Dr Hector Thomson Emergency Registrar Peer review: Dr Binula Wickramarachchi Babies do lots of funny movements. As an ACEM trainee working in a paediatric ED one of my greatest joys is learning all the cool baby reflexes from my RACP colleagues - fencing posture is my favourite so far! THE CASE In a recent shift as the waiting room doctor, I saw a 7-month-old who had been doing some “funny movements” over the past few weeks. They were happening more frequently and now interrupting feeds. She looked like a happy and well baby in the waiting room. Then the mum pulled up the videos she had taken. The little baby would suddenly throw its arms out and cry every few seconds. SO, WHAT IS GOING ON? Infantile spasms. These are a rare, but serious type of seizure, occurring in 1 in 2,000 children. The onset of IS peaks between 4 and 6 months, although these seizures can begin anytime in the first two years. 🤓 SIDE NOTE: HISTORY LESSON 🤓 English physician Dr W. J. West first described infantile spasms in 1840 with a letter to the Lancet outlining what he had observed in his own son. “The child is now near a year old; was a remarkably fine, healthy child when born, and continued to thrive till he was four months old. It was at this time that I first observed slight bobbing of the head forward, which I then regarded as a trick, but were, in fact, the first indications of disease; for these bobbings increased in frequency, and at length became so frequent and powerful, as to cause a complete heaving of the head forward toward his knees, and then immediately relaxing into the upright position, these bowings and relaxings would be repeated alternately at intervals of a few seconds, and repeated from ten to twenty or more times at each attack, which attack would not continue more than two or three minutes; he sometimes has two, three, or more attacks in the day; they come on whether sitting or lying; just before they come on he is all alive and in motion, making a strange noise, and then all of a sudden down goes his head and upwards his knees; he then appears frightened and screams out; at one time, he lost flesh, looked pale and exhausted, but latterly he has regained his good looks, and, independent of this affection, is a fine grown child.” WHAT DO THE MOVEMENTS LOOK LIKE? The seizures include repetitive, but often subtle movements. Typically sudden flexor or extensor spasms of the head, neck, trunk or extremities May include head nodding or facial or eye movements Commonly symmetrical, but may be asymmetric Often cries before or after Each event lasts 1-2 seconds, but these can cluster together, occurring every few seconds for periods of several minutes. Most commonly shortly after waking from sleep You can watch the YouTube clip of this gif here, or some further examples (including some that are pretty subtle) can be seen in videos here and here. DIFFERENTIAL DIAGNOSIS Non-epileptic episodes such as shuddering and benign myoclonus of infancy Benign myoclonic epilepsy of infancy Other infantile epilepsies POSSIBLE CAUSES Tuberous sclerosis complex -> Look for skin lesions Trisomy 21 -> Examine for dysmorphic features and ask about perinatal screening Genetic causes -> Ask about family history of seizures/Development delay Focal structural abnormalities -> Ask about early handedness Perinatal hypoxic-ischaemic encephalopathy -> Ask about perinatal complications Ask about milestones and chart the patient's head circumference. Source: https://dermnetnz.org/topics/tuberous-sclerosis COMPLICATIONS Associated with developmental delay in 80% of infants High rates of ongoing epilepsy SIDE NOTE: WHAT IS WEST SYNDROME? Described by our friend, Dr William James West (from your history lesson, above). West Syndrome is a triad (all good eponyms are) of: Infantile spasm Hypsarrhythmia on EEG Developmental arrest/regression Not all children with infantile spasm will have all features of West Syndrome. DIAGNOSIS 🚨 Suspicion needs an urgent neurology review - this is a neurological emergency - wake up on-call people for this 🚨 Urgent EEG Prompt MRI brain Other investigations for the underlying aetiology (if unknown), including: Chromosomal microarray Urine metabolic screen Consideration of other genetic testing TREATMENT This will be guided by the neurologists but first-line is high dose prednisolone Prompt treatment is required to minimise the adverse developmental impact Vigrabatrin is first-line in infants with Tuberous Sclerosis Complex ☝️ Practice Point: High dose prednisolone treatment is associated with increased risk of serious and/or opportunistic infections - if these kids present febrile or unwell, manage as sepsis. CASE CONCLUSION The baby got an urgent EEG in the ED which showed the classic hypsarrhythmia. They were admitted under the neurology team and high dose steroids commenced. Over the coming weeks the spasms decreased in frequency. TAKE HOME POINTS: If a picture is worth a thousand words, then a video is worth a million. Look for typically sudden, brief, bilateral and symmetric contraction of the muscles of the neck, trunk and extremities, occurring in clusters Infantile spasm requires an urgent neurology review and EEG Treatment is high dose steroids Early recognition and treatment can minimise