Clinical Topics

Carbon Monoxide

Carbon Monoxide poisoning is definitely one of those differentials that you consider when the patients books into ED with ‘?carbon monoxide poisoning’…… but how much do we really think about it in a patient that hasn’t been sent down to the ED with this specific thought in mind.

Rob Fenwick talks us through the key points of Carbon Monoxide poisoning and some recent evidence on the topic which will probably make us consider the possibility a bit more frequently! This podcast was based around the post Rob wrote for Jonathan Downham’s superb Critical Care Practitioner podcast. Go and have a look at the post for a lot more information on the topic.


  • CO poisoning is difficult to identify because of a number of factors.
  • When assessing patients with vague symptoms, it may be worthwhile taking that blood gas you were getting anyway, to the device that will also tell you their COHB..…. It might just surprise you.
  • A venous COHB is just fine,  save your patient that arterial sample.
  • The treatment is pretty simple, support ABC’s, give high flow oxygen and consider contacting a HBO centre.
  • Finally………..Refresh your knowledge on CO poisoning every once in a while, just to keep it in your list of differentials.


Blumenthal, I. (2001) Carbon monoxide poisoning. Journal of the Royal Society of Medicine. Volume 94, pp270-72.

Buckley, N. A., Juurlink, D. N., Isbister, G., Bennett, M. H & Lavonas, E. J. (2011) Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database of Systematic Reviews. Issue 4. Article number: CD002041.

Clarke, S. J. F., Crosby, A & Kumar, D. (2005) Early carbon monoxide intoxication: happy to be poisoned? Emergency Medicine Journal. Volume 22, pp754-755.

Harty, E., Haskins, K & Robinson, K. (2008) Carbon monoxide poisoning measurement. Emergency Medicine Journal. Volume 25, pp862.

Hampson, N. P. (1998) Pulse oximetry in severe carbon monoxide poisoning. Chest. Volume 114, pp1036-41.

Hampson, N. B & Weaver, L. K. (2007) Carbon monoxide poisoning: a new incidence for an old disease. Undersea & Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society. Volume 34, number 3, pp163-8.

Kaya, H., Coskun, A., Beton, O., Zorlu, A., Kurt, R., Yucel, H., Gunes, H & Yilmaz, M. B. (2016) Carboxyhaemoglobin levels predict the long-term development of acute myocardial infarction in carbon monoxide poisoning. American Journal of Emergency Medicine. Epub ahead of print. Available from: (last accessed 24/3/16).

Kumar, P & Clark, M. (2012) Clinical Medicine (8th Edition). Saunders. London.

Wright, J. (2002) Chronic and occult carbon monoxide poisoning: we don’t know what we’re missing. Emergency Medicine Journal. Volume 19, pp386-90.

Zorbalar, N., Yesilaras, M & Aksay, E. (2014) Carbon monoxide poisoning in patients presenting to the emergency department with a headache in winter months. Emergency Medicine Journal. Volume 31, e66-70.

NICE guideline; Major trauma assessment and initial management

So NICE has published it’s guidelines on ‘Major trauma; assessment and initial management’, obviously it would be ideal for you to run through the full document yourself but to give you a flavour of the key points that we think will affect our practice here are what we consider to be the headlines;

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 The document

So the guideline is split up into 10 major sections and we’ll take the key points from each 1 by 1….

1. Immediate destination after injury

Nothing major here but that the optimal destination for patients with major trauma is the major trauma centre, only exceptional circumstances or locations should they first go to the trauma unit for urgent treatment. A reasonable example would be inadequate airway management where local expertise at a trauma unit is required to secure the airway where it would be unsafe to convey the patient further to an MTC.

2. Airway management in pre-hospital and hospital settings

When an RSI is indicated this should be performed as soon as possible and within 45 minutes of the initial call to emergency services and preferably at the scene of the incident.

Transport the patient to a major trauma centre for RSI providing the journey time is 60 minutes or less & only divert to a trauma unit for RSI before onward transfer to if a patent airway can’t be maintained or the journey time is greater than 60 minutes.

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3. Management of chest trauma in pre-hospital settings

Regarding eFAST; only to be used if specialist team can utilise without delaying onwards transfer, beware that negative eFAST doesn’t rule out a pneumothorax.

Only perform chest decompression in a patient with suspected tension pneumothorax if there is haemodynamic instability or severe respiratory compromise and open thoracostomy instead of needle decompression should be used where expertise is available. Followed by a chest drain via the thoracostomy in patients who are breathing spontaneous (I’m not sure but it seems from the guidelines that this is recommended to be placed prehospitally).

Beware of conversion of an open pneumothorax to a tension once decompressed.

4. Management of chest trauma in hospital settings

In tension pneumothorax perform chest decompression before imaging only if they have haemodynamic instability or severe respiratory compromise (this is a strange one as a tension pneumothorax would be defined by haemodynamic instability or severe respiratory compromise….)

Consider CXR/eFAST as part of the primary survey assess chest trauma in adults with severe respiratory compromise.

Do not routinely use CT for 1st line imaging to assess chest trauma in children (under 16’s).

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5. Management of haemorrhage in prehospital and hospital settings

Regarding pelvic binders; if active bleeding is suspected from a pelvic fracture after a high energy trauma apply a purpose made binder or consider an improvised binder only if the purpose made binder does not fit.

Use TXA as soon as possible in patients with major trauma and active or suspected bleeding but not more than 3 hours after injury unless there is evidence of hyperfibrinolysis.

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Rapidly reverse anticoagulation in patients who have major trauma and active or suspected active bleeding; use prothrombin complex concentrate immediately for active bleeding needing reversal if vitamin K antagonists.

Fluid resuscitation should be with blood products. In pre-hospital settings only use crystalloids to replace fluid volume in patients with active bleeding if blood components are not available and once in hospital do not use crystalloids for patients with active bleeding.

In pre-hospital settings, titrate volume resuscitation to maintain a palpable central pulse (carotid or femoral).

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In hospital settings, move rapidly to haemorrhage control, titrating volume resuscitation to maintain central circulation until control is achieved and use a ratio of 1 unit of plasma to 1 unit of red blood cells to replace fluid volume.

Limit diagnostic imaging (such as chest and pelvis X‑rays or FAST [focused assessment with sonography for trauma]) to the minimum needed to direct intervention in patients with suspected haemorrhage and haemodynamic instability who are not responding to volume resuscitation.

Use interventional radiology techniques in patients with active arterial pelvic haemorrhage unless immediate open surgery is needed to control bleeding from other injuries.

6. Reducing heat loss in prehospital and hospital settings

Minimise ongoing heat loss in patients with major trauma.

7. Pain management in pre-hospital and hospital settings

Use intravenous morphine as the first‑line analgesic in major trauma and adjust the dose as needed to achieve adequate pain relief and if i.v. access has not been established, consider the intranasal route for atomised delivery of diamorphine or ketamine.

Consider ketamine in analgesic doses as a second‑line agent.

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8. Documentation in prehospital and hospital settings

The trauma team leader should be easily identifiable to receive the handover and the trauma team ready to receive the information.

Produce a written summary, which gives the diagnosis, management plan and expected outcome.

9. Providing support

If the patient agrees, invite their family member, carer or friend into the resuscitation room. Ensure that they are accompanied by a member of staff and their presence does not affect assessment, diagnosis or treatment.

10. Training and skills

So lastly the guidelines state as you might expect that all staff should be up to date with this guideline and should have up to date training for the interventions that they are required to deliver.

So as previously mentioned these are just a handful of the points and guidance contained within the document. Make sure you have a look through it yourself here and we’ll release a podcast summing up these points in the next week or so.


Cervical Spine Collars & Immobilisation

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C-spine Immobilisation and Clearance

Cervical collars have been used since the Vietnam War and after their implementation in the ATLS guidelines they have been considered the benchmark in trauma patients when there were any concerns about the C-Spine stability.

Studies about the real utility of these devices to date haven’t shown a clear benefit, mostly of them have been poorly conducted with a limited number of patients due to the potential catastrophic consequences of secondary spinal injuries. Subsequently the pre-hospital and intra-hospital management hasn’t changed for years.

So, collars have been introduced to prevent secondary injury to the spinal cord but what does the literature say about this practice? Are they really game-changing?

In a recent review by OTO (2015), the authors reviewed the published literature from 1979 till 2013 and they concluded that the cause of deterioration of the 24 c-spine injuries in a total of 12 different studies, were non specific and more importantly not care related.

They identified 3 categories of high- risk patients for secondary deterioration after c-spine trauma:

  • altered mental status
  • ankylosing spondylitis
  • iatrogenic manipulation.

And their conclusion about Secondary injury was mostly linked to:

  • thrombosis
  • hypotension
  • hypoxia
  • but NOT care related.

So, we don’t have a clear demonstration of their utility but what about their potential harm?

What we know so far……

  • increased intracranial pressure by reducing the venous drainage ( up to 4.5 mmHg)
  • aspiration/ respiratory compromise
  • limiting mouth opening. More difficult airway management.
  • pain from local ischaemia
  • hiding other injuries
  • claustrophobia
  • delays in transport

In this review by Benger (2009), the authors discuss the drawbacks associated with collars and immobilisation devices and suggest not to use them in co-operative patients even if an underlying cervical spine fracture is suspected for these reasons:

  1. Unstable C-spine injuries in awake and co-operative patients are rare (UK 10-15 per million per year spinal cord trauma. Half of them are cervical #).
  2. Unlikely, in awake patients, further movement will cause more harm than the initial force which created an unstable injury.
  3. Often cervical collars are poorly applied and even if well fitted, they don’t avoid neck movements (30 degrees flexion and extension are still permitted).
  4. Potential harms discussed previously.

Moreover in patient with a penetrating cervical trauma we already know the harms caused by general immobilisation hence the cervical collar must be avoided. Once of the most representative studies about this topic was published by Haut (2010). A retrospective analysis of penetrating trauma patients.

Primary outcome: mortality. Calculated NNT and NNH for spine immobilisation.

Total of 45,284 pts.

4.3% underwent spinal immobilisation. Overall mortality 8.1%

OR of death 2.06 if immobilised (95% CI: 1.35-3.13)

NNT 1.032

NNH 66

Evidence Surround C-Spine Clearance

In 2000 Hoffman et al published the NEXUS study (overall 34 069 blunt trauma patients).

Briefly, if patients meet all the 5 criteria, no imagining is needed and the C-spine can be cleared……..

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Sensitivity 99%

Specificity 12.9%

NPV 99.8%

PPV 2.7%

In 2001, Stiell et al published a study which became famous as the Canadian C-Spine rule (CCR). (in total 8924 awake blunt trauma patients)……

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In 2003 Stiell et al compared NEXUS vs CCR in a prospective cohort study (8283 patients) (12)


With CCR: 1 missed injury;

Nexus 16 missed injuries, 4 of which unstable

CCR was statistically more sensitive than the NEXUS in the detection of significant cervical spine injury.

C-spine Clearance and Guidelines

In 2009 the Eastern Association for surgery of trauma (EAST) published their guidelines about the management of cervical spine clearance in the traumatically injured patient.

The first edition can be easily summarised with these 4 points:

  • In awake, non symptomatic patients the c-spine can be cleared following the NEXUS criteria.
  • MDCT scan has got Class I Level I evidence of being superior to cervical x-ray.
  • In obtunded patients or awake but symptomatic a MRI should be done
  • Hard collar should be removed within 72 hrs and avoid prolonged immobilisation

There has been a long debate about the superiority of MRI towards CT.

