficient English, no internet, developmental delay, etc). EXPOSURE Bandage offering and immediate discharge. ComparisonRigid immobilisation with splint, back-slab or cast and follow up as per treatment centre protocol. OUTCOME Primary: Pain at 3 days, as measured by the WBFPS (Wong Baker Faces Pain Scale). Secondary Outcomes A collection of findings including days of school or childcare absence at 3 and 6 weeks, return to hospital at 1/3/6 weeks, and patient satisfaction using a 7-item Likert scale. FINDINGS Primary Outcome Children in the exposure group (bandage and discharge) had a mean WBFPS of 3.21, compared with 3.14 in the comparator group (rigid immobilisation), with CI -0.37, 0.17. Secondary outcomes: No significant difference in pain at any measured time-point. No significant difference secondary outcomes in function questionnaires. Statistically significant difference in parent satisfaction on day 1 and analgesia use on day 1. While not statistically significant, trend for bandage group to be more likely to have used analgesia (except D1), and have missed school. AUTHORS' CONCLUSIONS The authors report that their trial found equivalence in pain at 3 days in children with a torus fracture of the distal radius, between bandage and rigid immobilisation. They also report do between-group differences in pain or function during the 6 weeks of follow up. BOTTOM LINE This trial reaffirms that a bandage or tub-grip results in equivalent outcomes, save for some increase in use of basic analgesia. Splints here are a good option to have, but in this particular injury, rigid immobilisation is just not necessary – whether there is a concurrent ulnar fracture or not. Orthopaedic clinics are often full, and to be able to avoid unnecessary referrals to this clinic likely represents good stewardship of social resources. An equivalence trial has more steps than a traditional difference of means trial, in that one would need to disprove two null hypotheses rather than just one. The first null hypothesis to disprove is that the exposure increases the outcome variable by a certain measure of association. The second null hypothesis to disprove is that the exposure reduces the outcome variable by a certain measure of association. Disproving both, therefore shows that the exposure is equivalent to the comparator, to a certain statistical significance and minimum clinically important difference. 🎧 Podcast editor, Dave McCreary, also discussed this study on the RCEMLearning podcast, you can hear that here. 🎧 MID-ARM POINT IN PAEDIATRICS (MAPPAED): AN EFFECTIVE PROCEDURAL AID FOR SAFE PLEURAL DECOMPRESSION IN TRAUMA READ IT HERE CLINICAL QUESTION: Can the Mid Arm Point be used for landmarking ICC insertion in children? JOURNAL Emergency Medicine Australasia, November 2022 LEAD AUTHOR Nuala Quinn BACKGROUND In 2022, injuries were responsible for 33% of all deaths in Australian children {8}. Of those severely injured children, many are at risk of dying from thoracic injuries requiring emergency pleural decompression {9}. In one audit of a high-volume trauma service, 41% of intercostal catheters in children, were placed outside of the triangle of safety {10}. The Mid Arm Point is used in some adult trauma centres, and has been reported to be a reliable aid in placement {11}. DESIGN Prospective Cohort Study, compared to a presumed gold standard Population (Target)392 children aged ≤18 years, who attended one of four emergency departments in Australia and Ireland, who required a chest X-ray for any reason. POPULATION (TARGET) 392 children aged ≤18 years, who attended one of four emergency departments in Australia and Ireland, who required a chest X-ray for any reason. EXPOSURE Mid Arm Point measured and the chest wall marked at that level, a radio-opaque sticker was placed on the mark and an X-Ray was taken with the arms abducted. COMPARISON A presumed gold standard of intercostal space (ICS) 4–6, as identified on the chest x-Ray by a consultant radiologist. OUTCOME Primary Outcome: The proportion of markers localized to ICS 4–6 by interpretation of a consultant radiologist, versus those that identified as ICS 1-3 (too cranial) and those that were identified as ICS 7-8 (too caudal). Post Hoc Analysis: The proportion of markers localised to ICS 4–6 after a single ICS adjustment for age, chosen as ≥4 years. WHAT WERE THE FINDINGS? 712 markers were placed and xrayed following exclusion criteria, 353 (50%) Left sided 359 (50%) right sided. Using the MAP technique throughout all ages found 81% success, with malposition favouring more caudal placement - 14% in ICS 6th and 7th, with only 3% above 4th space. Patients between age 4-18 had higher rates of malposition and of those they were largely placed too caudal (22.6%). Post Hoc analyses showed an increased overall success rate to 91% if a MAPPAED rule was applied to ages 4-18 where the intercostal space above the marked space was used. AUTHORS' CONCLUSIONS Adopting the MAP and MAPPAED approach may improve these success rates of appropriate positioning in the safe zone, and reduce cognitive load on emergency and prehospital clinicians. The MAP rule requires a modification to ages 4-18 which likely represents non-linear relative discrepancies in growth patterns of upper limb and thoracic cage. CLINICAL BOTTOM LINE This is an excellent study. It is simple, straightforward, and represents a creative and pragmatic way to gather clinically useful evidence. For most emergency physicians, ICC insertion in children is rare. Using the Mid-Arm-Point in children <4 and moving 1 ICS superiorly to the Mid-Arm-Point in children ≥4 represents a significant reduction in cognitive load for what may be a complex resuscitation. Producing a good quality, prospective, randomised controlled trial in this patient group is fraught with challenges, if at all feasible. The MAPPAED study may well be some of the best evidence that exists in paediatric ICC insertion for some years to come. The primary limitation however, is