developmental impact INFANTILE SPASMS AWARENESS WEEK Infantile Spasms Awareness Week (ISAW) is held annually on December 1-7. During ISAW 2017, the ISAN introduced the "STOP Infantile Spasms" mnemonic, an easily remembered acronym, to raise awareness about this rare, yet serious seizure disorder. Source: https://www.epilepsy.com/learn/types-epilepsy-syndromes/infantile-spasms-west-syndrome#West-Story USEFUL RESOURCES RCH CPG: https://www.rch.org.au/clinicalguide/guideline_index/Infantile_Spasms/ Epilepsy Foundation: https://www.epilepsy.com/article/2020/11/infantile-spasms-awareness-week Dermnet: Tubular sclerosis: https://dermnetnz.org/topics/tuberous-sclerosis OTHER FOAMED CONTENT EMC Cases: https://emergencymedicinecases.com/em-quick-hits-april-2022/ REFERENCES Hancock EC, Osborne JP, Edwards SW. Treatment of infantile spasms. Cochrane Database of Systematic Reviews 2013, Issue 6. Art. No.: CD001770. doi: 10.1002/14651858.cd001770.pub3 Wilmhurs JM, Ibekwe RC, O’Callaghan FJK, Epileptic spasms – 175 years on: Trying to teach an old dog new tricks. Seizure 44(2017) 81-86. doi: 10.1016/j.seizure.2016.11.021 West WJ. On a peculiar form of infantile convulsions. Lancet. 1841;1:724–725 doi: 10.1016/S0140-6736(00)40184-4 (that's right, a doi for an 1841 article) 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.

Dr Hector Thomson Emergency Registrar Peer review: Dr David McCreary On a recent anaesthetic rotation during a paeds ENT list I heard a delightful description of laryngospasm. “Oh they are just a little squeaky… give them some PEEP it’ll be fine.” I immediately thought of the Toy Story 2 character, Wheezy, the adorable penguin who gets put on the shelf when his squeaker is broken! He tries squeaking for help but no one can hear him and the dust aggravates his condition! It took me a fair few lists before I stopped fearing the squeak! WHAT IS LARYNGOSPASM? Laryngospasm is a potentially life-threatening closure of the true vocal cords resulting in partial or complete airway obstruction. This is a primitive protective airway reflux that aims to protect against aspiration but can cause life-threatening hypoxia. ANATOMY REVISION In laryngospasm, either the true cords alone or the false cords slam shut and close the glottis. Most laryngeal reflexes are produced by stimulation of the superior laryngeal nerve which provides sensory innervation to the supraglottic region. This is a branch of the vagus nerve. The muscles involved are the lateral cricoarytenoid and thyroarytenoids (the adductors) and the cricothyroid (the vocal cord tensors). The cricothyroid muscle is the only tensor of the vocal cords. Gentle pressure from a jaw thrust may overcome moderate laryngospasm. The AIME Airway Course website has some amazing videos and images on airway anatomy. The vocal cords are white and triangular. Anteriorly sits the epligottis, laterally the aryepiglottic folds and posteriorly the cuneiform and corniculate tubercles and the interarytenoid notch. WHAT CAUSES IT? Local causes: Extubation: children with URTI symptoms (beware the snotty child) Airway manipulation (especially when under light anaesthesia) ENT procedures (usually involve lots of suctioning and prodding around the airway!) Secretions/blood/vomit in the airway Foreign body Near drowning Systemic causes: Drugs (rarely associated with ketamine sedation) Tetanus Hypocalcaemia Vocal cord dysfunction Risk factors: Past history of same Asthma Smoking GORD Recent URTI In the ED we will encounter this while performing procedural sedation. The feared situation being IM ketamine sedation and then laryngospasm that doesn’t settle with first-line measuring—leading to a scramble to gain IV access. There is also a case report from RCH of a case during nitrous oxide sedation. 🤓 TOP TIP: Give your ketamine slowly to reduce complications (Credit: Dr Shaun Baxter) Ed: In particular, this avoids the 'stunned apnoea' that a fast push can cause - which can cause some 🤨  in the room. HOW COMMON IS IT? Most of the studies are in the operating room. Bellolio in 2016 reported the rate of laryngospasm in ED procedure sedation is about 1.1 per 1,000 adult patients. In kids, it is estimated around 3.9 per 1,000 sedations and almost all were in ketamine sedations. 🤓  Ed: Andy Neill and I reviewed this 2017 paper by Bhatt et al. on the RCEMLearning Podcast back in February 2018. Of note this big dataset of over 6000 procedures from 6 tertiary paediatric emergency departments in Canada found the rate of laryngospasm to be a mere 0.1% (4 events overall). HOW DO WE RECOGNISE IT? Laryngospasm exists on a spectrum from partial to complete obstruction and occasionally presents atypically and without warning signs 🚨 Early warning = Loss of end-tidal CO2 🚨 Exam findings Inspiratory stridor/airway obstruction Increased inspiratory efforts/tracheal tug Paradoxical chest/abdominal movements Complete obstruction: No chest wall movements No airway sounds Inability to ventilate Late signs: Desaturation Bradycardia Central cyanosis In 189 cases reported to the Australian Incident Monitoring Study: 77% were clinically obvious 14% presented as airway obstruction 5% as regurgitation 4% as desaturation MY APPROACH Pause: Proceduralist stop the procedure Personel: Call for help – the