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Phemcast podcast on pain management in the pre-hospital environment.

Discussed around how pain present's differently and how it is a very individual feeling. Due to such each person will have a different management plan and approach.

It was also discussed that how often a missed treatment for managing pain is immobilisation, whilst obvious fractures are being treated, suspected might not be as well managed with immobilisation.

There is a range of different pharmacological treatment methods even in the pre-hospital setting, and the benefits vs risk will always need to be weighed before giving with a patient centric approach. Often this is in combination with none pharmacological intervention.

The use of 'bridging drugs' such as entonox or penthrox should not be overlooked, whilst other efforts are going on such as immobilisation or gaining access to get further long acting analgesics are administered.

Taking forward into practice, this can be added to the stepwise approach for pain management. Making use of bridging drugs whilst further analgesic management is implemented. Having a shared understanding with the patient to achieve an effective management plan.

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The International Association for the Study of Pain's revised definition of pain is available here.

If you'd like to read more about 'nocebo' i.e. the non-pharmacological adverse effects of an intervention, have a look at this article.

Penthrox

For more information on Penthrox, you can read about it in the BNF, The Emergency Medicines Compendium and on the manufacturers own website.

Jon is the author of the Pain and analgesia chapter in the 2nd edition of the ABC of Prehospital Medicine, to be published soon!

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This is the book Jon quotes, "Pain is a symphony..." The International Association for the Study of Pain's revised definition of pain is available here. If you'd like to read more about 'nocebo' i.e. the non-pharmacological adverse effects of an intervention, have a look at this article.

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I took time and listened to the Resus Room - Head Injury Updates; Roadside to Resus.

TXA should be considered in those who have experienced a head injury with a GCS Score of <12 who do not have active extracranial bleeding.

The TXA administered should be a 2g IV Bolus, not a 1g that paramedics are used to.

The direct access route from the community to radio imaging should cease and instead be sent to ED.

Those experiencing a head injury and are anti-coagulated or anti-platelet should have a scan within eight hours.

https://www.theresusroom.co.uk/courses/head-injury-updates/

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The last time we took a good look at head injuries was back in 2018 in our Roadside to Resus episodes and for all of the foundational stuff on incidence, assessment, management and loads more make sure you go and check that episode out.

But this episode is one of our new UPDATES episodes, because we're pretty old now... and whilst we've been having a go at this for a while evidence and guidelines will have progressed, which clearly have implications on how we manage certain cases and that's where these come in! So they'll focus mainly on the last 5 years of practice.

The new NICE head injury guidance has just been released and it's the first major overhaul since 2014. Now we know it's a UK guideline, but there's some really key practice updates and evidence in there that's relevant irrespective of where you find yourself listening this!

So in this episode we're going to be having a look at the most recent TXA evidence, with in terms of indications, timing and dosing. We'll be having a look at the risk of intracerebral injury with regards to anticoagulants and antiplatelet agents and a few other bits and pieces that can help us inform and improve our care.

Once again we'd love to hear any comments or questions either via the website or social media.

Enjoy!

Simon, Rob & James
Now that you have listened to the podcast, start the quiz to add it to your CPD Diary References NICE Head Injury Guidelines. 2023 Effect of Out-of-Hospital Tranexamic Acid vs Placebo on 6-Month Functional Neurologic Outcomes in Patients With Moderate or Severe Traumatic Brain Injury. Susan E Rowell. JAMA. 2020 Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial. CRASH-3 trial collaborators. 2019 Hypopituitarism After Traumatic Brain Injury. Sanjiv Gray. Cureus. 2019 Hypopituitarism Following Traumatic Brain Injury: Determining Factors for Diagnosis. Eva Fernandez-Rodriguez. Front Endocrinol (Lausanne). 2011 The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance. Neurology, Neurosurgery & Psychiatry. 2017 The Resus Room; October 2020 Papers of the month Risk of significant traumatic brain injury in adults with minor head injury taking direct oral anticoagulants: a cohort study and updated meta-analysis. Gordon Fuller. Emerg Med J. 2020 AHEAD Study: an observational study of the management of anticoagulated patients who suffer head injury. Mason. BMJ. 2017

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The last time we took a good look at head injuries was back in 2018 in our Roadside to Resus episodes and for all of the foundational stuff on incidence, assessment, management and loads more make sure you go and check that episode out.

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Cardiogenic shock in Trauma, an element covered by the Resus Room Podcast.

The discussion emphasised the different mechanisms of trauma-induced cardiogenic shock. These include blunt cardiac injury, also known as cardiac contusion, traumatic rupture of the heart or great vessels, and tension pneumothorax.

The podcast underscored the role of rapid and accurate diagnostic procedures in managing these patients. The use of bedside imaging techniques like focused assessment with sonography in trauma (FAST) and echocardiography were highlighted, with an emphasis on their importance in assessing cardiac function and identifying potential mechanical complications such as cardiac tamponade.

The complexity of managing trauma-induced cardiogenic shock was also discussed. Resuscitation measures, beyond the standard ALS principles, may include pericardiocentesis for cardiac tamponade, needle decompression or chest tube placement for tension pneumothorax, and immediate surgical intervention for cardiac rupture. (Beyond our scope but still interesting)

It  also highlighted that in the context of trauma, cardiogenic shock can often coexist with other types of shock, such as hypovolemic shock due to bleeding. This underlines the need for a comprehensive, multidisciplinary approach to these complex patients.