Several studies and meta-analysis failed to highlight any superiority of the former.

Finally, BADHIVALA (2015) completed a systematic review of 28 observational studies (3627 patients with blunt trauma and obtunded) 20 retrospective cohort and 8 prospective (0% significant injuries missed if CT negative).

The conclusion was: WELL-INTERPRETED AND HIGH-QUALITY SCAN can avoid prologued collar use and routine adjust images

Primary outcome: clinically significant (mechanical instability) c-spine injuries missed by CT scan and detected with other tests.

Limits: retrospective studies. Only in English. No paeds.

Morevoer, CCT requires less time to complete the exam and there is an all in all reduction of costs!

In September 2015, EAST published the updated guidelines for C-spine clearance in obtunded patients. The conditional recommendation is to clear the c-spine in the obtunded patient who sustained blunt trauma after a negative MDCT alone. (conditional due to the very low-quality evidence).

They based their suggestion on a Systematic Review. The lack of RCT and complete cohort study designs was stressed out

Of 52 studies identified, only 12 were included in the qualitative synthesis and data extraction. Of 5 articles with a total follow-up of 1,017 patients none reported changes after collar removal. Of 11 studies with a total of 1,718 patients, no unstable c-spine fracture missed.

NPP MDCT 100% for unstable injury

91% any stable injury.

Their primary outcomes were new neurologic changes after cervical clearance and identification of an unstable injury.

Secondary ones: stable C-spine injury and their treatment, post-clearance imaging, false-negative CT, pressure ulcers and time to cervical removal

strenghts: multilevel systematic dual-review of the literature

limitations: low quality data and bias. Possible type II error (underpowered studies). Non homogeneous interpretation of the term obtunded.

In conclusion

If all the NEXUS criteria are met or the CCS is negative: clear the c-spine

If MDCT is negative, c-spine can be cleared even in the obtunded patients without requiring any other imaging.

Further information in February 2016 when NICE will publish the “Spinal Injury Assessment”guidelines.



  1.  American College of Surgeons Committee on Trauma. ATLS–9th Edition 2012, American College of Surgeons, Chicago.

2.         Hauswald, M., and Braude, D. Spinal immobilization in trauma patients: is it really necessary? Curr. Opin. Crit. Care 2002 8; 566–57

3.       Oto B, Corey DJ, Oswald J et al. Early secondary neurologic deterioration after blunt spinal trauma: a review of the literature. Academic emergency Medicine. 2015; 22: 1200-1212.

4.     Abram, S., and Bulstrode, C. Routine spinal immobilization in trauma patients: what are the advantages and disadvantages? Surgeon 2010 8; 218–222

5.     Hunt, K., Hallworth, S., and Smith, M. The effects of rigid collar placement on intracranial and cerebral perfusion pressures. Anaesthesia 2001 56; 511–513

6.     Goutcher, C.M., and Lochhead, V. Reduction in mouth opening with semi-rigid cervical collars. Br. J. Anaesth. 2005 95; 344–348

7.     Benger, J., and Blackham, J. Why do we put cervical collars on conscious trauma patients? Scand. J. Trauma Resusc. Emerg. Med. 2009 17; 44-48

8.   Haut ER, Kalish BT, Efron DT, et al. Spine immobilization in penetrating trauma: more harm than good? J Trauma 2010;68:115–20.

9. HoffmanJR,WolfsonAB,ToddKH,MowerWR.Selectivecervicalspine radiography in blunt trauma: methodology of the National Emergency X-Radiography Utilization Study (NEXUS). Ann Emerg Med 1998;32:461-9

10. Hoffman JR, Mower WR, Wolfosn AB. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. NEJM 2000; 343 (2): 94-99

11. Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian C-spine rule for radiography in alert and stable trauma patients. JAMA 2001;286:1841–8.

12. Stiell IG, Clement CM, McKnight RD The Canadian C-spine rule versus the NEXUS low-risk criteria in patients with trauma. N Engl J Med 2003; 349:2510–2518

13. Como JJ, Diaz JJ, Dunham CM, et al. Practice management guidelines for identification of cervical spine injuries following trauma: update from the eastern association for the surgery of trauma practice management guidelines committee. J Trauma 2009;67:651Y659.

14. Panczykowski DM, Tomycz ND, Okonkwo DO. Comparative effectiveness of using computed tomography alone to exclude cervical spine injuries in obtunded or intubated patients: meta-analysis of 14,327 patients with blunt trauma. J Neurosurg. 2011;115:541-9.

15. Badhiwala JH, Chung KL, Alhazzani W. Cervical Spine clearance in obtunded patients after blunt traumatic injury. Ann Int Med 2015; 162: 429-437.

16. Patel MB, Humble SS, Cullinane DC et al. Cervical spine collar clearance in the obtunded adult blunt trauma patient: a systematic review and practice management guideline from the Eastern Association for the Surgery of Trauma. Trauma Acute Care Surg. 2015; 78(2): 430-441

Intraosseous Access

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Intraosseous (IO) access, in order to provide medication and fluid products to the central circulation, was first suggested in 1922 By Drinker. Between 1922 and the 1980’s there’s been sparse evidence mentioning IO due to the arrival of intravenous (IV) access devices able to deliver the same treatments. Since then, literature surrounding rapid infusion of fluids have refocussed on the use of IO access where IV  has been difficult, due to user failure and/or patients with poor circulatory volume. With the incidence of military conflict and the formation of specialist pre hospital care teams with enhanced skills, further evidence surrounding IO access has been published recognising the benefits in the severely shocked patients. Additionally, usefulness in scenarios where IV access is either technically or environmentally difficult is acknowledged. In 2005 in the United States of America and from 2011 in the United Kingdom IO use has been routinely recommended in the cardiac arrest patient, both adult and paediatric, where IV access may be delayed.


A device, which is inserted directly into the medullary space of bone, allowing the delivery of fluid and medications directly into the vascular system.


There is slight variation exactly when an IO device should be inserted. A consensus does exist though that in critically unwell patients with anticipated difficult IV access an immediate IO access is appropriate, or where 2 attempts have been undertaken and not been successful. In addition a consensus that in the arrested patient IO may be the first line access preference. This is more prevalent in the major trauma patient where early and aggressive fluid resuscitation with blood, as recommended in the new Major Trauma Cardiac Arrest algorithm .

Which site?

Don’t forget that different products are only recommended for certain sites… e.g. sternal access you can only use the FAST device…at the moment… Here is a little breakdown of which manufacturer recommends which site…

Site Device Advocated Landmark
Proximal Tibia EZIO, BIG, NIO, Cook ALS, PHTLS, ATLS, APLS, EPLS 2-3 cm below the tibial tuberosity on the antereomedial aspect (BIG 1cm/1cm paeds)
Distal Tibia EZIO PHTLS, EPLS 3 cm above the medial malleolus
Distal Femur EZIO, Cook, APLS, EPLS,Truemper et al. (2012) (Literature review) 3 cm above the lateral epicondyle
Humeral head EZIO, NIO ALS, Adduct and rotate the shoulder medially. Locate acromion and coracoid process. Midway-palpate distally towards elbow until reaching greater tuberosity.
Sternum FAST (Adults only) PHTLS At sternal notch, in the manubrium at the upper cephelad portion of the sternum.
Calcaneum Not disclosed Single case study. McCarthy, G et al. (1998) The Calcanium as a site for Intraosseus Infusion. Journal of Accident and Emergency Medicine. 15(6). 421. Medial aspect with external/rotation at the hip.
Iliac crest Mentioned in NIO Paper. Not advocated/licensed .Military experience NIO specific paper Above tubercle of Iliac Crest
Distal Radius Not disclosed Mentioned in one paper. Not specified

Manufacturer-sponsored video on Proximal Tibia and Humeral Head

Manufacturer-sponsored video on Sternal access

Volume and speed of infusion

From the literature reviewed the majority of the studies compared humeral head IO infusions rates with Tibia Plateau. Of the seven studies reviewed, six identified that humeral head site was preferable where infusion rates ranged from 41 mls/min to 213 mls/min for humeral head and 15 mls/min to 165 mls/min. The only studies that reviewed and compared the sternal site with other sites preferred the sternal site with 93.7 mls/min compaired with 57.1 mls/min in the humeral head as closets comparison. The studies unanimously agreed that in all cases delivery with 300mg/hg of pressure was essential to get effective effusion rates.

Speed to central circulation

We found 3 studies found looking at time to central circulation compared with IV routes looking at drug effect and serum concentration levels. They found IO administration equivalent to IV access. Of the sites the sternal site appears to be the fastest to central circulation, with humeral head being a close second.

Ease of use

The literature is pre hospital heavy when it comes to selecting a site and in this environment the studies have found that the tibial plateu is preferable. This was mainly due to an increase in dislodgments in the humeral head site and more difficulty in locating the landmarks. There is contradiction across the literature on time taken to insertion but what is conclusive is that IO access, from a time perspective is more efficient than IV access and definitely CVC access.


Of the three studies found there are issues surrounding sponsorship, methodology and interpretation of results when looking at using local anesthetic to flush the device with. The most painful point is the initial flush, which open up the medullary space with the volume of flush.

What was found is that the Humeral head is subjectively less painful than other sites.

It is more painful to insert an IO than to have an IV. Consider this when inserting into conscious patients. There is no clear, well constructed work done yet to determine the best way to mitigate and manage this

Bottom line

The humeral IO has good success rates on access, admittedly more dislodgments that tibia (in pre hospital studies) and good infusion rates from a volume and time to central circulation perspective. Additionally in the conscious patient, the small volume of literature does appear to suggest that the humeral head is less painful that other sites.

It has been suggested that the humeral head should be utilised where you can secure the IO device and minimize movement to reduce dislodgement. If this is not possible then the proximal tibia is probably your next best option.

On paper, the best site is the sternum IO to deliver fluids and drugs to the patient. However this can effect compressions during cardiac arrest, can be ineffective in the trauma patient with chest injuries and with only one product available currently, not commonly used results in other sites being preferred. So probably not one for the mainstream yet.

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Inserting an IO

1.         Know your device. Get it out. Look at it. Look at what the manufacturers recommend

2.         Secure the limb that you are inserting the device into.

3.         Keep it clean. Take a few seconds to make sure the site is cleaned prior to insertion.

4.         Draw back once inserted. Reasure yourself it is in place. Not all IO’s draw marrow back… Attempt to flush some volume then try to draw back again… You may have a plug on he device

5.         Use systemic analgesia / dissociative medication / amnesic / along with the flush if your patient is likely to have experienced discomfort on insertion. The evidence on local anesthetic use isn’t powerful enough.

6.         Secure, secure, secure. You’ve worked hard to get it in…don’t loose it now. (See pictures)

7.         Once in…if possible keep looking for IV access as you increase circulating volume 



References/Reading list

Advanced Life Support Group (ALSG) (2011) Advanced Paediatric Life Support Manual. 5th ed. John Wiley and Sons: Manchester.

American College of Surgeons (2012) Advanced Trauma Life Support. 9th ed.

Barnard, E. et al. (2014) Rapid Sequence Induction of Anaesthesia via IO access: A prospective observational study. Academic Emergency Medicine Conference. 21(5 SUPPL 1): S79

Burgert, J. et al. (2014) An evidence based review of epinephrine administered via the IO route in anal models of cardiac arrest [review]. Military Medicine. 179(1): 99-104.

Byars, D. et al. (2011) Evaluation of Success rate and access time for an adult sternal IO device deployed in Prehospital care setting. Prehospital and disaster medicine. 26(2):127-29.