situation can rapidly deteriorate An airway crisis needs a team and you will need but a team leader and an expert to manage the airway + drugs drawn up and equipment prepared Position: Jaw thrust/Chin lift + Suction blood and secretions Peep:100% O2 via mask with PEEP valve Consider a guedel airway Pressure point: Larson's point bilaterally while forming jaw thrust Propofol: 0.5mg/kg IV to deepen sedation/anaesthesia If rapidly developing hypoxia proceed to next step Paralyse 1.5mg/kg IV and intubate -> 3-4mg/kg IM has been suggested but remember you can put an IO in quickly Give atropine 20mcg/kg as bradycardia can develop with hypoxia. The anaesthetic approach has been suggested to get a low dose suxamethonium to break the spasm. My thought is if I am giving a paralytic for laryngospasm it is an airway emergency requiring intubation. WHAT COMPLICATIONS CAN ARISE? Desaturation (60%) Bradycardia (6%) Negative pressure pulmonary oedema (4%) Aspiration (3%) Cardiac arrest (0.5%) Ischaemic brain injury Death SIDE NOTE - WHERE IS LARSON'S POINT? In 1998 Dr Larson credits a Dr N. P Guadagni with showing him the technique 40 years earlier. Seems a bit rough for Dr Guadagni that he doesn’t at least get a partial naming credit! He describes the position as: “This notch is behind the lobule of the pinna of each ear. It is bounded anteriorly by the ascending ramus of the mandible adjacent to the condyle, posteriorly by the mastoid process of the temporal bone, and cephalad by the base of the skull. The therapist presses very firmly inward toward the base of the skull with both fingers, while at the same time lifting the mandible at a right angle to the plane of the body (i.e., forward displacement of the mandible or “jaw thrust”). Properly performed, it will convert laryngospasm within one or two breaths to laryngeal stridor and in another few breaths to unobstructed respirations.” Larson admits he doesn’t have a good scientific reason for why it works but postulates it may be forward displacement of the mandible, severe pain from the pressure applied to the facial nerve or even the glossopharyngeal nerve through the parotid. Image: from Larson’s original paper PREPARATION Don’t Forget the Bubbles have a fantastic section on procedural sedation. In it, they include a flowchart to be filled out for every patient prior to sedation. All the paediatric anaesthetists I worked with would check they had sux and atropine to hand and some would draw up emergency drugs to ward off the evil laryngospasm spirits. In ED I think this is a bit of a waste of medications but for every procedural sedation, I ensure I have sux, atropine and adrenaline to hand along with needles to draw them up. 🤓  Ed: I don't have the drugs drawn up (massive waste given the frequency of the event), and I don't have them on the side either. I do, however, specifically run through the steps we'd take for a laryngospasm event with the nursing staff as part of the pre-procedure timeout and in that I include that I could ask for sux and they should have eyeballed it and know where to get it immediately if needed. Source: Don't Forget The Bubbles SO REMEMBER – JUST STAY CALM AND DON’T FEAR THE SQUEAK! REFERENCES FOAMED RESOURCES First10 EM Don't Forget The Bubbles Life in the Fast Lane McCreary D, Neill A. NewinEM - Risk Factors for Adverse Events in Emergency Department Procedural Sedation for Children. RCEMLearning Podcast February 2018. PAPERS Hernández-Cortez E. Update on the management of laryngospasm. J Anesth Crit Care Open Access. 2018;8(2):1–6. DOI: 10.15406/jaccoa.2018.08.00327 N D’souza, R Garg. Perioperative Laryngospasm - Review of literature. The Internet Journal of Anesthesiology. 2008 Volume 20 Number 1. Laryngospasm With Apparent Aspiration During Sedation With Nitrous Oxide Babl, Franz E. et al. Annals of Emergency Medicine , Volume 66 , Issue 5 , 475 – 478. doi: 10.1016/j.annemergmed.2015.04.029 Bellolio MF, Gilani WI, Barrionuevo P. Incidence of Adverse Events in Adults Undergoing Procedural Sedation in the Emergency Department: A Systematic Review and Meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 23(2):119-34. 2016. doi: 10.1111/acem.12875 Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: laryngospasm. Qual Saf Health Care. 2005 Jun;14(3):e3. doi: 10.1136/qshc.2002.004275. PMID: 15933300; PMCID: PMC1744026. Al-Metwalli RR, Mowafi HA, Ismail SA. Gentle chest compression relieves extubation laryngospasm in children. J Anesth. 2010;24(6):854-857. doi: 10.1007/s00540-010-1036-9 Philip C. Larson; Laryngospasm-The Best Treatment . Anesthesiology 1998; 89:1293–1294 doi: 10.1097/00000542-199811000-00056Hector (the one on the left) is an Emergency Medicine Advanced Trainee at The Alfred. He's still clinging to the basic science knowledge he gained during primary exam prep and enjoys shoulder dislocations, trauma, rugby union, fresh pasta and good gin. He doesn't like vague allergies or cats. HECTOR THOMSON Emergency Registrar Hector (the one on the left) is an Emergency Medicine Advanced Trainee at The Alfred. He’s still clinging to the basic science knowledge he gained during primary exam prep and enjoys shoulder dislocations, trauma, rugby union, fresh pasta and good gin. He doesn’t like vague allergies or cats.