While some of the discussion was beyond the scope of standard practice as mentioned I feel that having at least an underlying knowledge of some of the most advanced techniques is probably beneficial from a personal development point of view and may help enhance the care I am able to provide within my own scope of practice.

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I watched “Major Burns” presented by Krissie Styles via CPDMe Unfortunately I couldn’t get a link working, but if you ever see this lady doing a burns presentation – definitely watch it.I find burns fascinating anyway – but this covered some really poignant elements. It was particularly effective as a presentation as it showed you the whole patient journey, as well as detailed pre hospital actions. You could really see the effect of 15 minutes cooling of a burn, as opposed to 30 minites of cooling on the long term recovery and skin healing / scarring. This is something I will caryy with me into practice. Also, I had never understood the absolute importance of times with burns, when it happened, how long cooling took place on scene, so hospital can understand how much further cooling needs to take place. Lots of visual material on types and depths of burns, the pros and cons of the different burns tools, and some visual examplees. Some examples of scalds. I found all of this very useful to aid my understanding of the different burns. They also covered CO2 and cyanide toxicity – one of the key presentations alongside inhalation injury at the Grenfell incident. Escharotomy was covered in detail, which whilst I have done  transfer where the patient had had this down, this gave me a better understanding of the reasoning behind it and the process, which wil help me with better understanding my road assessments and decisions. A good revision of the trauma triad resulting from severe blood loss, but the other highlight for me was the importance of not letting the patient get cold. A really high percentage (44%) of burns patients arrive at hospital cold (<36 degrees), the sheer balanceof cooling a wound but keeping the patient warm is tricky on the road and will rest in my mind on these jobs.  A heightened awareness of this difficulty will aid my care provision. Regular temperature checking, and using segmental cooling – something I had not honestly considered before. The importance of fluid therapy in burns and good wide bore access was covered – with reference to JRCacl guidelines. The third point that came through for me in this presentation is the importance of not missing life threatening injuries. Some examples were given of some pretty horrific burns, but the patient died because a chest injury or pneumothorax was missed. Overall I found this relly useful and it will profoundly improve my practice as I now have a better understanding of why certain actions are taken and the importance of something which in the moment may not seem so important. Without seeing the long term impact I am not sure I would have really understood the significance of these. 

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I watched “Major Burns” presented by Krissie Styles via CPDMe Unfortunately I couldn’t get a link working, but if you ever see this lady doing a burns presentation – definitely watch it.I find burns fascinating anyway – but this covered some really poignant elements. It was particularly effective as a presentation as it showed you the whole patient journey, as well as detailed pre hospital actions. You could really see the effect of 15 minutes cooling of a burn, as opposed to 30 minites of cooling on the long term recovery and skin healing / scarring. This is something I will caryy with me into practice. Also, I had never understood the absolute importance of times with burns, when it happened, how long cooling took place on scene, so hospital can understand how much further cooling needs to take place. Lots of visual material on types and depths of burns, the pros and cons of the different burns tools, and some visual examplees. Some examples of scalds. I found all of this very useful to aid my understanding of the different burns. They also covered CO2 and cyanide toxicity – one of the key presentations alongside inhalation injury at the Grenfell incident. Escharotomy was covered in detail, which whilst I have done  transfer where the patient had had this down, this gave me a better understanding of the reasoning behind it and the process, which wil help me with better understanding my road assessments and decisions. A good revision of the trauma triad resulting from severe blood loss, but the other highlight for me was the importance of not letting the patient get cold. A really high percentage (44%) of burns patients arrive at hospital cold (<36 degrees), the sheer balanceof cooling a wound but keeping the patient warm is tricky on the road and will rest in my mind on these jobs.  A heightened awareness of this difficulty will aid my care provision. Regular temperature checking, and using segmental cooling – something I had not honestly considered before. The importance of fluid therapy in burns and good wide bore access was covered – with reference to JRCacl guidelines. The third point that came through for me in this presentation is the importance of not missing life threatening injuries. Some examples were given of some pretty horrific burns, but the patient died because a chest injury or pneumothorax was missed. Overall I found this relly useful and it will profoundly improve my practice as I now have a better understanding of why certain actions are taken and the importance of something which in the moment may not seem so important. Without seeing the long term impact I am not sure I would have really understood the significance of these. 

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I listened to this Resus Room podcast about crush injuries.

They discussed different crush injuries and compartment syndrome but also the effects of long lie's for patients who have been on the floor for long periods of time which I found particularly interesting as that relates directly to a lot jobs we go to on the road.

Although there was no definitive answer as to the official length of a long lie or specific management and treatment as every case is different they did highlight some good points regarding possible treatment and management.

I also found it interesting how they explained treatment of a crush injury and how to manage it prior to the limb being released. Preparing fluids to get a head start on the haemorrhage shock, loosely placing a tourniquet on the area in case there is heavy blood loss on release, pre loading with pain relief.

Being able to properly understand the pathophysiology of a crush injury and rhabdomyolysis is great for me to understand what is happening to the body and what signs and symptoms to look our for. I will take this new knowledge and utilise it when I'm with patients who have suffered a long lie or crush injury in order to provide the best possible care.

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So in this episode we're going to be covering crush injury.

When you think about it, visions of falling rocks, industrial accidents and high speed RTCs may come to mind, but actually a crush injury can be sustained in a huge variety of ways without such vivid circumstances.

Definitions according to the Faculty of Prehospital Care are that;

'A crush injury is a direct injury resulting from crush.