Calkins, M. et al. (2000) IO infusion devices: a comparison for potential use in special operations. Journal of trauma Injury, Infection and Critical Care. 48(6): 1068-74.

European Resuscitation Council (2015) European Trauma Course Manual. v1.9. European Resuscitation Council: London.

Flamm, A et al. (2015) Utilizing the NIO to gain Intraosseous Vascular access.

Academic Emergency Medicine Conference: 2015. 22 (5 Suppl 1): S150.

Frascone, R. et al. (2007) Consecutive field trials using two different intraosseous devices. Prehospital Emergency Care. 11: 164-71.

Hafner, J. et al. (2013) Effectiveness of a drill assisted IO catheter vs manual IO catheter by resident physicians in a swine model. Western Journal of Emergency Medicine. 14(6): 629-32.

Hartholt, K. et al. (2010) Intraosseous Devices: A randomized control trial comparing three devices. Prehospital Emergency Care. 14: 6-13.

Helm, M. et al. (2015) EZ-IO intraosseous device implementation in German Helicopter Emergency Medical Services. Resuscitation. 88: 43-47.

Joint Royal College Ambulance Liaison Committee (JRCALC) (2013) UK Ambulance Services Clinical Practice Guidelines. JRCALC: Warwick.

Kehrl, T. et al. (2011). Relationship of body mass index and increased difficulty with IO needle placement: Assessment of tissue depth using US.

Annals of Emergency Medicine. 15(2): 278-281.

Lairet, J. et al. (2013)A Comparison of proximal tibia, distal femur, proximal humerous infusion rates using the EZIO IO device on the adult swine model.

Prehospital Emergency Care. 17(2): 280-4

Lairet, J. et al. (2013) Comparison of Intraosseous infusion rates of plasma under high pressure in an adult hypovolemic swine model in two different limb sites. Academic Emergency Medicine Conference. 20 (5 SUPPL 1): S13.

Lamhaut, L. et al. (2010) Comparison of IV and IO access by pre hospital medical emergency personnel with and without CBRN protective equipment. Resuscitation. 81(1): 65-8.

Lee, P. et al. (2015) IO vs CVC utilization and performance during inpatient emergencies. Critical Care Medicine. 43(6): 1233-1238.

Leidel, B. et al. (2010) Comparison of two IO access devices in adult patients under resuscitation in the ED: A prospective randomized study. Resuscitation 81(8): 994-999.

Macnab, A. et al. (2000) A new system for sternal IO infusion in adults. Prehospital Emergency Care. 4: 173-77.

Miller, L. et al. (2010) A two-phase study of fluid administration measurement during intraosseous infusion. Annals of Emergency Medicine. 53(3): S151.

National Association of Emergency Medical Technicians (US) (NAEMT) (2014) Pre Hospital Trauma Life Support. Instructor Course Manual. 8th ed. Jones and Bartlett Learning: Burlington.

Ong, M. E. (2009) An observational, prospective study comparing tibial and humeral intraosseous access using the EZIO. American Journal of Emergency Medicine. 27(1): 8-15.

Pasley, J. et al. (2015) Intraosseous infusion rates under high pressure. A cadaveric comparison of anatomical sites. The Journal of Trauma and Acute Care Surgery. 78(2): 295-9.

Paxton J. et al. (2009) Proximal Humerus IO infusion: A preferred Emergency Venous Access. Journal of Trauma, Infection and Critical Care. 67(3): 606-

Philbeck, T. et al. (2009) Hurts so good. Easing IO pain and pressure. Journal of Emergency Medical Services. 35: 58-62.

Philbeck, T. et al. (2009). Pain Management during Intraosseous infusion through the proximal humerous. Annals of Emergency Medicine. 54(3 Suppl 1): S128

Reades, R. et al. (2010) Comparison of first attempt success between tibial and humeral IO insertions during out of hospital cardiac arrest. Academic Emergency Medicine Conference. 17: S65

Reades, R et al. (2011) Comparison of first-attempt success between tibial and humeral intraosseous insertions during out of hospital cardiac arrest. Pre Hospital Emergency Care. 15(2): 278-281

Reades, R. (2011) IO vs IV access during Out-of-Hospital Cardiac Arrest. An RCT. Annals of Emergency Medicine. 58(6): 509-516.

Shavit, I. et al. (2009) Comparison of two mechanical IO infusion devices: a pilot, randomised crossover trial. Resuscitation. 80(9): 1029-33.

Tan, B. et al. (2012) EZIO in the ED: An observational, prospective study comparing flow rates with proximal and distal tibia IO access in adults. American Journal of Emergency Medicine. 30(8): 1602-06.

United Kingdom Resuscitation Council (2015) Advanced Life Support Course Materials. United Kingdom Resuscitation Council: London.

United Kingdom Resuscitation Council (2010) European Paediatric Life Support Course Materials. 3rd Ed. United Kingdom Resuscitation Council: London.

Von Hoff, D. et al. (2008) Does IO equal IV? A pharmacokinetic study. American Journal of Emergency Medicine. 26(1): 31-38.

Warren, D. et al. (1993) Comparison of fluid infusion rates among peripheral intravenous and humerous, femur, malleolus and tibial IO sites in norvovolemic and hypovolemic piglets. Annals of Emergency Medicine. 22(2): 183-6.

Waisman, M. et al. (1997) Bone Marrow infusion in adults. Journal of Trauma-injury Infection and Critical Care. 42: 288-93.


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DAS 2015 Guidelines

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So you’ll all probably be aware to the Difficult Airway Society (DAS) Guidelines for airway management. They centre around the need to have an airway strategy that is already determined for when an airway crisis occurs. As we’ve previously mentioned having those plans to hand makes stressful situations an awful lot easier by decreasing the cognitive load.


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Atrial Fibrillation in the ED

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The way in which patients with AF present unsurprisingly makes a huge difference to the appropriate treatment and management plan, this may range from nothing at all right through to DC cardioversion. It’s really important to manage this group correctly though and have a sound understanding on the topic as timely appropriate treatment can significantly reduce morbidity and mortality, whereas inappropriate treatment can lead to an increase in the M&M.


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Sux vs Roc

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What are we discussing today?

If you’re a regular subscriber to HEFT EMCAST you will be aware of our recent discussion regarding ED rapid sequence induction. For those you who haven’t listened to the podcast, or simply need a reminder, rapid sequence induction (RSI) is the preferred method of emergency tracheal intubation outside the operating room because it results in a rapid state of unconsciousness (induction) and neuromuscular blockade (paralysis). There’s loads more information about ED RSI on the earlier episode, which you can view here along with the accompanying blog.

In today’s episode we will be looking at neuromuscular blockade for the purposes of RSI in the emergency department. Specifically, we are going to look at the two neuromuscular blocking agents (NMBA) suxamethonium and rocuronium.

We’ve covered a number of papers including a systematic review so there’s lots of information to digest. This reflects the paucity of data specific to the ED. There are some useful take home messages that are summarised at the end.

Why is this an important topic?

The choice of NMBA has become an important and controversial topic. Historically, suxamethonium was the only available NMBA and consequently has established itself as the traditional and first line agent when performing RSI. Its reported major benefits over other agents are primarily:

  • Quick onset: <60 seconds
  • Quick offset: due to a T1/2 of 5-8 minutes

However, suxamethonium has a number of contraindications, is associated with myalgias, and post-paralysis pain due to its depolarising properties. Consequently, non-depolarising agents such as rocuronium have increased in popularity with a number of proponents arguing in favour of their use over suxamethononium:

  • Quick offset is not desirable in ED where failure to intubate in a critically unwell patient is not an option and will mandate progression along the difficult airway algorhythm
  • Fewer contraindications including hyperkalaemia and family history of malignant hyperthermia
  • Reduced incidence of oxygen desaturation with rocuronium

For more information about these controversies see the blog by @emswami via emDOCS as well this article from the journal of Anesthesia and Analgesia.

What are neuromuscular blocking agents?

A sound knowledge of basic physiology and pharmacology is required to understand how neuromuscular blockers work. The importance of this is underlined when identifying contraindications to NMBA use as well managing the various potential adverse effects associated with any individual agent.

Neuromuscular blocking agents act at the neuromuscular junction (NMJ), where acetylcholine (Ach) is released by the pre-synaptic neuron in response to motor nerve depolarisation. This causes an influx of calcium resulting in pre-synaptic release of acetylcholine into the synapse with subsequent binding at nicotinic Ach receptors on the motor end plate. This causes an influx of sodium (and some potassium) and hence depolarisation. When depolarisation is sufficiently large an action potential is generated and the muscle contracts. Acetylcholine is then broken down by acetylcholinesterase.

A simple way to remember the mechanism of action of all NMBAs is that they interfere with transmission at the NMJ and therefore decrease skeletal muscle tone.

There are two groups of NMBA:

  • Non-depolarising: e.g. rocuronium, vecuronium, atracurium (MOA: competitive inhibition of Ach at nicotinic Ach receptors. Paralysis is gradual)
  • Depolarising: e.g. suxamethonium (MOA: mimics the action of Ach, causing fasciculation of skeletal muscle, without breakdown by acetylcholinesterase)

Screen Shot 2015-08-07 at 12.01.37

So which NMBA should we use in ED?

Much of the data comparing different NMBAs in RSI comes from the anaesthetics literature. Data obtained from this specialty may not be valid or generalisable to the critically ill patient in the ED.

Circumstances that make RSI difficult are common in the ED:

  • Spinal/neck immobilisation
  • Unfasted patients
  • Critically unwell with high oxygen demands
  • Unreliable or absent past medical and drug histories

In such circumstances the correct choice of NMBA is critical to achieve optimal intubating conditions and differences between agents are likely to be magnified.

A major argument against rocuronium use in ED RDI, particularly at higher doses (1.2mg/kg), is its prolonged duration of action (>30 minutes) and the need for on-going ventilator support.

What does the literature say?

Paper 1

The first paper we are looking at was published in The Journal of Emergency Medicine in 2008 by William Mallon et al. It is a critical appraisal of four papers identified after searching pubmed.