in the post-hoc analysis in children ≥4 years. This is because a statistical test is most valid when tested against a pre-conceived single primary outcome, as opposed to identifying a group of retrospectively generated patterns. One could say that the MAPPAED rule, has been prospectively tested in children <4 years of age outside of a major trauma resuscitation, and that the MAPPAED adjustment, has been retrospectively identified in children ≥4 years of age outside of a major trauma resuscitation. EARLY POSTINJURY SCREEN TIME AND CONCUSSION RECOVERY READ IT HERE CLINICAL QUESTION: Does a reduction in screen time facilitate recovery from paediatric concussive head injuries? JOURNAL Pediatrics, November 2022 LEAD AUTHOR Molly Cairncross BACKGROUND Screen-time restrictions are often recommended by clinicians providing care for paediatric patients with a post-concussive head injury {6}. In 2021, a randomised trial of 125 patients between 12 – 25 years of age was conducted published in JAMA-Pediatrics, and provided some much-needed evidence for this recommendation {7}. However, the actual screen-time recorded for the screen-time restricted group was a median of 130 minutes per week (compared to 630 minutes in the screen-time permitted group). Unanswered questions into the optimal screen-time recommendation therefore persist. Design Retrospective Cohort Study - (Planned secondary data analysis of the Advancing Concussion Assessment in Pediatrics (A-CAP) study) POPULATION (TARGET) Seven hundred and twelve children aged 8 – 16 years, who presented to one of five Canadian Emergency Departments, between September 2016 and December 2018, with blunt head trauma and symptoms consistent with a concussion. Exclusion criteria were children with neurological deterioration, neurosurgical intervention, LOC > 30 min, amnesia > 24hrs, and abbreviated injury scale (AIS) > 4. EXPOSURE Self-reported screen-time measured weekly for 3 months, in patients with a diagnosed concussive head injury. COMPARISON Self-reported screen-time measured weekly for 3 months, in patients with a diagnosed orthopaedic injury. OUTCOME Primary: Differences in the association with the Health and Behaviour Scores, between the two groups, measured weekly for 3 months. Secondary Outcomes Secondary: A collection of other pre and post injury factors and measures of association with post concussive symptoms. WHAT WERE THE FINDINGS? Screen time was a significant but nonlinear moderator of group differences in post-concussion symptom severity for parent-reported somatic (P = .01) and self-reported cognitive symptoms (P = .03). Low and high screen time were both associated with relatively more severe symptoms in the concussion group compared to the OI group during the first 30 days postinjury but not after 30 days. Other risk factors and health behaviours had stronger associations with symptom severity than screen time. AUTHORS' CONCLUSIONS The interaction between self-reported screen time and post concussive symptoms is not linear. They recommend moderation in screen-time rather than abstaining from it. CLINICAL BOTTOM LINE This is a retrospective cohort study of an intervention – and the study design comes with many confounders. Concussive symptoms themselves may have many modifiers on both quantity and quality of screen time – they may be simply staring at the screen rather than engaging with it. Another challenge to the conclusions of the study are the nature of self-reported data on screen time. The fact that there was only a moderate correlation between parent and child – reported screen-time (Spearman’s r = .6) highlights this challenge. For now, it is likely reasonable to recommend moderation in screen-time for children who have suffered a concussion. REFERENCES Chung KC & Spilson SV. The frequency and epidemiology of hand and forearm fractures in the United States. J Hand Surg Am.2001; 26: 908-915 National Clinical Guideline Centre (UK). Fractures (non-complex): assessment and management. (NG38). 2016. Children’s Health Queensland Hospital and Health Service. Buckle Fractures . Accessed January 2023. Royal Children’s Hospital, Melbourne. Distal radius and / or ulna – metaphyseal fractures. (Clinical Practice Guideline). Accessed January 2023. Handoll HH, Elliott J, Iheozor-Ejiofor Z, Hunter J, Karantana A. Interventions for treating wrist fractures in children. Cochrane Database Syst Rev. 2018 Dec 19;12(12):CD012470. doi: 10.1002/14651858.CD012470.pub2. PMID: 30566764; PMCID: PMC6516962. Queensland Health. Recovery after a concussion (Patient Fact Sheet). Accessed January 2023. Macnow T, Curran T, Tolliday C, et al. Effect of Screen Time on Recovery From Concussion:A Randomized Clinical Trial. JAMA Pediatr. 2021;175(11):1124–1131. doi:10.1001/jamapediatrics.2021.2782 Australian Institute of Health and Welfare. Infant and Child Deaths. Accessed January 2023. Quinn N, Palmer CS, Bernard S, Noonan M, Teague WJ. Thoracostomy in children with severe trauma: an overview of the paediatric experience in Victoria, Australia. Emergency Medicine Australasia. 2020; 32: 117–26. Kong VY, Oosthuizen GV, Sartorius B, Keene C, Clarke DL. An audit of the complications of intercostal chest drain insertion in a high volume trauma service in South Aftrica. Annals of the Royal College of Surgeons of England. 2014; 96: 609–13. Bing F, Fitzgerald M, Olaussen A et al. Identifying a safe site for intercostal catheter insertion using the mid-arm point (MAP). Journal of Emergency Medicine, Trauma and Acute Care 2017.Danny is an Emergency Medicine Registrar at the Emergency and Trauma Centre and the current Senior Registrar for research. He trained in regional NSW before moving back to Melbourne to complete his training at the Alfred. DR DANNNY MARHABA Emergency Registrar Danny is an Emergency Medicine Registrar at the Emergency and Trauma Centre and the current Senior Registrar for research. He trained in regional NSW before moving back to Melbourne to complete his training at the Alfred.