Crush syndrome is the systemic manifestation of muscle cell damage resulting from pressure or crushing'

So in the episode we're going to run through all of the bits that we normally cover, from pathophysiology, to presentation and onto treatment. We'll also be looking at the controversy and evidence behind tourniquet use, fluid therapy, electrolyte management and much, much more!

Once again we'd love to hear any comments or questions either via the website or social media.

Enjoy!

Simon, Rob & James
Now that you have listened to the podcast, start the quiz to add it to your CPD Diary References Consensus Statement On The Early Management Of Crush Injury And Prevention Of Crush Syndrome. FPHC. 2003 Crush Injuries and the Crush Syndrome. S Rajagopalan. Med J Armed Forces India. 2010 LITFL; Crush syndrome Pharmacological interventions for the acute management of hyperkalaemia in adults. Cochrane Library. 2015 Management of crush victims in mass disasters: highlights from recently published recommendations. Mehmet Sukru Sever. Clin J Am Soc Nephrol. 2012 Severe crush injury in adults. Uptodate Crush syndrome in disaster. Yokota. JMAJ. 2005 Value and Use of Urinalysis for Myoglobinuria. Ron B Schifman. Arch Pathol Lab Med. 2019 Bench-to-bedside review: Rhabdomyolysis - an overview for clinicians. Huerta-Alardín AL. Crit Care. 2005

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So in this episode we're going to be covering crush injury. When you think about it, visions of falling rocks, industrial accidents and high speed RTCs may come to mind, but actually a crush injury can be sustained in a huge variety of ways without such vivid circumstances.

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I read an article on crush injuries provided by Ambulance CPD. The article provides important information about the incidence and pathophysiology of crush injuries and crush syndrome. It highlights that while crush injuries and syndrome are rare in European practice, they can occur in various settings such as natural disasters, war settings, industrial accidents, road traffic collisions and in elderly fallers. Understanding the potential scenarios where crush injuries can occur is crucial for paramedics to be prepared and respond effectively.

The article explains the difference between crush injury and crush syndrome. Crush injury refers to the direct injury resulting from the incident itself, which can cause significant pathophysiological issues affecting multiple systems of the body. On the other hand, crush syndrome is associated with the systemic effects of muscle cell damage due to prolonged compression. Recognising the three factors that contribute to the development of crush syndrome (compressive force, muscle mass involved, and duration of compression) is important in assessing the severity of the condition and its impact on the patient.

Understanding the pathophysiology of crush injuries and crush syndrome, allows paramedics to anticipate and recognise the potential complications and clinical features associated with these conditions. The article highlights that traumatic rhabdomyolysis and the subsequent release of muscle cell contents play a major role in the development of crush syndrome. The leakage of substances such as sodium, calcium, water, myoglobin, phosphate, and urate into the circulation can have detrimental effects on multiple organs and homeostatic functions.

Knowing the potential cascade of pathophysiological processes that can occur after the release of the crushing object is crucial for effective patient care. Paramedics should be aware of the risks of hypovolemic shock, cardiac arrest, metabolic imbalances (such as hyperkalaemia, hypocalcaemia, and metabolic acidosis), acute kidney injury, cardiac arrhythmias, acute respiratory distress syndrome (ARDS), coagulopathy, sepsis, and renal failure. This knowledge will allow paramedics to promptly recognise and manage these complications, improving patient outcomes.

Furthermore, understanding the differences between crush injuries and crush syndrome will help paramedics tailor their treatment approach. While immediate attention may be required to address the direct injuries and trauma associated with crush injuries, the release of toxins and metabolic disturbances in crush syndrome requires specific interventions such as fluid resuscitation, electrolyte management, and monitoring for organ dysfunction.

In summary, the knowledge provided in this article on crush injuries and syndrome equips paramedics with a deeper understanding of the incidence, pathophysiology, and potential complications associated with these conditions. This understanding enhances the ability to assess, manage, and provide appropriate care for patients presenting with crush injuries or syndromes. By applying this knowledge, paramedics can improve patient outcomes, minimise complications, and optimise patient care in challenging scenarios involving crush injuries.

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Although the likelihood of attending a patient with a crush injury or syndrome is uncommon, a patient presenting with crush injury or syndrome will cause significant challenge to the clinician on scene. There will be multiple factors to attend with, from personal safety, extrication and evacuation, treatment, joint agency response, and more. A crush injury patient can pose a significant challenge.
Incidence:
Crush injury and syndrome presentation remains a rare occurrence within European practice. Crush injury and syndrome is often seen in events of:

Natural disasters, such as earthquakes

In war settings

Building collapses following explosions

Industrial accidents

Road traffic collisions

Sometimes following collapses of patients where their own bodyweight has been trapping a limb over an extended period

Within the traumatic crush setting, statistically the legs are most commonly affected, with the arms being less frequent. Any crush injury to the head and/or torso often causes significant injury and destruction, resulting in trauma incompatible with life. This is often the scenario, however, there are some cases where patients have survived following a head or torso crush.

In the pathophysiology, crush injury and crush syndrome are different:

Crush injury is associated with the direct injury resulting from the incident. The injury itself can cause significant pathophysiological issues affecting multiple systems of the body depending on the MOI, location of injury, and amount of tissue involved. If the patient isn't immediately killed from the initial injury and tissue destruction, further complications will start to arise. The patient may begin to haemorrhage internally or externally from the trauma, organs may be injured and begin to fail, major blood vessels may be disrupted, and further complications may develop. In chest injury, a pneumo/haemothorax may develop, cardiac tamponade, etc.