  1. Rocuronium versus succinylcholine for rapid sequence induction of anaesthesia and endotracheal intubation: a prospective, randomised trial in emergent cases. Anesthesia and Analgesia, 2005.
  • Design: non-blinded, RCT of 234 adult patients undergoing emergent surgery under GA
  • Intervention: rocuronium for paralysis at 0.6mg/kg
  • Control: succinylcholine for paralysis at 1.0mg/kg
  • Primary outcome: intubating conditions as assessed by the intubating anaesthetist using numerical (nine-point scale) and qualitative scales
  • Secondary outcome: time to intubation
  • Exclusions (n=54): hyperkalaemia, neurologic disorder, burns, family history of malignant hyperthermia, difficult airway (known or anticipated)


Intubating conditions (numerical score) significantly better after administration of succinylcholine (8.6 +/- 1.1) than with rocuronium (8.0 +/- 1.5, p=<0.001)

Time to intubation: succinylcholine significantly (p=<0.0001) shorter (median, 95s) compared with rocuronium (median, 130s)

  1. Comparison of rocuronium and suxamethonium (succinylcholine) for use during rapid sequence induction of anaesthesia. Anaesthesia, 1998.
  • Design: double-blind, RCT of 348 adult patients scheduled for elective or emergency surgery requiring ET intubation.
  • Intervention: rocuronium for paralysis at two doses (0.6 and 1.0mg/kg)
  • Control: succinylcholine at 1.0mg/kg
  • Primary outcome: To compare the intubating conditions with the two doses of rocuronium using a three-point scale (excellent, good, poor) as assessed by a blinded observer 50s after injection of the NMBA
  • Secondary outcome: comparison of the better of the two doses of rocuronium with suxamethonium at a dose of 1.0mg/kg
  • Exclusions (n=34): elevated BMI, pregnancy, concomitant medications known to interact with NMBA, difficult airway (known or anticipated)


Rocuronium dose comparison: significantly higher frequency of good and excellent conditions in the higher dose (1.0mg/kg) group (p= <0.01)

Suxamethonium versus high dose rocuronium: Excellent grade intubating conditions significantly (p=0.02) higher in the suxamethonium group (80%) compared with the high dose rocuronium group (65%). The frequency of clinically acceptable intubating conditions (excellent and good) was similar between rocuronium (96.2%) and suxamethonium (96.9%, p=0.82)


  1. A comparison of succinylcholine and rocuronium for rapid sequence intubation of emergency department patients. Academic Emergency Medicine, 2009.
  • Design: Prospective cohort study of 520 patients of all ages undergoing RSI in the ED
  • Intervention: rocuronium for paralysis (average dose 1.0mg/kg) to all patients with contraindications to succinylcholine and those unable to give a history
  • Control: Succinylcholine for paralysis (average dose 1.7mg/kg)
  • Primary outcome: Assessment by means of a 10-point numerical descriptor for:

i)      The patient’s body movements during intubation

ii)     Vocal cord movement during intubation

iii)   The physician’s overall satisfaction with the extent of paralysis

  • Secondary outcomes:

i)      Time from drug administration to paralysis

ii)     Need for BVM

iii)   Pulse oximetry readings during intubation

iv)    Any complications

v)     Serum [K+] at time of intubation

  • Exclusions: none


Succinylcholine had a significantly faster onset time (39s, 95%CI 37-41s) than rocuronium (44s, 95%CI 39-50s), p=<0.04.

Succinylcholine resulted in significantly less (mean 9.1 +/- 1.1) movement than rocuronium (mean 9.1 +/- 1.5), p=0.01

There was no significant difference in vocal cord movement between succinylcholine (mean 9.2 +/- 1.6) and rocuronium (mean 9 +/- 1.6), p=0.15

Overall satisfaction was significantly higher with succinylcholine (mean 9.4 +/- 1.3) thank with rocuronium (8.8 +/- 2.0), p=<0.01

  1. Rocuronium versus succinylcholine for rapid sequence induction intubation. Cochrane Database of Systematic Reviews, 2008
  • Design: Systematic review of all patients of any age who underwent intubation by RSI either electively or emergently
  • Intervention: Search for RCTs or CTs relating to trials comparing succinylcholine and rocuronium for RSI intubation
  • Primary outcome: achievement of excellent intubating conditions using a three point scale (excellent, good, poor) during RSI comparing rocuronium and succinylcholine
  • Secondary outcomes: achievement of clinically acceptable (excellent or good) intubating conditions during RSI comparing rocuronium and succinylcholine
  • Exclusion criteria: 21 articles excluded


37 studies included for analysis. Succinylcholine was superior to rocuronium, with relative risk 0.86 (95%CI 0.80-0.92, n=2690).

No statistical difference in intubating conditions when succinylcholine was compared to the 1.2mg/kg rocuronium however, succinylcholine was clinically superior due to its shorter duration of action.

The second paper we are going to look at is from the journal of Critical Care, published in 2015 by Richard Lyon et al and a full open access version can be found via this link.

The paper is titled ‘significant modification of traditional rapid sequence induction improves safety and effectiveness of pre-hospital trauma anaesthesia’. The study took place in the context of pre-hospital RSI performed by dedicated helicopter emergency medical service (HEMS) teams. These teams serve a population of 4.5 million in South East of England and undertake around 1500 missions per year.

This was a comparative cohort study performed to compare the efficacy of two different RSI protocols over two separate 14-month periods three years apart:

  • Group 1, July 2007-October 2008: pre-hospital RSI using a protocol consisting of etomidate (0.3 mg/kg intravenously (IV)) and suxamethonium (1.5 mg/kg IV) followed by tracheal intubation
  • Group 2, February 2012-March 2013: pre-hospital RSI using a modified protocol consisting of fentanyl (3 mcg/kg), ketamine(2 mg/kg) and rocuronium (1 mg/kg) followed by tracheal intubation (3:2:1 regimen). A reduced dose of fentanyl (1 mcg/kg IV) and ketamine (1 mg/kg IV) was administered in patients with haemodynamic compromise (1:1:1 regimen)

The patient population included all consecutive trauma patients undergoing pre-hospital RSI during the defined study periods. All non-trauma patients were excluded. The decision to intubate was made by the attending on-scene risk-benefit assessment. Monitoring includedoxygen saturation, heart rate (HR), electrocardiogram and capnography.

The primary outcome measure was intubation success, and the acute haemodynamic response (hypertension, hypotension, tachycardia) to laryngoscopy and tracheal intubation.

So what did they find?

After exclusions (n=13) 261 patients were included for analysis (Group 1, n=116; group 2, n=145). The key results were:

  • Baseline characteristics: Group 2 were significantly older (39 years versus 45 year, p=0.03) and had significantly higher injury severity score (22 versus 26, p=0.019)
  • Intubating conditions: Laryngoscopy of patients in group 2 resulted in significantly better laryngeal views (p=0.013). Tracheal intubation was 100% successful within three attempts for both groups, however, first attempt intubation success was significantly higher in group 2 compared to group 1 (95% versus 100%, P = 0.007)
  • Haemodynamic response to laryngoscopy and tracheal intubation: Seventy-seven patients (66%) in group 1 and 111 patients (77%) in group 2 were administered a full-dose RSI protocol. Baseline haemodynamic measures were similar in the two groups. For each group, the haemodynamic response following a reduced-dose RSI was similar to the response observed following a full-dose RSI

o   A hypertensive response to laryngoscopy and tracheal intubation was less frequent following Group 2 RSI (79% versus 37%;
p < 0.0001)

o   A hypotensive response was uncommon in both groups (1% versus 6%; p = 0.05)

  • Outcome to hospital discharge: no significant mortality difference between the two groups; on subgroup analysis for head injury severity no significant difference was found

o   On univariate analysis the only factors significantly associated with mortality were age, initial Glagow coma score (GCS), injury severity score (ISS), and RSI dose

o   After adjusting for these variables, only age, initial GCS, and ISS remained independently associated with mortality

So what’s the take home message?

The findings of this study suggest that for pre-hospital RSI in trauma patients a combination of fentanyl, ketamine and rocuronium produced superior intubating conditions and a more favourable haemodynamic response to laryngoscopy and tracheal intubation.

Ketamine did not appear to have any adverse effects on head injury outcomes (although sample size on subgroup analysis was small).


  • The study compared the above RSI regimen with etomidate and suxamethonium, which is not the standard operating procedure in most UK A&Es
  • The study took place in the pre-hospital environment and not the ED
  • Retrospective cohort study
  • Group 1 patients had higher injury severity scores and were older

 Paper 2

The next article takes a look at whether suxamethonium use in RSI is associated with great oxygen consumption than rocuonium. The paper was published by S. Taha in the journal Anaesthesia in 2010.

Why did we include this paper?

Because suxamethonium is a depolarising NMBA that causes skeletal muscle fasciculation it has been postulated that this hastens desaturation after pre-oxygenation during RSI. This is a big issue for all patients undergoing general anaesthesia however, in the undifferentiated patient presenting to ED with critical illness (and therefore high oxygen demands) its manifestation could have profound effects.


A prospective partially blinded RCT of 60 ASA I or II patients admitted for elective surgery in a single centre. The country and location of the study is not described.


The primary outcome was to assess the time taken to desaturate to 95% folowing RSI. Patients were randomly assigned to one of three RSI protocols:

  1. Group R: lidocaine, 1.5mg/kg; fentanyl, 2mcg/kg; propofol, 2mg/kg; rocuronium, 1mg/kg
  2. Group S: lidocaine, 1.5mg/kg; fentanyl, 2mcg/kg; propofol, 2mg/kg; suxamethonium, 1.5mg/kg
  3. Group SO: saline, saline, fentanyl, 2mcg/kg; propofol, 2mg/kg; suxamethonium, 1.5mg/kg

Time of apnoea was measured from removal of the facemask after pre-oxygenation to when the patients desaturated to 95%; the tracheal tube was then attached to the ventilator.

Secondary outcomes included:

  • Intensity of visible muscle fasciculations: Four point score
  • Duration of muscle fasciculations
  • End expiratory oxygen and carbon dioxide after initiation of ventilation

The anaesthetist performing pre-oxygenation also scored the fasciculation score, duration of fasciculation, and duration of apnoea. They were blinded to the treatment arms.

What did they find?

Patient characteristics were similar for each of the three groups.

Median (IQR) time to 95% desaturation was significantly shorter in group S and SO compared to group R:

  • Group S vS Group R: 358s vs 378s (p=0.003)
  • Group SO vS Group S: 242s vs 378s (p=0.001)
  • Group SO vS Group R: 242s vs 358s (p=0.001)

The fasciculation score and duration of fasciculation were significantly greater in Group SO than in Group R and Group S, and greater in Group S than in Group R. Full data is available in the article.

What’s the take home message?

When suxamethonium is adminstered for RSI of GA, a faster onset of oxygen desaturation is observed during the subsequent apnoea compared with rocuronium. Co-adminstration of lidocaine and fentanyl with suxamethonium prolongs the time to desaturation.

Paper 3 

The final article we are going to discuss today was published in 2011 and is from the journal ACTA Anaesthesiologica Scandinavica titled ‘Desaturation following rapid sequence induction using succinylcholine vs. rocuronium in overweight patients.

Why did we include this paper?

To look at whether hypoxaemia is more common in RSI involving suxamethonium versus rocuronium. The reasons are exactly the same as the above paper except the patient population is slightly different.


This was a prospective double-blind RCT between August 2007 to February 2009. Sixty patients with BMI 25-30 kg/m2 were prospectively recruited; all patients were ASA grade I and II, aged 23-64 years, and undergoing elective surgery requiring general anaesthesia.

Exclusions included: contraindications to either suxamethonium or rocuronium, haemoglobin < 6.8mmol/l, pregnancy, significant cardiovascular disease, and known/anticipated difficult airway.


The time from administration of a NMBA to an oxygen saturation (SpO2) of 92% was defined as the ‘safe apnoea time’. The time taken from initiation of ventilation (when SpO2 reached 92%) to SpO2 reached 97% was defined as the ‘recovery period’.

The primary outcome measure was the ‘safe apnoea time’ and a 30 second difference was considered clinically relevant.

Patients were randomised to receive either 1.5mg/kg of suxamethonium or 0.9mg/kg of rocuronium. The RSI regimen comprised NMBA, propofol (to achieve a target serum concentration 5 micrograms/ml), midazolam (0.02mg/kg), fentanyl (1.5micrograms/kg).

Patients were intubated 60 seconds after administration of a NMBA. Following confirmation of tube placement the tracheal tube was left open to air until oxygen saturation fell to 92%. The patient was then connected to the ventilator.

A series of arterial blood gas (ABG) samples were taken to measure oxygen saturation at various points during the RSI:

  • ABG 1: At baseline, prior to pre-oxygenation
  • ABG 2: After 3-minutes pre-oxygenation
  • ABG 3: Once SpO2 fell to 92%

Times were recorded when oxygen saturation (SpO2) reached 98%, 96%, 94%, and 92%.