Dr Luke Phillips Emergency Physician Peer review: Dr David McCreary Welcome to Fast Fridays – a case-based, rapid review of a topic. The cases have been adapted from real patients but have been changed for anonymity and to emphasise key learning points. THE CASE An 84-year-old presents with a 4-day history of cough, shortness of breath and some fevers/lethargy. Family report that they have had decreased oral intake throughout that time and have had polyuria. They have a history of Type 2 DM (insulin-requiring) and their BSL is reading “high”. BASED ON THE ABOVE, WHAT DO YOU THINK IS HAPPENING? I am concerned that this patient has a developing or established hyperglycaemic hyperosmolar state (HHS) that is likely precipitated by chest sepsis (or COVID... it is 2022). I need to look for other precipitants of a HHS such as a myocardial infarction, surgical/GI issue that leads to excessive vomiting, evidence of stroke or intracranial pathology, any recent steroid use or compliance/changes with medications. I WISH IT WAS STILL CALLED HONK, BUT WHAT IS HHS? HHS is characterised by hypovolaemia, hyperglycaemia (>30mmol/L), mild or absent ketonaemia (Ketones < 3mmol) and a high osmolality (>320mOsm/kg). It differs from DKA due to its insidious onset and its pathophysiology is caused by a combination of reduced ability to utilise glucose and a disease state causing elevated counter-regulatory hormones (aggh – primary exams 🤯) leading to gluconeogenesis and glycogenolysis. The result is hyperglycaemia and an osmotic diuresis. You send some bloods. A formal glucose (it came with a bowtie 🤵‍♂️) is 40mmol/L and blood ketones are 2 mmol/L. Your venous blood gas is outlined below. WHAT ARE YOUR MANAGEMENT PRIORITIES? This process has happened over days, so you don’t want to correct everything too quickly. The principles of managing HHS are outlined below. Identify and Reverse the Underlying Precipitant Replace Fluid Deficits: Initial resuscitation may be needed to restore the circulating volume with 0.5-1L Normal Saline boluses. Then gentle rehydration to restore the deficits over the coming 24-48hrs. Rapid correction of this deficit can lead to osmolar shifts and cerebral oedema. Our hospital guidelines recommend normal saline for this. 45% sodium chloride can be considered if the osmolality is not declining despite a positive fluid balance and the fall in glucose at a rate of 4-6mmol/L per hour is not being achieved. 3. Electrolyte Monitoring and Replacement: Aim to lower osmolality by 3-8mOsm/kg per hour Sodium should not be lowered more than 10mmol in a 24hr period Commence potassium replacement early – Aim for K+ > 4mmol/L 4. Insulin Therapy: Commence an insulin infusion at 1-3 units/hr as per your local guidelines. Insulin should only be started after fluid hydration underway, and the serum potassium is > 3.5mmol/L Consider starting earlier if ketones > 1mmol/L Commence on 5% dextrose when BG < 15mmol/L 5. Ongoing Monitoring: This patient should be stabilised and monitored in a high-dependency area with cardiac monitoring. The patient needs hourly BSL and venous blood gas for the first 6 hours then stretch the time frame of these, depending on the patient’s condition. Close monitoring of urine output is also important to measure ongoing losses. ICU may be needed for patients with severe HHS, challenging to manage co-morbidities such as cardiac or renal failure or if they are frailer. 6. Thromboprophylaxis: Similar to your DKA patients, HHS patients are at high risk for developing venous thromboembolic events. THE OUTCOME Our patient was identified as having a missed anterior myocardial infarct with evidence of an established infarct on their ECG and a high-sensitivity troponin of 12000. A chest x-ray revealed evidence of pulmonary oedema, and this was confirmed with bedside ultrasound where there was widespread anterior B-lines and small effusions and a septal akinesis on echo. The patient was started on the above therapy and transferred to ICU for ongoing care given challenges with fluid management. During their inpatient stay they had an angiogram which confirmed mid LAD lesion, and this was stented, and they were eventually transferred to a rehab facility for cardiac rehab. REFERENCES AND FURTHER READING: Life in the Fast Lane: https://litfl.com/hyperosmolar-hyperglycemic-state/ Pulse Notes: https://app.pulsenotes.com/medicine/diabetes/notes/hhs Emergency Medicine Cases: Ep 147 HHS Recognition and ED management LUKE PHILLIPS Emergency Physician Dr Luke Phillips is an Emergency Physician at Alfred Health who has moved to the greener climes of Ireland. He is a passionate educator and has been fortunate enough to be able to combine this with his love of emergency ultrasound. Luke has a special interest in the use of focused ultrasound for critically unwell patients, in trauma management and in the use of ultrasound to guide procedures and improve patient safety in the ED. He is currently the Co-Chair of the Emergency Medicine Ultrasound Group (EMUGS.org) Board of Directors and holds a number of CCPU units through ASUM. Luke is also involved in the department’s international education program and has developed a Certificate of Emergency Medicine which is currently being run in both Germany and India. He also has interests in human factors, debriefing (particularly after clinical events), and simulation. His Twitter handle is @lukemphillips.