Crush syndrome is associated with the systemic effect of muscle cell damage from the crushing pressure. The are 3 common factors which lead to the development of crush syndrome, these include;

The degree of compressive force

The amount of muscle mass involved

The duration of the compression

When attending a potential crush syndrome patient, recognition of these 3 factors can help in determining the severity of crush syndrome and how adversely affected the patient may be. For example, a patient with a large concrete pillar crushing both legs over 4 days will be severely affected by crush syndrome compared to a patient crushing their finger in a vice for 2 hours.

The onset of crush syndrome usually occurs following reperfusion of injured muscle when the compressive force is released and the affected tissue's toxins, etc, re-enter the body's circulation. Depending on the factors above, this may result in acute and/or delayed-onset of clinical symptoms and presentations.

The clinical features of crush syndrome are mainly due to the result of traumatic rhabdomyolysis and subsequent damage and release of muscle cell contents. The mechanism behind this is the leakiness of the sarcolemmal membrane caused through the pressure or stretching from the incident. The Sarcolemma is the cell membrane which surrounds and contains skeletal muscle cells. Within this containment there is also the cytoplasm, or Sarcoplasm, mitochondria, myoglobin, calcium, and other components. As the membrane is stretched, sodium, calcium, and water leak into the sarcoplasm which traps extracellular fluid inside the muscle membrane. Additional to the influx of these substances into the cell, the cell releases potassium, and other toxic substances into circulation of the affected area such as myoglobin, phosphate, and urate.

From crush syndrome, a cascade of pathophysiological processes occur which can negatively affect numerous organs and homeostatic function. These numerous pathologies can present numerous opportunities of death to the patient. For example, when a patient is trapped from a significant crush injury, the crushed area increases permeability of the sarcolemmal membranes, allowing an influx of sodium and calcium creating a pressure head for water to follow by osmosis. The entire extracellular fluid volume may penetrate into the injured muscles within hours to days of injury. This leads to a rapid depletion of intravascular fluid, hypovolaemic shock and cardiac arrest.

On the release of the crushing object, the release of toxins, dead tissue cells, etc, will return to the body's circulation. This sudden influx of toxic material on the body's organs and tissues can result in numerous pathophysiology's such as shock, hyperkalaemia, hypocalcaemia, metabolic acidosis, Acute Kidney Injury, cardiac arrhythmias, etc. Later on issues which can result from crush syndrome include Acute Respiratory Distress Syndrome (ARDS), coagulopathy, sepsis, and renal failure.

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Crush Injury and Syndrome part 1 - Ambulance CPD

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Although the likelihood of attending a patient with a crush injury or syndrome is uncommon, a patient presenting with crush injury or syndrome will cause significant challenge to the clinician on scene. There will be multiple factors to attend with, from personal safety, extrication and evacuation, treatment, joint agency response, and more.

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Crush - roadside to resus

Resus room podcast

Difference between a crush injury and crush syndrome

A crush injury is a direct injury resulting from crush.

Crush syndrome is the systemic manifestation of muscle cell damage resulting from pressure or crushing

Crush syndrome Can be from a big injury sustain over a short time or a minor injury sustained over a long time such as long lie

Therefore must be aware in trauma patients and non injury fallers and recognised in a in-depth primary and secondary survey

Muscular injuries put patients in high risk of renal injury both from rhabdomyolitis and electrolyte disturbances. Prevention and reaction is important for improved patients

- no clear cut guidance for long lie patients therefore history and examination is important to pick up these injuries.

Prehospital treatment should include addressing haemorrhage using appropriate methods. Oxygen. Cannulation  or IO access to provide fluid therapy and transport to the most appropriate destination.

This new knowledge of crush injuries and crush syndrome gained from the podcast will make me more aware of symptoms and pre hospital care to improve recognition in patients.

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I listened to the COPD podcast as this particular respiratory disease is one we come across frequently and sometimes multiple times in a shift. There are different ways to manage a copd patient depending on their presentation. For example, Giving hydrocortisone if the patient is still struggling after nebulisers, and now a recent change in guidelines to leave patients at home with Prednisolone.

The Podcast was taking about the benefits between high concentrated and titrated oxygen in the pre hospital setting. They discussed a trail that resulted in less mortality rates with oxygen titrated than then giving them high concentrates of oxygen even when giving a patient just 2ltrs via nasal until hospital handover.  They were discussing the exacerbation is down to bacteria/viral, sputum and non- med compliance. Symptoms are breathlessness, tight chest, more inhaler use. However, it was discussed that some exacerbations can be ruled out through history as heart failure, PE, Pneumothorax could present as an exacerbation. The point on this is to undertake a full history before jumping to assumptions of its COPD. They discussed the use of the Dysphia scale to grade breathlessness and determine copd exacerbation. This will aid in potential safe discharge at home with GP involvement or need for hospital admission. The discussion around the Use of the Nice table to assist with safe discharge at home and provides safe netting if required. For example a patient that is on long term o2 use at home is a red flag if the patient is currently struggling. Another assessment tool is to use counting to 10 in one breath, rather than using speaking in full sentences. This is because counting to 10 can be easily reassessed and more accurate to the effectiveness of treatment.

The podcast was useful and given guidance on more assessment techniques that can be used in the pre-hospital setting when faced with copd patients. This is because I find that I assess a lot of COPD exacerbations and have limited knowledge and underconfident in safely discharging them at home. The other tools discussed in the podcats are definitely tools I will use in my daily practice and also looking further into the history of their COPD, and ask more questions in how long they have had copd, how they are normally, are there any activities that the patient currently can’t do and any recent changes. I will also ensure I ask the patient is they have a care plan for their copd and any alert cards. This is because some we need to determine if its an actual exacerbation of COPD or anxiety led.