    Dr Binula Wickramarachchi & Dr Luke Phillips Welcome to our Unlocking the ACEM Exams blog posts where we unlock the key study habits, resources and top tips from recent successful exam candidates.  This week we got to sit down with Dr Binula Wickramarachchi who recently completed a successful sitting of the ACEM fellowship OSCE exam (2022.1). Binula outlines some of his key tips to success in the post below. DR BINULA WICKRAMARACHCHI Binula is an Emergency Advanced Trainee and Education Fellow at the Alfred Hospital. He grew up among the verdant hills of Auckland, New Zealand, obtaining his medical degree and Postgraduate Diploma in Clinical Education at the University of Auckland. He also has a passion for point of care ultrasound, particularly echo and lung ultrasound. At home, Binula is a devoted parent to his two feline daughters, and is the household co-lead for the acclimatisation to a new human child. "HOW DID YOU PREPARE FOR THE EXAM?" A frequent, consistent and supportive study group is a must Don't underestimate the value of repeating stations, especially a day or two following a good learning encounter Identify your deficiencies early and work on these. It can be easy to keep patting yourself on the back for something you're already good at Practice with a range of FACEM's, including newer and more experienced ones. It is especially helpful to practice with ones that will be more critical with you, but try to avoid this closer to the exam "WHAT ARE YOUR TOP TIPS FOR SUCCESS?" Be adaptable - many of the cases you will face in the exam, you won't have seen before, or will be presented in a different context/format. You have to be able to answer the questions that are presented, not necessarily what you have practiced. Practice speaking confidently, concisely and in a structured manner. Appropriate language has a huge effect on how you're perceived. "DO YOU HAVE AN PEARLS ABOUT REFINING YOUR EXAM TECHNIQUE?" Use the pace of your speech effectively: (i) Slow down for empathy, (ii) Speed up for factual information, (iii) Use silence appropriately when breaking bad news or giving complex information. Use reading time effectively: (i) Actively read the stem and extract all the information you can from it. (ii) This can help you to pre-empt where you think the station will go, but be careful to not assume too much, and to adapt if it turns an unexpected corner If props are provided, extract all relevant information from them outside the room. This way, you can focus on answering the questions in the station, rather than spend time interpreting inside the room. For example: (i) Do the blood gas calculations, (ii) Interpret the X-rays/ECGs fully. Do as many trial exams as possible - each one will make you that much more comfortable with the exam process. (i) Speak to your DEMT or OSCE exam facilitator about how to get involved in these. "ANY RESOURCES YOU WOULD RECOMMEND?" Comm's Lab with Dr Hayden Richards (YouTube) - This is a gold mine of really useful communication strategies. End of life discussions Don Liew's personal coaching and trial exams - I found the coaching very individualised and helpful in practicing to iron out my weaknesses. As above, the trial exam was great for further practice. Various online question banks available - get your hands on these early and organise them so practice comes easily. Speak to recent exam graduates about how to get ahold of these resources.

  • Ventilation of the Obese Patient

    Dr Niraj Mistry Emergency Registrar Peer review: Dr Nick Erskine Editor: Dr Dave McCreary THE CASE You’re on for resus in the middle of a night shift and you receive an alert for a shocked diabetic male with respiratory sepsis and DKA who has been intubated and will be arriving soon. Your initial reaction to this news probably wouldn’t worry you too much (aside from how severe the DKA must be to lead to a tube) knowing that the hard work has been done pre-hospital until the paramedic ends the call with a very casual, “Oh by the way the patient is 280kg.” Suddenly, managing the patient has become that much harder and you’re in for a night of complicated respiratory physiology and unexpected challenges. I recently encountered just such a situation and the myriad of problems I encountered during the case left a lasting impression that motivated me to share my experiences in this blog post. FIRST, WHAT IF THE PARAMEDICS HADN’T BEEN SO KIND AS TO TUBE THIS PATIENT FOR ME? Intubation of the morbidly obese patient is a high-risk situation. You need an experienced airway operator and there are some considerations to optimise pre-oxygenation. Schetz et al.(1) recommend: At least 5 minutes of non-invasive ventilation (NIV) in an upright seated position with positive end-expiratory pressure (PEEP) support of 5-10cmH20 (3). Apnoeic oxygenation via the addition of high-flow nasal cannula (NC) to pre-oxygenation with NIV provided more effective pre-oxygenation and subsequently less oxygen desaturation then NIV alone (4). Furthermore, simple manoeuvres to improve the positioning of the patient such as ramping will optimise your first-pass success when it comes to intubating these tricky airways. OBESITY, THE RESPIRATORY SYSTEM & MECHANICAL VENTILATION The main issue with this patient was optimising ventilation. After trialling various modes of ventilation and PEEP settings to little avail I can honestly say that at the end of the night the Hamilton ventilator and I were not the best of friends. The physiological changes to the respiratory system in obesity explain why ventilating can be so difficult in these situations. Including(2): Increased oxygen consumption and carbon dioxide production Increased work of breathing Increased intraabdominal and intrathoracic pressures Decreased compliance Decreased functional residual capacity Schetz et al. eloquently summarise the most effective intubation/pre-oxygenation and ventilation techniques in obese individuals as such: PROTECTIVE VENTILATION The key to mechanical ventilation is a protective ventilation strategy using low tidal volumes of 6ml/kg of ideal body weight (as our image above illustrates, inside every obese patient is the non-obese patient we're trying to ventilate) with moderate-to-high PEEP support of >10cmH2O. This approach improves respiratory mechanics, alveolar recruitment, and gas exchange (6). Whilst Schetz et al proposed using PEEP flows of 10 or more it should be noted one study found that PEEPs around this level were inadequate in minimising atelectasis and optimising ventilation in obese ICU patients, and PEEPs as high as 20 cmH2O significantly improved lung volumes and oxygenation (7). BEWARE OF HIGH PEEP FLOWS Much like the respiratory system, the cardiovascular system undergoes changes in obesity which are detrimental to the patient, including: Haemodynamic changes – increase blood volume and cardiac output leading to hypertension and left ventricular hypertrophy Myocardial fibrosis secondary to myocardial fat accumulation Coronary atherosclerosis Pulmonary hypertension and right ventricular failure These changes ultimately manifest in ventricular dilatation and heart failure (obesity cardiomyopathy) (8). Whilst using higher PEEPs sounds great on paper, because of these changes to the cardiovascular system it would be careless