Dr Nick Erskine Emergency Registrar Peer review: Dr Luke Phillips You're working in a busy metropolitan ED. Your registrar colleague is currently cracking a chest open, the consultant is delivering a baby via resuscitative hysterotomy, and the intern in the next bay over is about to intubate someone in respiratory arrest. You sigh as you go to see the seizing patient who is flailing, arching their back and pelvic thrusting like they're doing the "Time Warp". "🙄 Pseudoseizures," you think to yourself... Let's fight the eye roll and take a closer look at what's going on with this patient...and we'll start with getting our nomenclature correct: what we suspect here is a Psychogenic Non-Epileptiform Seizure (PNES). HOW DO CLINICIANS AND PATIENTS FEEL ABOUT PNES? Perhaps an extreme example, but we know that healthcare providers carry preconceptions about functional seizures, and mostly receive little (or no) training about them.  A systematic review of healthcare providers' perceptions of psychogenic non-epileptiform seizures (PNES) showed five consistent themes[1]: We feel uncertain about the diagnosis and treatment of PNES, We think of PNES as a purely "psychological problem", We find patients with PNES "challenging and frustrating", We don't know who is responsible for treating patients long-term, and We think PNES is more deliberate/voluntary and less debilitating than epilepsy. Meanwhile, a meta-analysis of patients' experiences[2] showed that they felt: Frustrated in the diagnostic process, That communication of the diagnosis was poor and "difficult to make sense of", That their voice was "not heard" or not "taken seriously", That interactions with healthcare providers caused "considerable distress and persistent rumination" and were "not effective or supportive", That they perceived their condition as physical, and That they had lost their "freedom or independence" and that their condition markedly affected their lives. A somewhat damning assessment of us clinicians who swore to "first do no harm". So let’s tackle the nebulous beast that is functional seizures. A BIT OF HISTORY… To first address the ever-changing nomenclature: In the 19th century it was called "major hysteria", in the 20th it was "pseudoseizures". The early 21st century labelled it "psychogenic non-epileptiform seizures" and lately it has been moving towards either "functional seizures", "functional attacks", or "dissociative seizures". While the specific wording is up for debate, the general trend has been to move away from blaming the patient and more towards focussing on the functional impact the condition has. Like most of neuropsychology, the aetiology isn't yet clear. If you cut open a cadaver and squeeze its heart you can gain a reasonable understanding of how it works. Squeezing a cadaveric brain, however, just leads to a squashed cadaveric brain. The current proposed integrative cognitive model of psychogenic non-epileptic seizures[3] involves internal and external cues, threat perception, elevated arousal, inhibitory processing dysfunction, and a "seizure scaffold" shaped by remote patient factors like prior trauma. The end result is an involuntary state of reduced arousal and dissociation, frequently accompanied by seizure-like activity. Explaining it in a blog post for clinicians is hard enough, let alone to a distressed patient in a busy emergency department. The most readily understandable explanation I have come across is one proposed by Stone et al[4]. They describe epileptic seizures as a "hardware problem" – an abnormal electrical discharge that we can capture on an EEG. Non-epileptiform seizures, on the other hand, are a "software problem" characterised by dissociation or reduced arousal. From a patient perspective, the end result is the same though - your iPhone won't turn on, which sucks. SO, IN A PRACTICAL SENSE, WHAT DOES ALL THIS MEAN? Well for starters (as demonstrated by the paragraphs of preamble) - this is not an easy area of medicine. Not for us as clinicians, and certainly not for patients - 75% of whom actively resist the diagnosis<1>. Even making the diagnosis is easier said than done. Definitively diagnosing PNES may require repeat