COPD – The Resus Room

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CPD

What CPD is it: -

https://www.theresusroom.co.uk/courses/pre-alert/

Listened to a 1 hour long pod cast by the resus room around pre alerts (ATMISTS) this is useful as recently I have had some negative experiences with pre alerting. My experience has been that the HCP on the phone does not always allow the ambulance crew to give the relevant information in the ATMIST format and that when later speaking to these HCP’s that when receiving a pre alert each individual HCP wants different information in a different order. This information is sometimes based on previous experience.

What did you learn: -

The talk started with an ED doctor talking about there being no real defined criterial for what requires ATMIST. He refereed to a list but states they don’t fit all cases. The paramedic on the talk agreed that a set list was not always the best way to work.

Questions

What is a pre alert:-
My understanding
Pre alerts are a method for the OOH clinician to get the hospital ready for an immediate response on arrival for an unwell patient.

Podcast
A pre alert is made because you are experiencing a certain response when you arrive at the department, so they are ready to quickly treat a patient. Interesting information about how new pressures with long waits at hospital is causing paramedics so give “soft alerts” for patients who are unwell but not traditionally an ATMIST call to make sure there is room when the ambulance arrives. The Dr pointed out this was not helping with acceptance of ATMIST calls. The Dr explains that in the example of sepsis this can be treated on the ambulance. I would disagree with this statement as we cannot do bloods and are not able to administer ABX. Lost of talk around the “courtesy” pre alert in cases where for example a patient is technically FAST positive but the ambulance HCP has a high suspicion of it being something else.

My new thinking
I agree with the prehospital HCP that an ATMIST can only be decided by the one making the call. It should be made when you are so concerned about a patient that you want an immediate reaction when arriving at ED.

When should we pre alert: -
When there is an ABCDE issues that needs addressing as soon as the patient arrives. Spoke about pre alert fatigue where to many unnecessary pre alerts make the ED staff non-reactive to calls from paramedics. Likewise, there is concern of prehospital clinicians are starting to not pre alert through fear of a poor reaction on arrival. This carries huge risk to the patient.  It was pointed out that there is no formal training around giving ATMIST, this leads to poor pre alerts. Training should be included in the prehospital environment. Likewise, hospital staff don’t generally receive training on what an ATMIS is.

How did it benefit the patient: -
I have better understanding of the pre alert system and why some Dr’s react poorly. Also better understand as to what should be pre alert which in turn will lead to better patient care.

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Neck of Femur Fractures – The Resus Room

I listened to the resus room podcast surrounding neck of femur fractures. I chose this as it is relevant to my dissertation subject, so thought it may have been of some use.

From this I learnt to put some more consideration into the chosen methods of pain relief, with the discussion surrounding absorption of oral paracetamol sometimes being slowed when opioids are given very interesting to consider, as well as remembering to consider non pharmacological methods

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In this episode we'll be running through their presentation, discuss both the clinical and radiological diagnostics. We'll also be looking in depth about both pharmacological and non-pharmacological methods of pain relief and have a think about where fascia-iliaca compartment blocks sit with regards to pre and in- hospital practice.

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I listened to a Resus room podcast covering neck of femur injury. It was a nice reminder for how to decide if injury is more likely a NOF or dislocation and also information regarding previous hip surgery and potential for damage to be around the acetabulum. pain relief was discussed and treatment before conveyance. I would usually use a scoop for extrication, where possible but since listening to this I am likely to splint legs together whilst using the scoop and then transfer to vacuum mattress for support during the journey and ease of moving onto hospital trolley at the end. They touched on pain relief too and I'll be sure to use IV paracetamol where possible and follow up with some morphine. 

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I listened to a Resus room podcast covering neck of femur injury. It was a nice reminder for how to decide if injury is more likely a NOF or dislocation and also information regarding previous hip surgery and potential for damage to be around the acetabulum. pain relief was discussed and treatment before conveyance. I would usually use a scoop for extrication, where possible but since listening to this I am likely to splint legs together whilst using the scoop and then transfer to vacuum mattress for support during the journey and ease of moving onto hospital trolley at the end. They touched on pain relief too and I'll be sure to use IV paracetamol where possible and follow up with some morphine. 

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This has been beneficial for my recognition of ACS. Additionally, I have learnt how hospitals use tools such as the GRACE to improve diagnosis of ACS. Although, this podcast did not significantly alter my management of ACS, It has helped me widen my knowledge on this topic and aided in identifying literature that may be useful for my dissertation.

Enhancing my knowledge of ACS will be benefit service users, as this will improve my ability to identify likely ACS and manage it appropriately.

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So this time we're going to be looking at the HUGE topic of acute coronary syndrome (ACS)! ACS ranges from patients who appear well at the time of their presentation, to those that have arrhythmias, haemodynamic instability, to those that are in cardiac arrest!

There are around three quarters of a million ED chest pain attendances per year for acute chest pain and it accounts for around 25% of ED medical admissions!!

Some of the treatments we'll discuss for patients with ACS can have a huge affect on morbidity and mortality and we can make a real difference to our patients. The ESC guidelines are a fantastic resource to take a look at and we've listen the papers that form the evidence we cover in the podcast.

We worry about missing ACS and conversely, with so many 'suspected ACS patients', we also worry about overly suspecting it and the subsequent burden of admissions and investigations that it may mean. We're going to cover the approach to ACS in this episode in our standard format, all the way from definition, patho-physiology, assessment, investigations and management and cover aspects that are both new information and a sound revision of the topic.