not to acknowledge the effects high PEEP flows will have on haemodynamics. At higher PEEPs there is an increase in intrathoracic pressure. This compresses the inferior vena cava resulting in decreased venous return to the heart and reduced ventricular filling, a lower end-diastolic volume and less myocardial stretch before systole. As described by (primary exam trigger warning) Starling’s Law, this will result in a weaker strength of myocardial contraction and therefore reduced stroke volume and cardiac output. Ultimately this manifests as lower blood pressure – a situation I encountered first-hand in this case; every time I increased the PEEP the mean arterial pressure would drop so much so that I had to immediately dial up the Noradrenaline! Whilst on the topic of haemodynamics in obese patients it is important to mention that non-invasive blood pressures are not reliable. Blood pressure cuffs of appropriate size may not be readily available, and even when used the blood pressure cuffs are inaccurate in obesity(9). As such invasive blood pressure monitoring with an arterial line is the standard for haemodynamically unstable obese patients and this task should be prioritised. PATIENT POSITIONING Simple changes here can work wonders towards combating some of the above problems and improve the effectiveness of your ventilation. The increased body habitus in these patients adds to the intrathoracic pressures so any technique to offload some of that mass off of the thorax should used. In ED the simplest manoeuvre is the reverse Trendelenburg position (Figure 1). In this position, gravity will redistribute the apron of the patient away from the thorax and reduce the intrathoracic pressure exerted by the body habitus and thus reduce the work of breathing. Figure 1: THE ULTIMATE REPOSITION - PRONING A trickier, but more effective approach, would be prone positioning. This is advocated as the positioning of choice when mechanically ventilating obese patients with ARDS. Prone positioning of obese patients has been shown to improve the ratio of arterial oxygen pressure to the fraction of inspired oxygen (PaO2/FiO2) (10). In others words, less oxygen was required to achieve satisfactory arterial oxygenation. Prone positioning provides this benefit because of the dynamic advantages it provides over supine positioning (Figure 2) (11): Decrease gravitational pressure of the heart and mediastinum on the lungs Decrease compressive effects of abdominal organs on the lungs More evenly spread chest wall compliance due to the restriction of the anterior chest wall movements Figure 2: Venus et al. CMAJ 2020. However the logistics of proning an unwell, intubated, morbidly obese patient in a busy Emergency Department need to be considered. Pushing the “tilt bed” button on the bed control is significantly easier and safer than proning, and should be the first port of call. [Ed. – proning even an average-build intubated patient is complicated and requires training and experience that generally isn’t available in the ED. Proning is great in theory, but let’s leave this one to the ICU team.] SUMMARY Morbidly obese patients present many challenges. High-risk procedures such as intubation and ventilation become even trickier in these patients and failure to acknowledge the cardiorespiratory physiological changes which occur in obesity will lead you down a path of frustration and danger. By focusing on the simple things such as the importance of positioning and applying some of the recommendations I have highlighted in this post the effectiveness to which you can intubate and then ventilate obese patients can be greatly improved. In the end, the 280kg patient I encountered on my night shift eventually found himself in ICU but not until I had the pleasure of battling these challenges, and learning a heap in the process. On a more positive note, the case did provide me with my first experience of using an inflatable air mattress to transfer an obese patient and the utilisation of this equipment is the final, but probably most entertaining, recommendation I have to share when it comes to looking after morbidly obese patients. [Ed – I’ve had to use this a couple of times including once for a peri-arrest 180kg patient on the floor of our triage – it was an absolute game changer]. References Schetz M, De Jong A, Deane AM, Druml W, Hemelaar P, Pelosi P, Pickkers P, Reintam-Blaser A, Roberts J, Sakr Y, Jaber S. Obesity in the critically ill: a narrative review. Intensive Care Med. 2019 Jun;45(6):757-769. doi: 10.1007/s00134-019-05594-1. Epub 2019 Mar 19. PMID: 30888440. De Jong A, Chanques G, Jaber S (2017) Mechanical ventilation in obese ICU patients: from intubation to extubation. Crit Care 21:63 Delay JM, Sebbane M, Jung B, Nocca D, Verzilli D, Pouzeratte Y, Kamel ME, Fabre JM, Eledjam JJ, Jaber S (2008) The effectiveness of noninvasive positive pressure ventilation to enhance preoxygenation in morbidly obese patients: a randomized controlled study. Anesth Analg 107:1707–1713 Jaber S, Monnin M, Girard M, Conseil M, Cisse M, Carr J, Mahul M, Delay JM, Belafia F, Chanques G, Molinari N, De Jong A (2016) Apnoeic oxygenation via high‐flow nasal cannula oxygen combined with non‐invasive ventilation preoxygenation for intubation in hypoxaemic patients in the intensive care unit: the single‐centre, blinded, randomised controlled OPTINIV trial. Intensive Care Med 42:1877–1887 Groombridge C, Chin CW, Hanrahan B, Holdgate A. Assessment of Common Preoxygenation Strategies Outside of the Operating Room Environment. Acad Emerg Med. 2016 Mar;23(3):342-6. doi: 10.1111/acem.12889. Epub 2016 Feb 17. PMID: 26728311. Pelosi P, Croci M, Ravagnan I, Cerisara M, Vicardi P, Lissoni A, Gattinoni L (1997) Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 82:811–818 Pirrone M, Fisher D, Chipman D, Imber DA, Corona J, Mietto C, Kacmarek RM, Berra L (2016) Recruitment maneuvers and positive end‐expiratory pressure titration in morbidly obese ICU patients. Crit Care Med 44:300–307 Piche ME, Poirier P, Lemieux I, Despres JP (2018) Overview of epidemiology and contribution of obesity and body fat distribution to cardiovascular disease: an update. Prog Cardiovasc Dis 61:103–113 Bur A, Hirschl MM, Herkner H, Oschatz E, Kofler J, Woisetschlager C, Lag‐ gner AN (2000) Accuracy of oscillometric blood pressure measurement according to the relation between cuff size and upper‐arm circumference in critically ill patients. Crit Care Med 28:371–376 De Jong A, Molinari N, Sebbane M, Prades A, Futier E, Jung B, Chanques G, Jaber S (2013) Feasibility and effectiveness of prone position in morbidly obese patients with ARDS: a case–control clinical study. Chest 143:1554–1561 Venus K, Munshi L, Fralick M. Prone positioning for patients with hypoxic respiratory failure related to COVID-19. CMAJ. 2020 Nov 23;192(47):E1532-E1537. doi: 10.1503/cmaj.201201. Epub 2020 Nov 11. PMID: 33177104; PMCID: PMC7721267. NIRAJ MISTRY Emergency Registrar Niraj is an emergency medicine doctor from the United Kingdom. He spent his childhood in the United States where he discovered his first love in life – basketball. He also has a weird fascination with numbers and has combined these two interests into an annual NBA Almanac which he publishes for free every year, you can find the latest edition here.