examinations, expert epilepsy assessment, and video EEG. Importantly there is no single clinically pathognomonic feature of PNES. Frontal lobe seizures can present with bizarre semiology and mimic a lot of the "classic pseudo seizure signs." And medial frontal, and amygalic epileptic foci are also not well detected on routine scalp EEG - so a "normal" video EEG may be insufficient. ☝️ PRACTICE POINT: If in doubt, reach for the benzos and levetiracetam. The presumption is therefore that all seizure activity is epileptiform until a functional aetiology is "ruled in" (as opposed to "ruling out" epilepsy). The tables below summarise some patient factors and examination findings that may sway you more towards functional seizures but are by no means a foolproof checklist. ☝️ PRACTICE POINT: Remember that patients having a functional seizure are in a reduced arousal state but do retain memories of events at the time. Be calm, and reassuring. Reduce stimuli such as bright lights and harsh sounds from the monitors. Avoid derogatory terms like “faking it”, and don’t go slapping them with their hand. Ask around precipitating events such as injury and emotional state (anxiety, hyperventilation) as well the usual "seizure questions" (loss of awareness, tongue bite, incontinence, post-ictal confusion etc.). Specifically ask about medical and psychiatric co-morbidities, as well as somatization tendencies or other medically unexplained conditions (e.g.: Fibromyalgia). Patients will often become defensive when asked about mental health, due to the perception that we feel their symptoms are "all in their heads" (which ironically is truer in the case of epileptic seizures). It is best to save this till later in the history once a rapport is formed, and preface it with phrases such as "I want to ask a bit about mood and anxiety because we know it’s important in seizure disorders" and use questions like "what was life like for you growing up?" rather than bluntly asking "have you been traumatized in the past?" HOW DO I EXPLAIN THE DIAGNOSIS TO PATIENTS? When it comes to explaining the diagnosis, the following steps have been recommended: Name the condition (EG: Functional seizures) State clearly that functional seizures are common, real, and treatable Empathically explain that you do not believe the patient is "crazy" or "making up their symptoms" Acknowledge the physical and emotional impacts functional attacks have on the patient Give specific examples from the patient that lead you to your diagnosis (EG: "you mentioned that you remembered what people were saying while you were seizing...") You can expect initial resistance to their diagnosis - and this is ok. Take the time to pause, reflect on their concerns, and reiterate what you have said. Draw from common examples of the body's physical response such as nausea before an exam. Be prepared for questions such as "What is the cause of my seizures" and practice explaining it in a way that doesn't involve a lengthy blog, flow charts or a table of references. Use patient-centric education materials on functional seizures such as those found on www.neurosymptoms.org to reinforce what you're saying. WHAT ABOUT A DISCHARGE PLAN? Refer patients for an acute assessment by Neurology and/or Psychiatry. A 10-minute consult in a loud Emergency Department resuscitation bay is never going to work and will leave patients with that feeling that the initial communication was poor and "difficult to make sense of." Patients with a new diagnosis of functional seizures will likely require repeated discussions about the diagnosis, as well as confirmatory investigations such as video EEG. They will need a comprehensive treatment plan involving Neurology, Psychiatry, and Physical Therapy. A poorly executed, rapid discharge will leave patients without a clear plan and perpetuates repeated presentations to the ED.[5] Now you have that sorted you can go stop that intern from blindly intubating someone. REFERENCES AND FURTHER READING: Health care practitioners' perceptions of psychogenic nonepileptic seizures: A systematic review of qualitative and quantitative studies https://pubmed.ncbi.nlm.nih.gov/29750340/ What patients say about living with psychogenic nonepileptic seizures: A systematic synthesis of qualitative studies https://pubmed.ncbi.nlm.nih.gov/27522576/ Reuber, M. "Are non-epileptic seizures a manifestation of neurologic pathology." Controversies in epilepsy and behaviour. New York: Elsevier (2008): 151-75. The bare essentials: Functional symptoms in neurology https://pubmed.ncbi.nlm.nih.gov/19448064/ The Inpatient Assessment and Management of Motor Functional Neurological Disorders: An Interdisciplinary Perspective https://pubmed.ncbi.nlm.nih.gov/29628294/ 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.