Once again we'd love to hear any thoughts or feedback either on the website or via twitter @TheResusRoom.

Enjoy!

Simon, Rob & James
Now that you have listened to the podcast, start the quiz to add it to your CPD Diary References NICE. Acute Coronary Syndrome Guidelines 2020 2020 Acute Coronary Syndromes (ACS) in Patients Presenting without Persistent ST-Segment Elevation (Management of) Guidelines TheNNT; Aspirin Given Immediately for a Major Heart Attack (STEMI) The NNT; Thrombolytics for Major Heart Attack The contemporary significance of Framingham risk factors. Barbra E Backus. Eur J Emerg Med. 2021 Do risk factors for chronic coronary heart disease help diagnose acute myocardial infarction in the Emergency Department? Richard Body. Resuscitation. 2008 The role of cardiac risk factor burden in diagnosing acute coronary syndromes in the emergency department setting. Jin H Han. Ann Emerg Med. 2007 LITLF; MI localisation The NNT; Acute Coronary Syndrome Does This Patient With Chest Pain Have Acute Coronary Syndrome?: The Rational Clinical Examination Systematic Review. Alexander C Fanaroff. JAMA. 2015 Evaluation of the impact of the GRACE risk score on the management and outcome of patients hospitalised with non-ST elevation acute coronary syndrome in the UK: protocol of the UKGRIS cluster-randomised registry-based trial. Colin C Everett. BMJ Open. 2019 Does a strict glycemic control during acute coronary syndrome play a cardioprotective effect? Pathophysiology and clinical evidence. Alfredo Caturano. Diabetes Res Clin Pract. 2021 Impact of call-to-balloon time on 30-day mortality in contemporary practice. Richard W Varcoe. Heart. 2017 Pre-hospital thrombolysis delivered by paramedics is associated with reduced time delay and mortality in ambulance-transported real-life patients with ST-elevation myocardial infarction. Erik Björklund. Eur Heart J. 2006 Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Jean-Philippe Collet. EHJ. 2020 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Borja Ibanez. EHJ. 2017 P2Y12 platelet inhibition in clinical practice. Peter Damman. J Thromb Thrombolysis. 2012 Role of beta blockers following percutaneous coronary intervention for acute coronary syndrome. Peck. Heart. 2021 PRe-hospital Evaluation of Sensitive TrOponin (PRESTO) Study: multicentre prospective diagnostic accuracy study protocol. Abdulrhman Alghamdi. BMJ Open. 2019 Diagnostic Performance of Prehospital Point-of-Care Troponin Tests to Rule Out Acute Myocardial Infarction: A Systematic Review. Abdulrhman Alghamdi. Prehosp Disaster Med. 2020 St. Emlyns; Troponins RCEMLearning; Acute Coronary Syndromes

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So this time we're going to be looking at the HUGE topic of acute coronary syndrome (ACS)! ACS ranges from patients who appear well at the time of their presentation, to those that have arrhythmias, haemodynamic instability, to those that are in cardiac arrest!

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Listened to general broadcast podcast- fall non-injuries

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Listened to general broadcast podcast- fall non-injuries

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http://www.generalbroadcast.org.uk

70% of accidental deaths in the over 75s are attributed to a fall

Those over 65 who fall, 5% will suffer a fracture

95% NoFs are caused by falls

Those who have fallen twice in the last 12 months, are at higher risk of falling again. Therefore it is important to identify these patients and risk stratifying.

Falls are very rarely purely ‘mechanical’ in nature and are often multi-factorial. Falling is not a normal part of getting older and investigations need to take place to discover why and how they have fallen and what can be done to prevent a fall in the future (better lighting, change in glasses strength, Assessment of urinary continence- is there a way trips to the bathroom can be reduced? Are they on diuretics? Significant increase in falls risk for patients who report 2 or more night time trips)

Assessment of osteoporosis risk is easy- Increases in advancing age favouring women 4:1 especially post-menopausal. Steroid use, smoking, Cushing syndrome and anorexia increase risk. If at risk of OP and falls, look at their medication- referral to GP for review if they need to be on OP management.

Encourage patient to assist themselves off the floor and educate them techniques of how to get off the floor- This prevents the reinforcement that they need an ambulance to get off the floor and reduces risk of long-lies.

This CPD is beneficial as 7-9% of calls are to ‘elderly fallers’ so we attend them frequently. The service user will benefit from doing this CPD as it highlights the importance of a thorough assessment to stratify risk and adequately safety net to prevent future falls.

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Left Bundle Branch block (LBBB) is a electrocardiogram (ECG) abnormality in which the electrical signal that normally passes through the left bundle branch is disrupted, resulting in a widened and sometimes flattened or abnormally shaped QRS complex.

A left bundle branch block (LBBB) can be identified on an ECG by looking for a widened QRS complex greater than 0.12 seconds and an absence of an initial R wave in leads I, VL, V4-6.

If an ECG shows LBBB, the Sgarbossa Criteria can be used to determine if acute myocardial infarction (MI) is present. The Sgarbossa Criteria is a scoring system that incorporates ST-segment deviation and concordance between the ST-segment and the QRS complex.

Sgarbossa Criteria assigns scores between 1 and 3 to ST segment deviation and QRS concordance.

If the total score is 3 or more, it is suggestive of an MI and further investigation is warranted.