    DR HOLLY BANNON-MURPHY & DR LUKE PHILLIPS Welcome to our Unlocking the ACEM Exams blog posts where we unlock the key study habits, resources and top tips from recent successful exam candidates.  This week we go to to sit down with Dr Holly Bannon-Murphy who recently completed a successful sitting of the ACEM fellowship written exam (2022.1). Holly outlines some of her key tips to success in the post below. DR HOLLY BANNON-MURPHY Emergency Registrar Holly  is a dual emergency and ICU registrar. She has an interest in prehospital and global emergency medicine, and enjoys working in diverse places such as the Royal flying doctor service in central Australia and teaching trauma assessment in Chennai, India. She is an assistant editor for the Global emergency literature review and for the trainee edition of Emergency Medicine Australia journals. She loves travel, mountain biking, ski mountaineering and trail running. "HOW DO YOU PREPARE FOR THE EXAM?" I initially started just choosing a topic a week and reading through Dunn's and Cameron's textbooks and summarising them. I would recommend against this as a single tactic as I found it really ineffective. I changed tact around 4 weeks in and looked at the Geelong syllabus who do SAQs weekly. I did each of those every week and read around what I didn't know. I also did a topic a week of Dunn's but instead of summarising loads, I made Anki deck flashcards. I then started doing the Anki flash cards daily to revise as I went along for spaced repetition. "WHAT ARE YOUR TIPS FOR SUCCESS?" Continuity of study but have days off for the eventual fatigue. Factor in a week here and there to be a human being so you don't peak too early. "DO YOU HAVE ANY PEARLS ABOUT REFINING YOUR EXAM TECHNIQUE?" Just do a billion exam questions. You can find at least 80 past papers on doctors writing website. Do the questions and exam to time always from the beginning and learn to ditch superfluous words early. Make sure you keep up with your hospitals fellowship questions/programs and get them marked by experienced consultants. The more marked papers the better! Do lots of recall MCQs; they're always in the exam. "ANY RESOURCES YOU WOULD RECOMMEND?" Doctors writing website Geelong Exam Syllabus Anki (search for previous ACEM fellowship decks including Chris Parry's which was a great place to start). I'm also happy to pass on my deck. AFEM was good (was useful summarising course with the chance to do MCQ and SAQ to time).

  • Intractable Hiccups

    Dr Binula Wickramarachchi Emergency Physician Peer Review: Dr David McCreary THE CASE A 72-year-old man presents to the emergency department with persistent hiccups for 4 days. As you walk over to his cubicle, you think back to all the different ways you’ve tried to cure your own hiccups. What does holding your breath, drinking water upside down and getting frightened have in common anyway? AREN'T HICCUPS NORMAL? Hiccups are a normal everyday experience, usually attributed to a trigger such as a carbonated drink or spicy food. The vast majority of hiccups will last minutes to hours, and almost all benign cases of hiccups will last less than 48 hours. There are a number of theories as to the specific function of hiccups, with the most interesting being that it is a vestigial reflex, primarily involved in the maturation of the respiratory tract in utero. This is thought to be the reason that frequent hiccups in a foetus are a hallmark of the third trimester of pregnancy, as well as in the early neonatal weeks. WHAT ARE HICCUPS? Hiccups (AKA ‘singultus’ for those of you who are Latin-inclined) are spontaneous, involuntary and spasmodic contractions of the diaphragm and intercostal muscles, predominantly affecting the left hemidiaphragm. These spasms result in a sudden inspiration, which is immediately followed by the abrupt closure of the glottis, creating the onomatopoeic ‘hiccup’ sound. This process occurs in a reflex arc involving: An afferent limb: phrenic & vagus nerves and the sympathetic chain. A central mediator: thought to be within the medulla, near the respiratory centre. An efferent limb: the phrenic nerve, as well as neural connections to the glottis and inspiratory intercostal muscles. Anatomy of the hiccups reflux arc. M. Steger et al. 🤓 PHYSIOLOGY PEARL The sudden closure of the glottis is thought to be a protective reflex to prevent the hyperventilation that would result from hiccups. Patients with tracheostomies have been shown to develop hypocapnoea secondary to hiccups, as their airway bypasses the glottis. WHAT CAUSES HICCUPS? There are a multitude of causes of hiccups, but the underlying principle is that one or more parts of the above reflex arc are activated. This most commonly includes vagus or phrenic nerve activation due to gastro-oesophageal causes (gastric distension, GORD, gastritis, peptic ulcer disease or gastric cancer), but can also be due to inflammation or mass effect on these nerves anywhere in their course within the neck and thorax. Central nervous system aetiologies are also important to consider. Structural lesions such as tumour, aneurysm and vascular malformations in the medulla are of particular concern, and hiccups are specifically implicated in lateral medullary infarction. Hiccups in this category will however very rarely be an isolated symptom. The most significant consideration is that of malignancy. This can range from locally invasive gastro-oesophageal, pancreatic and lung cancers, to more advanced metastatic malignancies with significant thoraco-abdominal lymphadenopathy. The prevalence of hiccups in this population has been reported as high as 1 – 9%1. Other less frequent causes include: Medication-related Dexamethasone Diazepam, midazolam Tramadol Metabolic Hyponatraemia, hypokalaemia, hypocalcaemia & renal impairment Psychogenic These hiccups typically disappear during sleep Post-operative Related to irritation of the phrenic nerve ASSESSMENT Features on assessment that are important to elicit are: Characterise the hiccups and their effects – time course, relieving factors, effects on quality of life (eating, drinking and sleeping) Explore possible aetiologies – to exclude any treatable causes, as well as identify any features of malignancy Examination – seeking features of infection or inflammation in the head, neck, chest or abdomen. Paying particular attention to potential mass lesions or lymphadenopathy. Investigation with pathology and imaging can then be guided by the findings above. If the initial assessment is unremarkable, consideration should be given to initiating empirical treatment while further investigations are undertaken. If a patient is known to have advanced malignancy, the aetiology of intractable hiccups is likely multifactorial. It is generally recommended that the focus should be on symptomatic treatment of these patients, rather than exhaustive ongoing evaluation. MANAGEMENT The mainstay of treatment for hiccups of less than 48 hours is physical manoeuvres. Many of these will be familiar to us as home-cures for hiccups! These can be divided into: Inducing hypercapnia via breath-holding or breathing into a paper bag. This is thought to interrupt the hiccup reflex arc due to its effect on the medulla and the respiratory centre Stimulating the nasopharynx via drinking cold water, pulling on the tongue or performing a Valsalva. This increases vagal stimulation to interrupt the reflex arc. 