So what did they find?

Mean safe apnoea time was significantly less with the succinylcholine group (283 seconds, 95%CI 257–309 seconds) compared with the rocuronium group (329 seconds, 95%CI 303–356 seconds; p=0.01).

The mean recovery period was significantly longer in the succinylcholine group (43 seconds, 95%CI 39-48 seconds) compared with the rocuronium group (36 seconds, 95%CI 33-38; p=0.002)

What have we covered?

  • Neuromuscular blocking agents are used in RSI and result in paralysis of skeletal muscle
  • The use of rocuronium in RSI is increasing. From the ED perspective, this may be advantageous:
  • Quick offset is not desirable in ED
  • Fewer contraindications including hyperkalaemia
  • Reduced incidence of oxygen desaturation with rocuronium
  • From the papers we have looked at:

 Suxamethonium was favourable to rocuronium in most instances however, data is largely from the anaesthetics literature

A higher dose of rocuronium (1.2mg/kg) may produce comparable intubating conditions compared to suxamethonium at standard dose (1.0mg/kg)

In the pre-hospital environment, a modified RSI protocol utilising rocuronium resulted in favourable intubating conditions and haemodynamic response to laryngoscopy and tracheal intubation

Rocuronium may, in overweight patients, increase the safe apnoea time compared to suxamethonium however, the best study looking into this is not of high enough quality to inform practice.

Take home messages

Use of a modified RSI protocol utilising rocuronium instead of suxamethonium may be advantageous in a specific group of patients in certain environments. Whether this translates into an advantage in the ED is debatable.

Those undertaking RSI in the UK should be proficient in the skill, which includes rescue techniques, before considering its application.



  1. Swaminathan A. 2014. Roc Rocks and Sux Sucks! Why Rocuronium is the Agent of Choice for RSI. emDOCS. Accessed 11th July 2015.
  2. Mohammad EO, Connolly LA. 2010. Rapid Sequence Induction and Intubation: Current Controversy. Anesth Analg. 2010 May 1;110(5):1318-25
  3. Mallon W, Keim S, Shoenberger J, et al. 2008. Rocuronium vs. succinylcholine in the emergency department: a critical appraisal. J Emerg Med. 37(2):183-8
  4. McCourt KC, Salmela L, Mirakhur RK, et al. 1998. Comparison of rocuronium and suxamethonium for use during rapid sequence induction of anaesthesia. Anaesthesia. 1998 Sep;53(9):867-71
  5. Lyon R, Perkins Z, Chatterjee D, et al. 2015.   Significant modification of traditional rapid sequence induction improves safety and effectiveness of pre-hospital trauma anaesthesia. Critical Care. 015, 19:134
  6. Taha S, El-Khatib MF, Baraka AS, et al. Effect of suxamethonium vs rocuronium on onset of oxygen desaturation during apnoea following rapid sequence induction. Anaesthesia, 2010, 65:358-361
  7. Tang L, Li S, Huang S, et al. Desaturation following rapid sequence induction using succinylcholine vs. rocuronium in overweight patients. Acta Anaesthesiol Scand 2011; 55: 203–208


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EMS Handover; make a difference to all alerted patients

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In Emergency Medicine we pride ourselves on treating the undifferentiated acutely ill patient. The ones that no clinician has seen and it’s up to us to ascertain exactly what’s going on but is that really the case?

EMS professionals (Paramedics and technicians in the UK) provide a service to the truly undifferentiated patient. Irrespective of the situation and problem that confronts them the EMS are forced to work in isolation forming a rapid assessment, management plan and deliver that patient to the correct destination if deemed necessary.

As Emergency Medicine clinicians we can at times take this service for granted. We receive a pre alert for the sickest of the EMS patients, arming us with the key bits of information along with treatments that have been instituted.

The ETC (The European Trauma Course) is based upon the principles of team leading and team working and talks about using the pre alert time to prepare equipment and staff for the incoming patient. This time can helps to ensure that the team is able and prepared for the case and contact any further help that may be required.

Screen Shot 2015-07-30 at 10.14.36

The ETC also talks about reception and transfer of patients in a structured fashion. The course recommends a ‘5 second round’ in which the following are identified;

  • Is the patient in cardiac arrest?
  • Are there signs of massive external haemorrhage or severe hypovolemic 
  • Is their airway clear, acceptable or
obstructed needing immediate intervention?
  • Is ventilation and oxygenation 
adequate or unacceptable?
  • Are there any major deformities of 
head, neck, trunk or limbs?
  • Note their skin colour and temperature 
while feeling the pulse.

If one of the above major issues is identified then a few specific actions may take place to include;

  • Start cardiopulmonary resuscitation (CPR) if required
  • Control external haemorrhage
  • Securing the airway, support of 
  • Request further help or support e.g. 
massive transfusion protocol.

However if none are present then the team leader’s next task is to take the MIST handover which is defined as the following;

  • Mechanism of injury
  • Injuries identified to date
  • Signs and symptoms
  • Treatments administered and the response so far

This structure enables all members involved in the patient care, both in hospital receiving teams and those delivering the patient to that care, to work in an expected and structured fashion with a dependable format.

It is likely that EDs receive major trauma in the most regimented and professional manner in comparison to other acute presentations. Trauma carries a sexy image and receives a significant amount of publicity and attention as a result. But think for just a moment about the other alerts you receive, sepsis, respiratory distress, cardiac arrests, do you handover in a such a regimented and pre determined fashion? Is there a tendency to eye roll and downplay what the EMS have taken time and skill to evaluate and formed a working diagnosis over? And if so what gives us the right to make such sweeping assumptions and is it fair to give a different service to those outside of the trauma cohort.

As EM clinicians we experience these assumptions from receiving specialities from time to time and it is disappointing to think that occasionally we may also be guilty of such behaviour. Don’t get me wrong, I’m not saying as a speciality that we’re all poor at receiving handovers from EMS providers I just think it’s an area that we could probably pay more attention to.

This podcast follows reflection on a recent case and hopefully will make me better at receiving handovers.

There are some really useful papers out there on this topic and we’ll run through a few;

; Alix J. E. Carter, PREHOSPITAL EMERGENCY CARE 2009;13:280–285

This paper looked at patients with a full trauma team activation at a level 1 trauma centre in the US

They conducted a literature search in order to determine the key prehospital data elements that have prognostic value and thus would be key for hospital staff to hear and receive. They identified a list of 16 key data elements including;

  • Prehospital hypotension
  • GCS score
  • Patient age
  • End tidal CO2value
  • Pulse rate
  • Respiratory rate
  • Oxygen saturation
  • Blood loss in the field (quantity)
  • Death of an occupant in the same compartment
  • Mechanism of injury
  • Intrusion
  • Extrication time
  • Estimated crash speed
  • Anatomic location of injury
  • Preexisting disease
  • Prehospital intubation

The study included adult patients for whom videotaped documentation of the whole trauma was available from the initial arrival to the departure of the trauma bay. Two physicians reviewed the tapes noting which of the 16 key data elements (that were relevant to the case) were verbally transmitted to the receiving team, 2 further clinicians blinded to the results of this checklist then reviewed the notes to ascertain which of the key 16 data points had been noted/received by the trauma team.

They reviewed a total of 113 handovers. They found an average of 4.9 data points were handed over per trauma. Most frequent pieces of information that were handed over were;

  • Mechanism
  • Anatomic location of injury
  • Age

An average of 72.9% of these data points were received (i.e a loss of nearly a quarter of the key points)

Maintaining eye contact: how to communicate at handover, Erin Dean. EN1910Mar2012 06-07

This papers talks about the degradation of information during handover, again following a study of 100 video analysis of handovers. Key findings were;

  • Variance in handovers from paramedics – all started with identification of the patient, 2 thirds then identified the presenting complaint, just over half went on to discuss presenting complaints in detail and in about a quarter the paramedics then provided information on the patients’ vital signs
  • ED staff asked questions during or after 93 percent of handovers – 1/3 of the time this information had already been provided
  • Times for handover varied between 26 seconds to 4 minutes, with more senior paramedics tending to take longer to handover
  • The amount of eye contact influenced the length of handover with greater eye contact associated with shorter handover times

The recommendation was made following the review that a 20 seconds of hands off time was instituted where ED staff minimize physical contact and are not allowed to interrupt but that maximum eye contact should be made.

Following these recommendations a protocol was also set up for handovers to include the following;

  • Identity of the patient
  • Mechanism of injury or complaint
  • Injuries
  • Signs and symptoms
  • Treatment and trends
  • Allergies
  • Medication, background history
  • Other information

After institution a secondary analysis of handovers showed;

  • Average duration of handovers had reduced from 96-83 seconds
  • Amount of eye contact had increased between ED staff and paramedics and reports that ED staff more fully understood handovers
  • The number of handovers in which ED staff asked questions reduced from 93-41%)
  • The number of paramedics needing to repeat information halved

The handover process and triage of ambulance-borne patients: the experiences of emergency nurses. Karin Bruce .2005 British Association of Critical Care Nurses, Nursing in Critical Care 2005 Vol 10 No 4

This paper explored the experiences of nurses receiving patients who were brought into hospital as emergencies by ambulance crews. It was a qualitative descriptive study that centered on structured interviews of ED nursing staff on the topic of handover. The trends they found were;

  • Pre alerts by EMS crews were well structured, brief and informative and required very little extra questioning
  • Less information was desirable on the patients past medical history and rather information centered around the presenting complaint was felt valuable

Review article: Improving the hospital clinical handover between paramedics and emergency department staff in the deteriorating patient, Sarah Dawson,
 Emergency Medicine Australasia (2013) 25, 393–405

This was a review of the literature with the following 2 objectives

  • what aspects of the clinical handover between paramedics and ED staff impact on the effective transfer of a patient in a state of physiological deterioration
  • how these aspects might be improved in the future

The main conclusions were under the following headings

  • Professional relationships, respect and barriers to communication, having experience, being confident and succinct (paramedics), and actively listening (ED staff) was key to efficient handover
  • Structure to handover/a tool was needed
  • Multiple/repeated handovers and identification of staff in ED, leads to information being lost
  • Education and training in handovers, one journal found that only 19% of ambulance staff in their study had formal training in giving a handover. In those without training regarding handover 83% felt a need for it.
  • Vital signs, were found in many studies to be some of the most fundamental and valued piece of information communicated in handover
  • Documentation and other data display formats, ideas such as displaying the prehospital observations on a computer screen in the ED were reviewed and comment was passed upon the nature of field observations being written on gloves/bedsheets/remembered and that these methods would lead to inaccuracies and inefficiency of data gathering and transfer.


Handover is your chance to glean as much information as possible about the patient coming into your care, to find out what the symptoms/signs/working diagnosis is, it’s also a chance to see how they have responded to the treatment given so far.

The importance of active listening, eye contact, not interrupting and taking the information on board cannot be overestimated. Not only is this in your patient’s interest but it also helps build solid working relationships with your EMS staff and will help you forge great working relationships for the future.

You can work on this with simple steps, welcome the EMS staff to your resus room, make it clear who will be receiving handover, challenge yourself to stay silent and maintain eye contact during handover until all of the information is given(I guarantee you’ll struggle!). Consider standard positions in the handover,

Screen Shot 2015-07-30 at 10.19.32maybe the nurse or EDP taking the head end of the patient on the slide over to the ED trolley by the monitor and the clinician/team leader taking the feet to easily adopt the end of bed/leadership position with ease.

Try it and let us know how you get on!