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Smith-Modified Sgarbossa Criteria

Concordant ST elevation ≥ 1 mm in ≥ 1 lead

Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3

Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave

Background

In patients with left bundle branch block (LBBB) or ventricular paced rhythm, infarct diagnosis based on the ECG can be difficult

Abnormal depolarisation should be followed by abnormal repolarisation, manifesting as ST-segment and T-wave deviations that do not necessarily indicate acute ischaemia ("appropriate discordance")

Image: ECGMedicalTraining.com

However, serial ECGs may show dynamic ST segment changes during ischaemia

In 1996, Elena B Sgarbossa first described criteria to assist clinicians to diagnose infarction in the setting of LBBB

Original Sgarbossa Criteria
The original three criteria used to diagnose infarction in patients with LBBB are:

Concordant ST elevation > 1mm in leads with a positive QRS complex (score 5)

Concordant ST depression > 1 mm in V1-V3 (score 3)

Excessively discordant ST elevation > 5 mm in leads with a -ve QRS complex (score 2)

These criteria are specific, but not sensitive (36%) for myocardial infarction. A total score of ≥ 3 is reported to have a specificity of 90% for diagnosing myocardial infarction.
Image: ECGMedicalTraining.com

During right ventricular pacing the ECG also shows left bundle brach block and the above rules also apply for the diagnosis of myocardial infarction during pacing, however they are less specific.

Smith-Modified Sgarbossa Criteria

As discussed in this article by Stephen Smith, the Smith modified Sgarbossa criteria for Occlusion Myocardial Infarction (OMI) in LBBB have been created to improve diagnostic accuracy. The most important change is the modification of the rule for excessive discordance.

The use of a 5 mm cutoff for excessive discordance was arbitrary and non-specific - for example, patients with LBBB and large voltages will commonly have ST deviations > 5 mm in the absence of ischaemia. The modified rule is positive for "STEMI" if there is discordant ST elevation with amplitude > 25% of the depth of the preceding S-wave.
Smith-Modified Sgarbossa Criteria:

Concordant ST elevation ≥ 1 mm in ≥ 1 lead

Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3

Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave

See the modified Sgarbossa criteria in action in this excellent case study by Stephen Smith and references for the 1) Derivation and 2) validation of the Smith-Modified criteria

1. Smith SW et al. Diagnosis of ST Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block using the ST Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Annals of Emergency Medicine 2012;60:766-776

2. Meyers HP, Limkakeng AT Jr, Jaffa EJ, Patel A, Theiling BJ, Rezaie SR, Stewart T, Zhuang C, Pera VK, Smith SW. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170(6):1255-1264.

ECG Examples

Example 1
Positive Sgarbossa criteria in a patient with LBBB and troponin-positive myocardial infarction:

This patient presented with chest pain and had elevated cardiac enzymes.

Previous ECG showed typical LBBB

There is 1mm concordant ST elevation in aVL (= 5 points)

Other features on this ECG that are abnormal in the context of LBBB (but not considered "positive" Sgarbossa criteria) are the pathological Q wave in lead I and the concordant ST depression in the inferior leads III and aVF.

This constellation of abnormalities suggests to the authors that the patient was having a high lateral infarction

Example 2

ECG courtesy of Dr Andrew Coggins, FACEM
Positive Sgarbossa criteria in a patient with a ventricular paced rhythm:

There is concordant ST depression in V2-5 (= Sgarbossa positive).

The morphology in V2-5 is reminiscent of posterior STEMI, with horizontal ST depression and prominent upright T waves.

This patient had a confirmed posterior infarction, requiring PCI to a completely occluded posterolateral branch of the RCA.

Example 3

Example 4

Cases

Related Topics

References

Advanced Reading

Online

Textbooks

Mattu A, Tabas JA, Brady WJ. Electrocardiography in Emergency, Acute, and Critical Care. 2e, 2019

Brady WJ, Lipinski MJ et al. Electrocardiogram in Clinical Medicine. 1e, 2020

Straus DG, Schocken DD. Marriott's Practical Electrocardiography 13e, 2021

Hampton J. The ECG Made Practical 7e, 2019

Grauer K. ECG Pocket Brain (Expanded) 6e, 2014

Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography 1e, 2009

Surawicz B, Knilans T. Chou's Electrocardiography in Clinical Practice: Adult and Pediatric 6e, 2008

Mattu A, Brady W. ECG's for the Emergency Physician Part I 1e, 2003 and Part II

Chan TC. ECG in Emergency Medicine and Acute Care 1e, 2004

Smith SW. The ECG in Acute MI. 2002 [PDF]

LITFL Further Reading

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Smith-Modified Sgarbossa Criteria Concordant ST elevation ≥ 1 mm in ≥ 1 lead Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3 Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding

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What CPD?

https://www.theresusroom.co.uk/courses/lactate/

Lactate podcast​

What learn?

Pathophysiology of aerobic and anerobic metabolism. Why lactate can be raised (Liver disease, Accelerated Glycolysis, Congenital disorders, Thiamine deficiency, Anerobic metabolism, Toxic and drug effects, Extracellular alkalosis, Sepsis) and not just linked to Sepsis.

Benefit to service user?

Not able to access pre-hospital lactate measurements but podcast affirms that focus should be on clinical picture of the patient. Focus on signs of hypoperfusion such as hypotension and hypoxia which we can manage pre-hospitally. Importance of recording interventions/treatments as they can impact lactate measurements and in turn improve outcomes.