🤓 FUN FACT The mechanism of frightening someone out of their hiccups is believed to occur due to the interruption of the reflex arc at the sympathetic chain, which forms part of the afferent limb of the arc. For those patients with hiccups for more than 48 hours, empirical pharmacological treatment can be initiated. The evidence base for the use of many of these are not well established. Both single-drug therapy as well as multi-modal therapies may also be trialled. The main options here are: Proton-pump inhibitors (PPI) Baclofen Gabapentin Metoclopramide Chlorpromazine Various other medications have also been trialled, with very variable reports of efficacy in the literature. Some of these options are: haloperidol, amitriptyline, pregabalin, phenytoin, sodium valproate and carbamazepine. THERE'S AN ALGORITHM FOR THAT... BACK TO THE CASE The patient tells you of their unfortunate recent diagnosis of advanced pancreatic cancer, and that they’re awaiting their initial oncology appointment in 2 days. The patient was started on regular pantoprazole and metoclopramide, with a plan for the oncology team to initiate baclofen if the hiccups had not resolved by the time of his oncology appointment. SIMPSONS CONSULT And finally, further proof that the Simpsons have always been ahead of their time and have an answer for everything... REFERENCES Calsina-Berna, A., García-Gómez, G., González-Barboteo, J., & Porta-Sales, J. (2012). Treatment of chronic hiccups in cancer patients: a systematic review. Journal of palliative medicine, 15(10), 1142-1150 Steger, M., Schneemann, M., & Fox, M. (2015). Systemic review: the pathogenesis and pharmacological treatment of hiccups. Alimentary pharmacology & therapeutics, 42(9), 1037-1050. Kahrilas, P. J., & Shi, G. (1997). Why do we hiccup?. Gut, 41(5), 712-713. Polito, N. B., & Fellows, S. E. (2017). Pharmacologic interventions for intractable and persistent hiccups: a systematic review. The Journal of Emergency Medicine, 53(4), 540-549. BINULA WICKRAMARACHCHI Emergency Physician Binula is an Emergency Physician at the Alfred Hospital. He grew up among the verdant hills of Auckland, New Zealand, obtaining his medical degree and Postgraduate Diploma in Clinical Education at the University of Auckland. He also has a passion for point of care ultrasound, particularly echo and lung ultrasound. At home, Binula is a devoted parent to his two feline daughters, and is the household co-lead for the acclimatisation to a new human child.


    DR LUKE PHILLIPS EMERGENCY PHYSICIAN PEER REVIEW: DR EANNA MAC SUIBHNE 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 23-year-old presents with knee pain and swelling post landing awkwardly on their right knee playing football. They now have pain and swelling to the knee and have difficulty weight bearing. On exam they have a large joint effusion and tenderness to lateral joint line. They can straight leg raise but any other assessment of knee joint integrity is limited by the swelling and pain. WHICH PATIENTS ACTUALLY NEED A KNEE X-RAY? Our Canadian friends, led by Stiell et al, have developed the Ottawa Knee Rule to identify low risk patients who may not need a knee X-ray. A knee x-ray series is only needed for knee injury patients with any of these findings: Age ≥ 55, OR Isolated tenderness of patella (no bone tenderness of knee other than patella), OR Tenderness of head of fibula, OR Inability to flex to 90°, OR Inability to bear weight both immediately after injury and in the ED for 4 steps (unable to transfer weight twice onto each lower limb regardless of limping. In an external validation study of the rule, the authors found a relative reduction in knee X-rays of 26.4% and a sensitivity of 100% for detecting knee fractures and a specificity of 48%. THE PATIENT MET CRITERIA FOR IMAGING AND X-RAYS WERE PERFORMED Case courtesy of Dr Luke Phillips, From the case rID: 99008 WHAT ARE THE KEY FINDINGS ON THESE X-RAYS? There is a moderate to large knee joint effusion. Avulsion fracture of the tibial spine at the distal ACL attachment. Avulsion fracture from the lateral knee capsule (Segond fracture)\ What is the significance of this fracture pattern? Segond fractures are avulsion fractures of the proximal-lateral tibia and represent a bony avulsion of the anterolateral ligament. It is associated with severe rotational instability of the knee. Identification of this finding on plain film radiographs should prompt further evaluation as they are rarely isolated injuries. They are pathognomonic for an Anterior Cruciate Ligament (ACL) tear, present in 75-100% of cases. Conversely, 9-12% of ACL ruptures have an associated Segond fracture. The presence of a tibial spine fracture and large haemarthrosis also indicates a likely ACL injury. EPONYMOUS OLD WHITE MAN ALERT Paul Ferdinand Segond (1851–1912) was professor of surgery at the University of Paris and surgeon in chief at the Saltpetriere. Although Segond was one of the foremost “knee specialists” in 19th century France, his significant contributions in this area were overlooked, and he is chiefly remembered for his contributions to gynaecologic surgery. WHAT ARE THE KEY MANAGEMENT OPTIONS? Management initially should be supportive, encouraging ice application, elevation compression and simple analgesia. Patients should be having restricted weight baring (initially using crutches but can toe touch, then progress to foot down if standing) and if there is complete knee instability or loss of extensor mechanism (ie patella fracture or quad/ patella tendon rupture) they should be provided with a Zimmer splint in the short term. They should be encouraged to retain some movement while sitting/ lying.  