Information loss in emergency medical services handover
of trauma patients
; Alix j. e. Carter, Prehospital Emergency Care 2009;13:280–285

Maintaining eye contact: how to communicate at handover, Erin Dean. EN1910Mar2012 06-07

The handover process and triage of ambulance-borne patients: the experiences of emergency nurses. Karin Bruce .2005 British Association of Critical Care Nurses, Nursing in Critical Care 2005 • Vol 10 No 4

Handover from paramedics: Observations and emergency department clinician perceptions, Guohao Yong
. Emergency Medicine Australasia (2008) 20, 149–155

Handover from paramedics: Observations and emergency department clinician perceptions, Guohao Yong
. Emergency Medicine Australasia (2008) 20, 149–155

Review article: Improving the hospital clinical handover between paramedics andEmergency department staff in the deteriorating patient, Sarah Dawson,
 Emergency Medicine Australasia (2013) 25, 393–405

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Sepsis in the ED

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There’s no doubt that a case of sepsis will pass through your ED in the next hour or so. It’s a disease that carries a high mortality rate and requires prompt and effective care. In this podcast we’ll run through the following

  • Definition
  • SIRS
  • Severity levels
  • The Sepsis 6
  • Which patients require treatment within the hour
  • What is Early Goal Directed Therapy (EGDT)
  • Relevant literature to EGDT that may raise questions over it’s importance?

We’ll look at the following papers

  • Marik – CVP
  • Nguyen – Lactate clearance
  • Jones – Lactate clearance
  • TRISS – Hb transfusion thresholds
  • Bai – nor adrenaline in patients with septic shock
  • Recent trials specifically challenging EGDT, the Process, Arise and Promise trials
  • The Surviving Sepsis Campaign and their recent update

There are some fantastic resources out there. The Surviving Sepsis Campaign is resource that must be investigated as a body that sets the standards in the management of sepsis in the UK and further afield.  The RCEM Sepsis Toolkit gives a fantastic overview of sepsis care with specific relevance to its implementation in the Emergency Department.   References Rivers, Emanuel, et al. “Early goal-directed therapy in the treatment of severe sepsis and septic shock.” New England Journal of Medicine 345.19 (2001): 1368-1377. Marik, Paul E., and Rodrigo Cavallazzi. “Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense*.” Critical care medicine 41.7 (2013): 1774-1781 Nguyen, H. Bryant, et al. “Early lactate clearance is associated with improved outcome in severe sepsis and septic shock*.” Critical care medicine 32.8 (2004): 1637-1642. Jones, Alan E., et al. “Lactate clearance vs central venous oxygen saturation as goals of early sepsis therapy: a randomized clinical trial.” Jama 303.8 (2010): 739-746. Holst et al. Lower versus Higher Hemoglobin Threshold for Transfusion in Septic Shock. October 2014 371(15):1381 Bai, Xiaowu, Wenkui Yu, Wu Ji, Zhiliang Lin, Shanjun Tan, Kaipeng Duan, Yi Dong, Lin Xu, and Ning Li Early versus delayed administration of norepinephrine in patients with septic shock. Critical care, 2014, 18:532 The ProCESS Investigators N Engl J Med 2014; 370:1683-1693May 1, 2014DOI: 10.1056/NEJMoa1401602 The ARISE Investigators and the ANZICS Clinical Trials Group N Engl J Med 2014; 371:1496-1506October 16, 2014DOI: 10.1056/NEJMoa1404380 ProMISe Trial Investigators N Engl J Med 2015; 372:1301-1311April 2, 2015DOI: 10.1056/NEJMoa1500896  

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Sepsis SMACCback

So we’re here at SMACC being treated to a fantastic conference and some superb talks. Last night (Day 1) closed with a superb panel of experts from across the globe talking on sepsis including Melvyn Singer, Paul Marik, John Myburgh, Simon Finfer, Kathryn Maitland & Flavia Machado. The panel challenged current global practice on sepsis including the use of SIRS criteria, antiobitic prescribing patterns and the utility of lactate.

This led to a phenomenal response on twitter with many left wondering what to do with their sepsis care.

I’m here at the conference with Tim Nutbeam and Clare Bosanko who are both EM physicians down in the south west in Derriford Hospital. We came together to discuss what yesterday means for our sepsis care.

It is of note that Tim is a founding member of the UK sepsis trust and has been involved in the new sepsis guidelines produced by RCEM, RCP, RCGP, RCN & COP and the associated toolkits.


ResusMe Causes of a raised lactate 



Peripheral vasopressors and preshospital LMA vs ET Tube in Cardiac Arrest

Over the last few episodes we’ve talked about the use of vasopressors and their utility in resuscitation. It is a commonly held belief that giving vasopressors peripherally puts patients at high risk of extravasation and secondary skin necrosis. In an ideal world patients would have a central line placed and then have their vasopressors commenced, sadly life in the ED doesn’t always mean that time permits this luxury.

If you’re presented with a patient that requires vasopressors should you wait until that central access is gained or is it acceptable to commence peripheral vasopressors, obtain central access as quickly as is feasible and then convert over?

An RCT of just over 250 patients in 2013 looked at the complication rate when patients were randomly assigned to either peripheral iv access or central as their initial venous access in ITU. They showed a significant increase in complications (all be it non life threatening) when choosing the peripheral route and concluded ‘In ICU patients with equal central or peripheral venous access requirement, central venous catheters should preferably be inserted: a strategy associated with less major complications’. They defined complications with a relatively long list of events, including such things as a need to resite the iv site and difficulties insertion (defined as >2 attempts in gaining a peripheral iv) but included extravasation of fluid. This study wasn’t specifically looking at vasopressor infusions and looked at complications over a 28 day period.

This however isn’t the situation we’re faced with in ED, what we’re deciding is whether the vasopressors should be delayed to gain the gold standard access to ensure it’s safe delivery or if the risk is small enough to warrant commencing vasopressors before central access is gained.

A recent paper by Loubani, published in the Journal of Critical Care, gives us a greater understanding of the sort of risks we might be taking. The authors looked at adults with a spontaneous circulation who were receiving vasopressors either via a central venous catheter or peripherally. It was a systematic review of all published reports of both local tissue injury and extravasation. This obviously leads the paper wide open to reporter bias but as the authors state, current practice and concern over peripheral vasopressor is based only upon case reports and expert opinion.

The paper reviewed 325 separate events of local tissue injury or extravasation. They found the average duration of vasopressor infusion to be 56 hours prior to local injury occurring with a secondary major disability reported in 4.4% of events.

They also looked at the sites in which these events occurred and noted that the saphenous vein was the most commonly reported area of complications but that as a rule peripheral sites were more commonly affected than more proximal sites.

Whilst it’s difficult to make a firm statement about the safety or lack of it for administering peripheral iv vasopressors it’s probably reasonable that in the patient requiring urgent vasopressors, when the ability to gain central access will interfere with time critical interventions, running an infusion through a peripheral access (sited as proximally on the body as possible) for as short a period a time before switching to a central line seems reasonable. It’s key to make sure that the cannula is well sited and there are regular checks to ensure there isn’t any local damage or extravasation during its limited use. As with all of medicine it’s about weighing up the potential risks against the benefits to the patient.

The second paper we looked at by Benoit, published in Resuscitation, looked at outcomes when comparing patients in cardiac arrest who had EMS ET tubes placed compared with the use of supraglottic airway devices.

This was another systematic review and they found 10 relevant papers, including over 70, 000 patients and found some interesting associations.

Patients who received ET tubes rather than supraglottic devices had significantly better chances of ROSC, survival to hospital admission and neurologically intact survival to hospital discharge.

The authors point out that the 10 articles were all observational cohort studies with relatively low level evidence and that there will have been a number of confounders that could have influenced the results.

So although this isn’t necessarily a game changer, it’s interesting to see the association of patients receiving an ET tube in cardiac arrest, with a greater survival which isn’t widespread current teaching in the UK. It could of course be that seemingly simple airways led the EMS providers to feel more confident in performing an intubation, there may have competency levels that led those with a greater skill set to perform intubation which may reflect a greater underlying level of care that those patients received, or it may be that the benefit in ventilation and oxygenation inferred by intubation in arrests is genuine. It’s fair to say that more work will be needed in this area until we truly understand the relationship.

That’s it for this time, we’ll be back soon with some more Resuscitation based EBM and maybe I’ll bump into you next week in Chicago!!!!

Take care



Loubani, Osama M., and Robert S. Green. “A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheters and central venous catheters.” Journal of critical care 30.3 (2015): 653-e9.

Ricard JD, Salomon L, Boyer A, Thiery G, Meybeck A, Roy C, et al. Central or peripheral catheters for initial venous access of ICU patients: a randomized controlled trial. Crit Care Med 2013;41:2108–15.

Benoit, Justin L., et al. “Endotracheal Intubation versus Supraglottic Airway Placement in Out-of-Hospital Cardiac Arrest: A Meta-Analysis.” Resuscitation(2015).

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RSI in the ED; should EM be taking the lead?

What is an RSI?

Rapid sequence induction, or RSI, is the preferred method of emergency tracheal intubation outside the operating room because it results in a rapid state of unconsciousness (induction) and neuromuscular blockade (paralysis).

The Scottish Intensive Care Society defines RSI as follows;

‘Rapid sequence intubation is the administration of a potent induction agent (anaesthetic) followed by a rapidly acting neuromuscular blocking agent (usually suxamethonium) to induce unconsciousness and motor paralysis for tracheal intubation. It is assumed that the patient has a full stomach, and is thereforeat risk of aspiration of gastric contents. The aim is to render the patient unconscious and paralysed so that they can be intubated’

Securing the airway by means of RSI is particularly useful in patients with an intact gag reflex, ‘full’ stomach and a life threatening illness requiring immediate airway control. Common indications for RSI include:

  • Inability to maintain airway patency
  • Ventilatory compromise
  • Reduced GCS
  • Status Epilepticus
  • Anticipated loss of airway patency

It is important to remember that RSI performed outside of the operating theatre has many additional challenges. Internationally, there is huge variation in who is performing RSI in this circumstance. In the UK in most institutions, an anaesthetist, regardless of environment, performs RSI most commonly. Reasons for this are historical, political, and educational. Given the importance of emergency airway management however, one might expect emergency physicians (EPs) to perform RSI more regularly.

EM training in the UK involves ST2 which is a year dedicated to anaesthetics and ITU, a whole host of acute skills are learnt which also involves the need to gain the Royal College of Anaesthetist’s IACC (Initial Assessment of Clinical Competency). The IAAC is typically completed by a trainee after 3 months training and includes the ability to perform an RSI and failed intubation drill.

It would seem a shame to devote such time to achieving airway skills to then let them dwindle later on in your practice and once achieving competency one must ensure, as John Hinds stated at the recent RCEM conference in Belfast, that a clinician performing an RSI in the ED has ‘competence, confidence and currency’.

With a relative infrequency of RSI’s to perform in the ED with comparison to the exposure anaesthetists see in the operating theatre, one could be forgiven for thinking there is no place for a laryngoscope in the hand of an EM clinician.

A few issues however fuel the appetite for the EM clinician to remain involved in RSIs. Firstly we perform countless sedations in the ED, guidance from the Royal College of Anaesthesia states;

‘Because sedation is a continuum, it is not always possible to predict how an individual patient will respond. Hence all practitioners intending to produce a certain level of sedation should be able to rescue patients whose level of sedation becomes deeper than originally intended. Practitioners therefore require skills to recognize and manage airway, respiratory and cardiovascular problems caused by over sedation.’