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So when people talk about patients having a high lactate we think about them being sick, it can at times be easy to slip into thinking that this equals sepsis or maybe ischaemia. And whilst the presence of a high lactate in the context of infection and ischaemia is important to note, there is a lot more to interpreting a raised lactate than may first be apparent... So in this episode we're going to delve down into lactate, have a think about what it is, what normal and raised levels are, consider the mechanisms behind it's formation and breakdown and think about the causes of raised lactate. We'll then put this all together and have a think about how we can interpret and lactate levels ensuring we give the best treatment to our patients! Enjoy!

Simon, Rob & James
Now that you have listened to the podcast, start the quiz to add it to your CPD Diary References Etiology and therapeutic approach to elevated lactate. Lars W. Andersen. Mayo Clin Proc. 2013 Lactate physiology in health and disease. Phypers. Continuing Education in Anaesthesia Critical Care & Pain. 2006 Initial pH, base deficit, lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury. Kaplan. Crit Care Med. 2004 Clinical practice guideline: endpoints of resuscitation. Tisherman. The Journal of trauma. 2004 Etiology and therapeutic approach to elevated lactate. Lars W. Andersen. Mayo Coin Proc. 2014 Determinants of prehospital lactate in trauma patients: a retrospective cohort study. E Ter Avest. BMC Emerg Med. 2020 St. Emlyns; Lacthate Understanding elevated lactate; Resus.Me Lactate and lactic acidosis; LITFL

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So when people talk about patients having a high lactate we think about them being sick, it can at times be easy to slip into thinking that this equals sepsis or maybe ischaemia. And whilst the presence of a high lactate in the context of infection and ischaemia is important to note, there is a lot more to interpreting a raised lactate than may first be apparent...

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What did you learn?

The new NICE head injury guidance has been released and it’s the first major overhaul since 2014.  It’s a UK guideline, but there’s some key practice updates. This podcast included:

·       A look at the most recent TXA evidence

·       Indications, timing and dosing of TXA

·       The risk of intracerebral injury with regards to anticoagulants and antiplatelet agents.

How will it benefit the patient?

Keeping up to date with recent changes of guidance such as NICE is exceptionally important working as a prehospital clinician. Head injuries are commonplace jobs for the ambulance service. With a range of ages presenting with head injuries. Knowing current changes to NICE enables us to understand any changes of policy/procedure. For example, on checking JRCALC, it is an indication to consider the use of TXA for a head injury, of a patient aged 18 or above, with a GCS of 12 or less. Understanding drugs such as TXA and their uses, will benefit future head injury patients in practice.

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The last time we took a good look at head injuries was back in 2018 in our Roadside to Resus episodes and for all of the foundational stuff on incidence, assessment, management and loads more make sure you go and check that episode out.

But this episode is one of our new UPDATES episodes, because we're pretty old now... and whilst we've been having a go at this for a while evidence and guidelines will have progressed, which clearly have implications on how we manage certain cases and that's where these come in! So they'll focus mainly on the last 5 years of practice.

The new NICE head injury guidance has just been released and it's the first major overhaul since 2014. Now we know it's a UK guideline, but there's some really key practice updates and evidence in there that's relevant irrespective of where you find yourself listening this!

So in this episode we're going to be having a look at the most recent TXA evidence, with in terms of indications, timing and dosing. We'll be having a look at the risk of intracerebral injury with regards to anticoagulants and antiplatelet agents and a few other bits and pieces that can help us inform and improve our care.

Once again we'd love to hear any comments or questions either via the website or social media.

Enjoy!

Simon, Rob & James
Now that you have listened to the podcast, start the quiz to add it to your CPD Diary References NICE Head Injury Guidelines. 2023 Effect of Out-of-Hospital Tranexamic Acid vs Placebo on 6-Month Functional Neurologic Outcomes in Patients With Moderate or Severe Traumatic Brain Injury. Susan E Rowell. JAMA. 2020 Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH-3): a randomised, placebo-controlled trial. CRASH-3 trial collaborators. 2019 Hypopituitarism After Traumatic Brain Injury. Sanjiv Gray. Cureus. 2019 Hypopituitarism Following Traumatic Brain Injury: Determining Factors for Diagnosis. Eva Fernandez-Rodriguez. Front Endocrinol (Lausanne). 2011 The screening and management of pituitary dysfunction following traumatic brain injury in adults: British Neurotrauma Group guidance. Neurology, Neurosurgery & Psychiatry. 2017 The Resus Room; October 2020 Papers of the month Risk of significant traumatic brain injury in adults with minor head injury taking direct oral anticoagulants: a cohort study and updated meta-analysis. Gordon Fuller. Emerg Med J. 2020 AHEAD Study: an observational study of the management of anticoagulated patients who suffer head injury. Mason. BMJ. 2017

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The last time we took a good look at head injuries was back in 2018 in our Roadside to Resus episodes and for all of the foundational stuff on incidence, assessment, management and loads more make sure you go and check that episode out.

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1. Podcast based around leadership and followership in healthcare.
2. I learnt that positive patient outcomes have been shown when cognitive load is shared. I have also learnt that affirming those in a position of leadership is important as feedback from followers or those who may be assumed to be stepping into the leadership role can have a positive impact on those who are leading.
3. This will benefit the service user as it has taught me how to better lead/follow at critically unwell patients and how this can be improved in the ambulance service. This will ultimately lead to higher levels of cohesion whilst managing these patients and lead to hopefully better outcomes.

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We talk a lot about the different skills involved in the management of the critically unwell patient; CPR, airway management, defibrillation, chest drains, RSI etc, etc.....but there is another aspect which is arguably as important and that is the non-technical skills involved in resuscitation.