Gentle movement against gravity will help preserve quad strength, reduce effusion, retain range of movement & proprioception. Early Physio for “prehab” ("pre-op rehabilitation") is really important. This makes the operation easier and can  improve recovery in the longer term. Often patients will have operative management delayed until good ROM & strength similar (>90% of unaffected side). Patients should have an early orthopaedic referral for consideration of operative management including open repair of the fracture along with the ACL. There is no evidence for fixing the Segond fracture itself, any surgical intervention undertaken is aimed at repairing associated injuries. MRI will likely assist in further differentiating the injury and decision-making about ongoing management. Prognosis-wise, although Segond fractures are associated with a highly unstable knee, post-operative studies suggest no difference in tested stability after the ligamentous injury is addressed. Good news for our 23-year-old footballer! THE OUTCOME The patient was discussed with orthopaedics, discharged from the ED with a Zimmer Splint and was made non-weight bearing. A week later they underwent knee arthroscopy and repair of the tibial spine/ACL. The meniscus was intact. REFERENCES AND FURTHER READING: Davis DS, Post WR. Segond fracture: lateral capsular ligament avulsion. J Orthop Sports Phys Ther. 1997 Feb;25(2):103-6. doi: 10.2519/jospt.1997.25.2.103. PMID: 9007767. Shaikh H, Herbst E, Rahnemai-Azar AA, Bottene Villa Albers M, Naendrup JH, Musahl V, Irrgang JJ, Fu FH. The Segond Fracture Is an Avulsion of the Anterolateral Complex. Am J Sports Med. 2017 Aug;45(10):2247-2252. doi: 10.1177/0363546517704845. Epub 2017 May 12. PMID: 28499093. Arneja SS, Furey MJ, Alvarez CM, Reilly CW. Segond fractures: not necessarily pathognemonic of anterior cruciate ligament injury in the pediatric population. Sports Health. 2010 Sep;2(5):437-9 Filbay SR, Grindem H. Evidence-based recommendations for the management of anterior cruciate ligament (ACL) rupture. Best Practice & Research Clinical Rheumatology. 2019 Feb;33(1):33–47. 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 ( 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 Hector Thomson Emergency Registrar Peer review: Dr Binula Wickramarachchi While recent cases of Japanese Encephalitis have caught headlines, I recently stumbled across a disease I was embarrassed to say I had never heard of. My paediatric-trained colleagues all seemed to have heard of it, but I could scarcely find a mention in my ED textbooks, maybe because the diagnosis is never made downstairs and we call it viral meningitis pending a culture. With a waiting room full of kids with viral URTIs, I now have a new disease to look out for along with PIMS-TS. Let me tell you about some more scary capital letters: ADEM. So, what is ADEM? ACUTE DISSEMINATED ENCEPHALOMYELITIS (ADEM) ADEM is an autoimmune demyelinating disease of the central nervous system (CNS) which is monophasic (has a single occurrence) but multifocal in nature. So, lots of cool neurological signs but then they don’t go away; in contrast to MS, for example,  where they may fluctuate. It's most commonly seen in children, though adults can also be affected. It was first described by Mr James Lukas, a surgeon in Leeds in the 18th Century, as "uncommon symptoms succeeding the measles". CRITERIA FOR DIAGNOSIS All of the following are needed, along with reasonable exclusion of other possible neurological conditions: A first multifocal clinical CNS event of presumed inflammatory demyelinating cause Encephalopathy: stupor and/or lethargy or behavioural changes unexplained by fever, systemic illness or postictal symptoms An abnormal MRI brain during the acute phase (3 months) No new clinical or MRI findings >3 months after clinical onset CAUSE It isn’t clear what exactly causes ADEM but as with many autoimmune conditions, the current theory is that an infectious or environment trigger in a genetically susceptible child causes an autoimmune attack on the CNS resulting in demyelination. The disease typically starts with an abrupt onset within a day to weeks after a viral infection (75%) or immunisation. Common viruses (Epstein-Barr, measles, mumps, rubella, and Coxsackie B) are the most common pathogens associated with postinfectious ADEM. COVID has been reported as a cause but a review this year only found 31 reported cases. Bacterial triggers are rare and less than 5% of ADEM cases follow immunisation. These have most often been associated with the MMR vaccination. PRESENTATION The classic presentation is a 2-5 day prodrome where fever, nausea, vomiting, headache, and weakness may be present, followed by acute-onset, rapidly progressive encephalopathy and multifocal neurological symptoms. Encephalopathy comprises change in behaviour and/or conscious state and can range from lethargy and irritability to coma. A wide variety of neurological deficits can be manifested, determined mainly by the localization of lesions.  80% will have a motor deficit, 50-60% ataxia, and up to 50% will have a cranial nerve deficit with optic neuritis, often bilaterally. Yes, that means you have to go find the tendon hammer and try and get those grumpy toddlers to walk for you! Systemic features are common, with fever (50%), headache (40-50%) and vomiting (30%) occurring frequently. 10-30% will have seizures and case series have shown between 3-25% have concurrent spinal cord involvement. UK data suggests 25% of children with ADEM will need ICU level care. The majority of cases follow a monophasic course, but patients may have recurrence of initial symptoms (recurrent ADEM) or a second episode (multiphasic ADEM). EPIDEMOLOGY ADEM can occur at any age but is most common in children (mean age 5–8 years old), with a slight male predominance. Tracking the rate of ADEM is difficult as the majority of paediatric encephalitis hospitalisations never have a cause identified. Australian data identifies the incidence of ADEM at 0.68-0.79 per 100 000 person years in people aged < 14. Higher than quoted numbers in the US, UK and Asian countries. INVESTIGATIONS The diagnosis of ADEM is clinical but MRI seems to be the most important investigation. T2 and FLAIR sequences will show multiple areas of demyelination in the brain and spine. CT is not sensitive and can be reported as normal.  Lumbar puncture may show pleocytosis and increased protein. EEG may show non-specific diffuse or less commonly focal slowing of background activity. Someone may ask you to order MOG IgG and aquaporin-4 (AQP4) IgG serum autoantibody. For me, these go into the bag of the “did ya” tubes. 