It is unrealistic to expect anaesthetic and ITU colleagues to always be on hand immediately should a patient in the ED need an RSI with little advanced notice and if an EM clinician can perform an immediate safe and effective RSI, expedite care and reduce complications from undue delays then that would seem in everyone’s interests.

A recent online survey that we conducted at HEFT showed that when considering which departments to work in, the draw of an MTC was equally matched by the draw of departments that perform ED led RSIs. And if departments are considering how to be driving EM forward then developing the service is a hugely positive step.

Finally, the ED is a familiar and comfortable environment within which we as a speciality can develop and drill routines for procedures such as RSI. The RCoA set a standard of at least 2 monthly team practices for RSI and major trauma management using case scenarios, simulation and debrief which fits in well with current practices in EM.

As with many things in your EM career there will come a point at which you will need to decide consciously to keep upto date with your skills of RSI. This can either be achieved in an adhoc random fashion or as a structured joint specialty vision and working. If Emergency Medicine in the future is to hold RSI as a competence utilised skill then encorporating it into our regular department practice needs to occur sooner rather than later.

For this reason we’ve waded through some papers on the topic to see whether the aspiration holding on to that laryngoscope by the Emergency Clinician is something that is appropriate and safe for our patients. Make sure you take a look at the recent St Emlyns post on the Kerslake paper we cover as well.

Kovac, 2004.

In this review article the authors tackle the historical precedent that has contributed to the dogma associated with EPs performing RSI using neuromuscular blocking agents (NMBA). The authors provided narrative as well as reviewing the evidence that supports ED RSI.

Before delving into individual articles the authors spent some time discussing the important topic of airway management training.  In a survey performed by the authors they report that only 16% of EPs reported having received formal airway management education during higher education.  They go on to say that postgraduate education in airway management, including airway courses such as ATLS, are in isolation unlikely to equip clinicians with the necessary skills to competently manage the airway.  They point out that such courses focus on the procedure of RSI and neglect the other important aspects of airway management including:

1) Recognizing the need for airway management

2) Understanding the indications for and contraindications to RSI

3) Developing skills in bag-valve maskventilation and laryngoscopy

4) Developing an approach to the difficult andfailed airway

5) Developing and maintaining cognitive andpsychomotor skills

It’s important to recognise the old saying of ‘use it or lose it’ when thinking about maintaining clinical competency. For an interesting podcast about this go to #RCEMBELFAST podcast with John Hinds where he coins the phrase ‘currency’ when discussing this topic.

The body of the article then goes on to discuss a number of articles looking at RSI performed by the non-anaesthetist.  A summary of the data is presented in the following table:

Author Design Variables RSI (%) Sedation (%) Nastracheal (%)
Walls, et al. 2000 Prospective observational (n=6294) Methods 69.5 6.8 5.1
Success 98.7 90.2 87.2
Attempts (>3) 2.1 10.7 14.3
Complications 15.3% overall
Li, et al.1999 Prospective observational (n=233) Methods 71 29
Success 99 72
Attempts (>3) 2 24
Complications 28 78
Sakles, et al. 1998 Prospective observational (n=610) Methods 83.4 15.2 1.3
Success 99.4 91.4 75
Attempts (>2) 5.3% overall
Complications 9.3% overall
Tayal, et al. 1999 Prospective observational (n=596) Methods 70 NA NA
Success 100 NA NA
Attempts (>3) 3 NA NA
Complications 15.8 NA NA

Table: Airway management in the emergency department

Whilst the table above does not present data directly comparing the success, complication, and failure rates between anaesthetists and non-anaesthetists, it does provide encouraging results to support both the use of RSI over sedation or other techniques as well as the efficacy of RSI performed by the non-anaesthetist.

The authors emphasise the importance of on-going education and collaborative work between departments to ensure EPs are competent and current in managing all aspects of airway management.

Reid, 2004

The next paper we review is by the well known #FOAMed contributor @cliffreid et al.

The authors conducted a prospective observational study looking at RSIs performed by critical care doctors outside the operating theatre over a six month period in a large UK teaching hospital.

Of relevance to UK EPs, this paper presented RSI data for both anaesthetists and non-anaesthetists making comparison between groups possible. Given this methodology, it has the potential to be more relevant and generalisable to UK ACCS training and CME.

For the purpose of the study:

  • An anaesthetist was defined as a doctor with at least six months’ prior training in a pure anaesthesia post
  • A non-anaesthetist was defined as a doctor whose intubation skills were acquired in the intensive care unit or emergency department environment, or both, and who had not been employed as a trainee in anaesthesia at any time

What did they find?

Data was available for 208/211 patients who met the inclusion criteria.

Indication Number (% of total)
GCS <8 67 (26.3)
Falling GCS 30 (11.8)
Hypoxia 67 (26.3)
Respiratory failure 40 (15.7)
Transfer 19 (7.5)
Multiple injuries 9 (3.5)
Other 23 (9.0)

Table: Major indications for emergency RSI

Immediate complications

The intubating doctor was a non-anaesthetist (either unsupervised or supervised by another non-anaesthetist or an anaesthetist) in 75% of intubations. The likelihood of a failed intubation was greater in groups NA and M; p = 0.007 and p = 0.04 respectively.

No deaths occurred during RSI and no patient required a surgical airway. There were no failed intubations. Most common immediate complications were hypoxaemia (19.2%), hypotension (17.8%), and arrhythmia (3.4%).

Difficulty Group A number (%) Group NA number (%) Group M number (%)
>1 attempt at laryngoscopy 4 (7.8) 11 (13.4) 22 (29.3)
Unsuccessful intubation attempt (UIA) 2 (3.9) 9 (10.8) 15 (20)

Table: Difficulties in RSI according to physician group. Groups NA and M have a higer incidence of multiple attempts and UIAs. X2 analysis shows these differences are significant (p=0.007 and p=0.004, respectively)


Group A number (%) Group NA number (%) Group M number (%)
Arryhythmia 2 (3.9) 2 (2.4) 3 (4.0)
Hypoxaemia 7 (13.7) 18 (22.0) 22 (28.6)
Hypotension 8 (15.7) 16 (19.5) 13 (16.9)
Complicated RSIs 17 (33.3) 28 (34.2) 37 (49.3)
Total in group 51 82 75

Table: Complication rates of RSI performed by each physician group. There is no difference between the complication rates between the groups. X2 analysis p = 0.232.

What does this mean for us?

These results suggest that complications rates from emergency RSI are similar between anaesthetists and non-anaesthetists. Prior training in a formal anaesthesia post did not significantly affect complication rates, although there were more episodes of hypoxia when intubation was attempted by non-anaesthetists.

It is important to note that in this paper intubating teams comprised junior (SHO) doctors who received two weeks training in emergency airway management prior to the study period. These trainees were then supervised throughout the study until such time they were deemed competent and thus capable of independent practice. Whether this training and close supervision is provided to all clinicians undertaking RSI is unknown and may impact the generalisability of these results to other institutions.

The authors point out that “training programmes for non-anaesthetists should be defined and standardised to optimise the safe and timely securing of the airway in emergency situations rather than debating which specialists should do it”

Kerslake, 2015.

The last paper we discuss is a very large prospective observational study of tracheal intubation in a UK ED. It is the largest study of its kind in the UK to date with data collected over 12 years between 1999 and 2011.

It’s fair to say that in this Edinburgh ED, joint working with the anaesthetics and critical care departments is likely to have contributed to the extremely high rates of RSI performed by EPs (a whopping 78%). Of the 3738 intubations included, 2749 (74%) were RSIs, 361 (10%) were other drug combinations, and 628 (17%) received no drugs.   Compare these results with those North American studies discussed by Kovac above and you’ll see they aren’t hugely dissimilar.

The authors of this study found that tracheal intubation was successful in nearly all patients (99.6%) with a first time success rate of 85%; 98% of patients were successfully intubated with two or fewer attempts. Failed intubation was extremely rare (n=14); only five patients (0.13%) had a surgical airway performed.

Complications rates were extremely low (8%) and were directly related to the number of attempts made; 7% in one attempt, 15% in two attempts, and 32% in three attempts (p < 0.001). If we compare these results to the Reid article we can see that Kerslake reports far fewer complications (8% versus 33% for non-anaesthetists). The types of complications encountered (hypotension and hypoxaemia) however, were similar.

Overall, Kerslake provided excellent and encouraging data to support ED RSI performed by non-anaesthetists with extremely high success rate and low failure and complications rates. Such results are likely to have been achieved through the adoption of excellent collaborative ways of working between emergency physicians and their anaesthetic and critical care colleagues.

So putting this all together what have I taken away from these papers?

To summarise it neatly the above papers demonstrate that RSI involving NMBA is the preferred modality for securing the airway. When performed by non-anaesthetists outside the operating room RSI has high success rates and low complication and failure rates. These results are encouraging for EPs developing and maintaining skills in airway management.

It is clear from the two UK papers that practice differs and as such so do success and complication rates. A common theme across each of the papers is that of education, training, and maintenance of skills. Until departments achieve collaborative ways of working, and training programmes including ACCS and CME initiatives such as ATLS unify their approach to education, results will remain varied.

Thanks for reading.

James Rudge

References & Further Reading

Kovacs, George, et al. A randomized controlled trial on the effect of educational interventions in promoting airway management skill maintenance. Annals of emergency medicine 36.4 (2000): 301-309.

C Reid; The who, where and what of rapid sequence intubation: prospective observational study of emergency RSI outsode the operating theatre. Emerg Med J 2004; 21:296-301

Kerslake, Dean, et al. “Tracheal intubation in an urban emergency department in Scotland: A prospective, observational study of 3738 intubations.” Resuscitation (2015).

Scottish Intensive Care Society: RSI

Difficult Airway Society Guidelines

RCOA Anaesthesia in the Emergency Department Guidelines; Chapter 6.1

John Hinds on RSI at RCEM 2015 Belfast

St Emlyns blog post on Kerslake paper

AAGBI Pre-hospital Anaesthesia Guideline


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Presyncope, what does it mean for our patients in ED?

What does presyncope mean to you?

If you ask this question to a handful of doctors you’ll get a multitude of different answers, you’ll also get a huge variety of opinion as to their understanding of it’s significance or associated morbidity and mortality. As with most areas of greyness in medicine this is contributed to significantly by a paucity of evidence on the topic.


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Vasopressors & Inotropes in the ED

In this podcast we are going­­­­­­­­­­­­­­­ to be talking about inotropes and vasopressors. And we’re going to be talking about them with respect to septic shock.

In the UK we use the definition of septic shock as a patient who is hypotensive following the administration of 30 mils per kilo of IV fluids. You might wonder why we can’t continue giving these patients more and more IV fluids, but as with most things in medicine there are side effects and consequences to this. This fluid (and even more so in sepsis) is going to moving from the intravascular space to other fluid compartments and can give rise to problems such as pulmonary oedema. Inotropes and vasopressors in themselves are not harmless but they do have a role in supporting the cardiovascular system in haemodynamic compromise and the surviving sepsis campaign would ask us to consider them went 30 mils per kilo has been administered to patients without the resultant rise in BP.

Inotropes and vasopressors can be used to increase cardiac output both by increasing the rate of cardiac contractility and also the degree of contractility..