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 https://www.poisonsinfo.nsw.gov.au/First-Aid/Pressure-Immobilisation.aspx) 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 https://www.aihw.gov.au/reports/injury/contact-with-living-things [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 (https://litfl.com/approach-to-snakebite/,  https://litfl.com/snakebite/, https://litfl.com/snakebite-envenoming-challenge/) 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.

Dr Stephen Gilmartin Emergency Registrar Peer review: Dr Mehul Srivastava Editor: Dr David McCreary THE CASE A 22-year-old female medical student attends the emergency department. She is unable to close her mouth after yawning in one of her biochemistry lectures. She is in some distress and is struggling to speak clearly. You have seen many a bored medical student, so you are able to quickly diagnose a temporomandibular joint (TMJ) dislocation. Before we get down to the fun part of relocation let’s explore the background of this injury. ANATOMY The TMJ is a ginglymoarthroidal (yes, that's a real word) joint, this means it is made up of two joints, one moving in a hinge motion and the other in a gliding motion. The Condylar process articulates with the glenoid fossa and is cushioned by an articular disc. HOW IS STABILITY NORMALLY MAINTAINED? The synergistic movement of the joint’s dynamic stabilisers (pterygoid and masseter muscles) ensures the TMJ remains stable during opening and closing of the jaw. Image 2: Anatomy of Pterygoid Muscles Image 3: Anatomy of Masseter Muscles DISLOCATION Spontaneous anterior TMJ dislocation has a reported annual incidence of 5.3 per 1,000,000 patients who present to the emergency department (ED)(2).  Dislocation is most commonly bilateral but can also be unilateral. MECHANISM When movement of the stabilising muscles becomes uncoordinated, this leads to an increased risk of TMJ dislocation.  Dislocations can occur in any direction but anterior is by far the most common.  This involves the condylar process moving anteriorly out of the fossa and sitting anterior to the articular eminence. Most dislocations occur spontaneously following yawning, eating seizures or intraoral procedures.  Infrequently dislocations have an associated fracture. REDUCTION The optimal reduction technique will be safe and performed with appropriate analgesia and sedation.  We will not discuss analgesia and sedation techniques here, instead we will focus on the reduction methods themselves. We would advise attempting the extraoral methods first (Methods 1 & 2 below) prior to attempting the intraoral method.  This is for two reasons; the intraoral method is invasive and usually requires some level of sedation. EXTRA-ORAL 1. Our first method was first described in 2007 by Chen et al(4).  They reported a case series of seven patients who were all successfully reduced using this extraoral technique. They did not comment on success rates among all comers, time taken or any complications. This technique involves: Sitting the patient upright with their head against a solid surface Apply steady pressure with your thumb to the anterior ramus of the affected side. With your other hand, you do two things. First is to provide counter pressure with your thumb on the patient’s cheek. The second is to apply an anterior and rotational force to the contralateral angle of the mandible with your fingertips. You should feel a clunk. If it is a bilateral dislocation, you now perform the same procedure on the opposite side. You can see a great video of an extra-oral method from AliEM here: 2. Our next extra-oral technique was described more recently (2014), the 'syringe technique': Once again, the patient is placed in a comfortable seated position. The clinician places a syringe between the posterior upper and lower molars on the affected side. The patient is then instructed to gently bite down and grasp the syringe while rolling it back and forth in their mouth. This should result in reduction after a few minutes. The authors describe an impressive success rate of 97% (30/31), (the unsuccessful patient had no teeth!), 70% (24/31) were relocated in less than one minute with nil complications reported (5). INTRA-ORAL METHOD Finally, we have the traditional intra-oral method described in the textbooks. (Ed. - and the technique I use regularly as it works every time, sorry, novel-techniquers!): Sitting the patient upright with their head against a solid surface. This is to avoid retraction away from the clinician. While wearing gloves, the clinician places their thumbs into the patient’s mouth and applies pressure to the patient’s inferior molars An inferior and anterior force is applied Once you feel the condyle is disengaged you can apply posterior force to relocate. You should feel a clunk and the patient will be immediately relieved. A video of the traditional method can be seen here. ☝️ Editor's note: Practice Point Yes, this is putting your thumbs between the patient's molars so you want to have some gauze over your digits. My way of doing this is to put on a pair of gloves, put the gauze over your thumbs, and put a second pair of gloves over this. This prevents you having loose gauze floating around the patient's mouth and gives you more dexterity for performing the technique. CASE CONCLUSION You relocate the TMJ using the extraoral technique. The patient is delighted and can now (carefully) sing your praises. Before she goes you advise her to avoid eating large or chewy foods for the next few days and to apply superior pressure to her chin when yawning. She asks does she require surgery and you reassure her that this is rarely warranted, and simple self-help techniques as described are more effective. REFERENCES Minye HM. Neuroplasticity and central sensitization in orofacial pain and TMD. OBM Neurobiol. 