🤓 DEFINITION: “DID YA” TUBES. A Hectorism. When taking blood, the process of storing excess in a serum storage tube in anticipation of a specialty registrar calling you back to ask for extra tests they have just read about on UpToDate. DIFFERENTIAL In the emergency department, you will be faced with an encephalopathic child with focal neurology. The important differential to rule out in these children is acute CNS infection and these children should always be covered with antibiotics and antivirals. The list of differentials is extremely long. The consensus guidelines for investigation of encephalitis list hits every major disease group. Other key things to rule out are: Space occupying lesion Traumatic brain injury Metabolic encephalopathy Seizure disorder It may be useful to frame this rare disease with something more familiar. Doesn’t this so far just sound like MS? Well yes, but there are important differences. The most relevant being that in MS there should not be any features of encephalopathy. Image courtesy of: Dale RC, Branson JA Acute disseminated encephalomyelitis or multiple sclerosis: can the initial presentation help in establishing a correct diagnosis? Archives of Disease in Childhood 2005;90:636-639 TREATMENT Corticosteroids are the established first-line therapy (this is neurology, after all). There are no RCTs, but small paediatric case series dictate the standard protocol as being IV methylprednisolone followed by oral prednisolone for 4 weeks. The use of immunoglobulin and plasmapheresis have only been published in very small case series in children, and mostly in those that have not responded to steroids. PROGNOSIS The good news is that thankfully, most of these kids do very well. 65-85% of paediatric ADEM patients have a good functional outcome and improvement is usually seen within a few days of starting treatment. Whether this is just the natural course of the illness or due to the steroids is a point of debate. Mild neurocognitive deficits and behaviour problems are not uncommon, with children younger than 5 being at higher risk. SCARY FORM In a small proportion, the course is more fulminant, frequently resulting in death. In such cases, the lesions may demonstrate haemorrhage and the condition is then known as acute haemorrhagic leukoencephalitis (Hurst disease). This disease appears to have overlap with cerebral vasculitis. ED PERSPECTIVE I don’t think we should, or are likely to be making this diagnosis. It definitely helps to know it exists, though. In the 4-year-old with irritability and focal neurological findings our job is to not send them home, empirically treat dangerous infections and facilitate appropriate investigations. Accessing sedation and imaging lists can be challenging for inpatient teams, so do your best to help with facilitating these, and advocate for these patients. I’m going to try and remember this as the drunk toddler who just got over a cold. Irritable, staggering around and can’t see straight. TAKE HOME MESSAGES ADEM often presents 1-4 weeks after a febrile illness Do your best to do a complete a neuro exam on the irritated toddler – focal findings should make you stop and think hard about not just “another URTI” ADEM remains a clinical diagnosis, however, early MRI is key for early diagnosis and prompt initiation of treatment. We should do our best to help facilitate these tests Empirically give antibiotics and antivirals ADEM is treated with high dose steroids +/- IVIG or plasmapheresis REFERENCES / WANT TO READ MORE? GUIDELINES Krupp LB, Tardieu M, Amato MP, Banwell B, Chitnis T, Dale RC, et al. International pediatric multiple sclerosis study group criteria for pediatric multiple sclerosis and immune-mediated central nervous system demyelinating disorders: revisions to the 2007 definitions. Mult Scler. 2013;19(10):1261–7. Britton PN, Eastwood K, Brew B, Nagree Y, and Jones CA. Consensus guidelines for the investigation and management of encephalitis. Med J Aust 2015; 202 (11): 576-577. || doi: 10.5694/mja14.01042 Filippi, M., Rocca, M.A. (2020). Acute Disseminated Encephalomyelitis. In: White Matter Diseases . Springer, Cham. doi: 10.1007/978-3-030-38621-4_5 CASE SERIES McLendon LA, Rao CK, Da Hora CC, Islamovic F, Galan FN. Post-COVID-19 Acute Disseminated Encephalomyelitis in a 17-Month-Old. Pediatrics. 2021 Jun;147(6):e2020049678. doi: 10.1542/peds.2020-049678. Epub 2021 Mar 24. PMID: 33762311. Huynh W, Cordato DJ, Kehdi E, Masters LT, Dedousis C. Post-vaccination encephalomyelitis: literature review and illustrative case. J Clin Neurosci. 2008 Dec;15(12):1315-22. doi: 10.1016/j.jocn.2008.05.002. Epub 2008 Oct 30. PMID: 18976924; PMCID: PMC7125578. Bisker Kassif, O., Orbach, R., Rimon, A., Scolnik, D., & Glatstein, M. (2019). Acute disseminated encephalomyelitis in children - clinical and MRI decision making in the emergency department. The American Journal of Emergency Medicine, 37(11), 2004–2007. doi: 10.1016/j.ajem.2019.02.022 Absoud M, Parslow RC, Wassmer E, Hemingway C, Duncan HP, Cummins C, Lim MJ; UK & Ireland Childhood CNS Inflammatory Demyelination Working Group and the the Paediatric Intensive Care Audit Network. Severe acute disseminated encephalomyelitis: a paediatric intensive care population-based study. Mult Scler. 2011 Oct;17(10):1258-61. doi: 10.1177/1352458510382554. Epub 2010 Sep 27. PMID: 20876155. George T, Basin A, Avva U, Taylor M, Muhammed J, Ogedegbe C. Early Recognition and Treatment of Acute Disseminated Encephalomyelitis in Pediatrics: A Case Series. Pediatr Emerg Care. 2019 Apr 9. doi: 10.1097/PEC.0000000000001771. Epub ahead of print. PMID: 30973501. Tenembaum S, Chamoles N, Fejerman N. Acute disseminated encephalomyelitis: a long-term follow-up study of 84 pediatric patients. Neurology. 2002;59(8):1224–31 Ravaglia S, Piccolo G, Ceroni M, Franciotta D, Pichiecchio A, Bastianello S, et al. Severe steroid-resistant post-infectious encephalomyelitis: general features and effects of IVIg. J Neurol. 2007;254(11):1518–23. Keegan M, Pineda AA, McClelland RL, Darby CH, Rodriguez M, Weinshenker BG. Plasma REVIEWS Leake JA, Albani S, Kao AS, Senac MO, Billman GF, Nespeca MP, Paulino AD, Quintela ER, Sawyer MH, Bradley JS. Acute disseminated encephalomyelitis in childhood: epidemiologic, clinical and laboratory features. Pediatr Infect Dis J. 2004 Aug;23(8):756-64. doi: 10.1097/01.inf.0000133048.75452.dd. PMID: 15295226. Berzero G, Cortese A, Ravaglia S, Marchioni E. Diagnosis and therapy of acute disseminated encephalomyelitis and its variants. Expert Rev Neurother. 2016;16(1):83–101. Koelman DL, Mateen FJ. Acute disseminated encephalomyelitis: current controversies in diagnosis and outcome. J Neurol. 2015;262(9):2013–24. Britton PN, Khoury L, Booy R, et al. Encephalitis in Australian children: contemporary trends in hospitalisation. Archives of Disease in Childhood 2016;101:51-56. 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.

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