2020;4(2):1. Papoutsis G, Papoutsi S, Klukowska-Rötzler J, Schaller B, Exadaktylos AK. Temporomandibular joint dislocation: a retrospective study from a Swiss urban emergency department. Open Access Emerg Med OAEM. 2018;10:171. Oliphant R, Key B, Dawson C, Chung D. Bilateral temporomandibular joint dislocation following pulmonary function testing: a case report and review of closed reduction techniques. Emerg Med J. 2008 Jul;25(7):435–6. Chen Y-C, Chen C-T, Lin C-H, Chen Y-R. A safe and effective way for reduction of temporomandibular joint dislocation. Ann Plast Surg. 2007 Jan;58(1):105–8. Gorchynski J, Karabidian E, Sanchez M. The “syringe” technique: a hands-free approach for the reduction of acute nontraumatic temporomandibular dislocations in the emergency department. J Emerg Med. 2014;47(6):676–81. STEPHEN GILMARTIN Emergency Registrar Stephen is an emergency medicine doctor from Ireland. He has interests in trauma, ultrasound and medical education. He’s amazed that your brain is active 24/7, 365 days of the year until your death, the only two times it stops is during an exam and when you’re trying to write a funny bio!

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: https://www.hospitalbedscn.com/news-posts/put-a-patient-in-reverse-trendelenburg-position/ 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).

Miller spoke to The Sydney Morning Herald from Beirut about his day-to-day experiences working in the refugee camp with the International Committee of the Red Cross. As the only field hospital servicing the camp, it has treated more than 2000 patients since opening on May 30, and Miller said it was treating “a huge amount” of children. A boy, 10-year-old Omar, was in a wheelchair when he arrived at the hospital, “He was one of the first patients to undergo surgery. He had an old fracture. We removed a piece of dead bone and fixed his leg and put him in a cast and he’s soon to be walking. “Those moments are very special where you can see the difference you’ve made,” Miller said. After a month in the camp, he was on his way home to Melbourne, where he works at The Alfred hospital. Read the whole article in the Sydney Morning Herald.

It may be the ‘land of the unexpected’, but a lot of positive change can occur in a short amount of time in Papua New Guinea. In only three years, the Mount Hagen Public Hospital (MHPH) has gone from an ED lacking in systems, leadership and direction, to a department with all of the foundations for a promising future. Read the whole article: The road to paradise: Developing Emergency Medicine in the highlands of Papua New Guinea in the “Your ED” magazine. By Dr Rob Mitchell – Emergency physician at the Alfred Emergency and Trauma Centre in Melbourne and Project Lead for the Mount Hagen Emergency Department Triage Development Initiative. Learn more about the project.

Professor Peter Cameron, Academic Director of Alfred Health’s Emergency and Trauma Centre, was recognised in The Australian as the best Australian researcher in the field of Emergency Medicine. This is an area of real strength for Australian universities where many institutions, including some outside of the research- intensive ones, do well. Read the whole article: Health & Medical Sciences: Australia’s Research Field Leaders (2019)

IMPLEMENTING ED SYSTEMS IN PAPUA NEW GUINEA Situated in the Western Highlands of Papua New Guinea only accessible to the capital Port Mosby by air, the Mount Hagen Public Hospital (MHPH) services more than 400,000 people in this remote region. In November 2019, the MHPH has officially launched new triage and patient flow systems, designed to help identify patients with urgent healthcare needs so that they can be prioritised for assessment and treatment. The new systems were initially developed by the World Health Organization, Médecins Sans Frontières and the International Committee of the Red Cross. Adaption and implementation support was supported by a team from the Australasian College for Emergency Medicine (ACEM) including Alfred Emergency physician, Dr Rob Mitchell and nurse, Jean-Phillipe Miller. The new systems include: A three-tier triage system, recently developed by the World Health Organization for resource-limited settings An electronic ED patient registration system, to record patient presentations and monitor ED performance A system for presenting complaint coding, to provide burden of disease data and enable disease surveillance The implementation of these systems will not only enable a rapid response to urgent patients, but will also support the provision of safe and efficient emergency care in Mt Hagen and other sites in Papua New Guinea. They are assisting the emergency department to save lives daily through a fast, high-quality triage process, patient registration system and data registry. “It may be the ‘land of the unexpected’, but a lot of positive change can occur in a short amount of time in Papua New Guinea.” Dr Rob Mitchell Learn more about this project