Heart rate (HR) x stroke volume (SV) = cardiac output (CO)

Blood pressure (BP) = cardiac output (CO) x total peripheral resistance (TPR)


BP = HR x SV x TPR

If delivery of blood flow to organs is determined by an adequate perfusing blood pressure then this can be addressed in the above 3 ways. It makes sense that it is targeted at the factor that is most deficient. For example there’s no point targeting an increase in HR in a septic patient who has already got a racing tachycardia-especially if their TPR is in their boots

It’s important to remember that numerical values are easy to talk about but shock is a clinical picture and there is no substitute for looking closely at the patient, and making a clinical judgement including those features that are harder to quantify in EBM such as cold clammy peripheries, and appearing peripherally shut down


Catacholamines – are derived from the amino acid tyrosine. They are neurotransmitters and hormones. Include epinephrine/adrenaline, norepinehirine/noradrenaline and dopamine. The first two are released from the adrenal medulla. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are comparatively few in number and their cell bodies are located in relatively small cerebral areas, but affect many other areas of the brain and exert powerful effects on their targets

L-dopa is released converted to dopamine this can be further broken down to noradrenaline and then even adrenaline

They have a half life of a few minutes when in the blood stream and are used in the fight/flight response, and increase HR, BP, glycaemic levels.

They have a range of actions but act on alpha and beta receptors and at a very basic level have the following effects

α1 α2 β1 β2
Blood vessels Constrict Constrict Dilate
Heart Increase contractility & rate Increase contractility & rate
Bronchi Constrict relax


These different Catacholamines have different affinities for different receptors and therefore exert different effects in the cardiorespiratory system.

More information on vasopressors and inotropes can be found here.

Vasopressors are agents that cause a constriction of the vascular system, and they can be used in this way to increase the venous return to the heart by constricting capacitance vessels. The venous system can be thought of as a huge reservoir of blood th­­­­­­­­­­at can be mobilised when required, in this way by squeezing this volume of blood back to the heart, Increasing venous return, increasing/volume and increasing cardiac output can help deliver a rising BP and improvement of oxygen delivery to the tissues.

A typical resus case

You are in resus reviewing a 65-year-old gentleman who has septic shock due to a left lower lobe pneumonia. His wife tells you that he has been unwell for three days with a productive cough that has been getting worse. She tells you he takes a few tablets for a ‘weak’ heart but is otherwise quite well.

When Mr Jones arrived via ambulance he was unresponsive (GCS 8/15), febrile (38.9), tachycardic (HR 140) and hypotensive (BP 60/30 [MAP 40]).

The resus team were quick to act and completed the sepsis 6 within 15 minutes of arrival to hospital but unfortunately, after an hour of aggressive resuscitation including 2.1L of crystalloid, his numbers haven’t improved. In fact, he is anuric and the repeat VBG you have just done demonstrates that his lactate has increased from 4 to 5.

Things are bleak; he has an associated mortality of about 50%. You remember that his poor lactate clearance points towards a worse prognosis. His blood pressure is so low that he isn’t perfusing his vital organs. You are under pressure to act but have a feeling that more fluids aren’t going to cut it. You are aware that the surviving sepsis campaign advocates use of a vasopressor to maintain a MAP >65mmHg in septic shock patients with refractory hypotension after initial resuscitation. You have some key questions you wished you could answer, specifically:

What vasopressor should you use?
When should you begin a vasopressor?
What are you hoping to achieve with a vasopressor?
Does existing cardiac dysfunction change the approach?
You can remember from medschool days that different organs require different perfusion pressures which are approximately

Heart: MAP 65
Kidneys: MAP 65-75
Brain: MAP 50

1. Which vasopressor should you use?

Noradrenaline has demonstrated the best efficacy in the literature and is recommended by the surviving sepsis campaign (SSC) [1,2].

2. When should you begin a vasopressor?

A more difficult question to answer. The SSC recommends starting a vasopressor within six hours of septic shock onset. There is a paucity of data on this topic but the following article attempts to answer the question.

Bai, Xiaowu, Wenkui Yu, Wu Ji, Zhiliang Lin, Shanjun Tan, Kaipeng Duan, Yi Dong, Lin Xu, and Ning Li Early versus delayed administration of norepinephrine in patients with septic shock. Critical care, 2014, 18:532


213 adult patients admitted to a large, tertiary centre surgical ITU with septic shock defined as:

sBP <90mmHg or drop of >40mmHg from baseline or MAP <65mmHg
Persistent hypotension despite 30ml/kg crystalloid

Administration of NA as first line inotrope for persistent hypotension despite ongoing fluid resuscitation.


Retrospective cohort study comparing survivors versus non-survivors. Primary outcome measure was 28-day mortality.


Measure 28 day survivors 28 day non-survivors P value
Time to NA being commenced (hours) 2.7 +/- 2.1 3.8 +/- 2.9 0.002
NA duration (days) 2.4 +/- 0.6 3.4 +/- 0.9 <0.001
Effective antimicrobial therapy (%) 97 45 0.012

Twenty-eight-day mortality was significantly higher in patients who received norepinephrine ≥2 hours after septic shock onset and increased when compared to those who received it <2 hours after onset

o OR of death (NA >2 hours) = 1.86 (1.04 to 3.34; P =0.035)

o OR of death (NA >3 hours) = 2.16 (1.23 to 3.81, P =0.007)

o OR of death (NA >6 hours) = 3.61 (1.45 to 8.95, P =0.004)

The OR of death was 1.20 per hour delay (1.07 to 1.35, P =0.002)

o I.e. every 1-hour delay = 20.4% increased probability of death

MAP was significantly higher a 1, 2, 4, and 6 hours after the onset of septic shock and serum lactate levels at 2, 4, 6 and 8 hours after onset of septic shock were significantly lower in the early NA group than in the late NA group (p<0.05)

Early administration of NA increases survival rate for septic shock patients

For every one hour delay in norepinephrine initiation within six hours after the onset of septic shock, the mortality increased by 5.3%.

Early NA initiation can increase MAP, shorten the duration of hypotension and, thereby, may improve vital organ perfusion and decrease serum lactate levels.

3. What are you hoping to achieve with a vasopressor?

Monnet, Xavier; Jabot, Julien; Maizel, Julien; Richard, Christian; Teboul, Jean-Louis. NA increases cardiac preload and reduced preload dependency assessed by passive leg raising in septic shock patients. Critical Care Medicine. 2011 Vol 39, 4.


25 mechanically ventilated septic shock patients admitted to the ITU with:

Circulatory shock: sBP<90mmHg / fall >50mmHg in known hypertensives
NA in place and running
Delta BP <40mmHg – justifying dose increase in NA
Positive PLR: i.e >9% increase in cardiac index – indicating fluid responsiveness

Measurements of haemodynamic status were undertaken at several points during NA administration:

Baseline NA dose and then during a passive leg raise test (PLR)
Increased Noradrenaline dose and during a second PLR test
After volume expansion with 500ml saline infusion

Haemodynamic variables at different study times in response to NA dose and saline infusion were compared.


PLR1(p <0.05) Increasing NA (p <0.05) PLR2(p <0.05) Saline(p <0.05)
MAP +12% +/- 10% +38% +/- 17% +6% +/- 9% +10% +/- 6%
LVEDA +17% +/- 10% +9% +/- 6% +9% +/- 7% +22% +/- 11%
CI +19% +/- 6% +11% +/- 7% +13% +/- 8% +26% +/- 15%

The results show that increasing NA:

Significantly increased the right and left cardiac preload
Increased cardiac index
Caused a smaller increase of cardiac index to PLR compared to baseline NA. I.e. NA reduced cardiac preload reserve
The ability of PLR test to predict fluid responsiveness in those receiving NA was excellent:

Sensitivity: 95 [76 –99]%
Specificity 100 [30–100]%
Positive predictive value 100 [83–100]%
Negative predictive value 75 [20 –96]%

In septic patients with cardiac preload reserve, NA:

Increased cardiac preload (GEDVI/LVEDA) – increased venous return by acting as an endogenous fluid challenge analogous to PLR
Increased cardiac index (systolic function) – increased cardiac output
Decreased preload reserve – reduced response to fluids

4. How will this impact our patient’s prognosis?

Olfa Hamzaoui, Jean-François Georger, Xavier Monnet, Hatem Ksouri, Julien Maizel, Christian Richard, Jean-Louis Teboul. Early administration of NA increased cardiac preload and cardiac output in septic shock patients with life-threatening hypotension. Critical Care. 2010; 14:R142.


105 septic shock patients admitted within 6 hours to a medical ITU with life-threatening hypotension defined as MAP <65 mmHg


Measurement of haemodynamic variables after early commencement of NA to restore critical hypotension, in particular diastolic BP <40mmHg, regardless the degree of prior volume resuscitation

PiCCO was used for recording dynamics measurements of haemodynamic status

Data analysis

Haemodynamic variables were measured before (T1) and after introduction or increase in dose of NA (T2) providing the MAP target of >65mmHg was achieved. This time did not exceed two hours.
o The cohort was split into two groups based on the median value of MAP achieved. I.e. group 1 MAP < median MAP and group 2 MAP > median MAP. Haemodynamic variables were then analysed depending on whether the median MAP was achieved

o The cohort was also subdivided into two groups based on LVEF </> 45% at T1 and haemodynamic variables analysed at T2 depending on whether the median MAP was achieved


Haemodynamic variables were compared before (T1) and after introduction of or increase in dose (T2) of noradrenaline once the target MAP >65mmHg was achieved.

Haemodynamic variables were analysed according to baseline LVEF above or below 45%.

The paired Student T test or Wilcoxon Test was used for data analysis.


Achieved MAP <75mmHg (n=53) Achieved MAP >75mmHg (n=52)
Before NA After NA Before NA After NA
MAP 51  ± 7 68  ± 4 57 ± 7 83 ± 6
GEDVI 698 ± 139 752 ± 161 691 ± 157 743 ± 181
CFI 4.7 ± 1.8 4.9 ± 1.7 4.8 ± 1.3 5.1 ± 1.5

All values p < 0.05 versus before NA


LVEF <45% (n=34) LVEF >45% (n=71)
Before NA After NA Before NA After NA
MAP 54  ± 9 75 ± 9 54 ± 7 76 ± 9
GEDVI 719 ± 161 768 ± 190 683 ± 140 731 ± 157
CFI 4.2 ± 148 4.4 ± 1.5 5.0 ± 1.6 5.4 ± 1.6

All values p < 0.05 versus before NA

When subdividing the group with LVEF <45% in function of their median MAP value (75mmHg), haemodynamic variables significantly increased in those with MAP <75mmHg (n=17). No change in CI, SVI, GEDVI, or CFI was observed in the 17 patients with baseline LVEF ≤45% for whom values of MAP ≥75 mm Hg were achieved with norepinephrine.


Early administration of NA aimed at rapidly achieving a sufficient perfusion pressure in severely hypotensive septic-shock patients is able to increase cardiac output
The increase in cardiac output with NA seems to be related to increases in both cardiac preload and cardiac contractility
These positive effects can be observed even in patients with poor cardiac contractility, except when values of MAP ≥75 mm Hg are achieved


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Havel C, Arrich J, Losert H, Gamper G, Müllner M, Herkner H. Vasopressors for hypotensive shock. Cochrane Database of Systematic Reviews 2011, Issue 5. Art. No.: CD003709
Sandifer JP, Jones AE. Dopamine versus norepinephrine for the treatment of septic shock EBEM commentators. Ann Emerg Med. 2012. Sep;60(3):372-3
Bai, Xiaowu, Wenkui Yu, Wu Ji, Zhiliang Lin, Shanjun Tan, Kaipeng Duan, Yi Dong, Lin Xu, and Ning Li Early versus delayed administration of norepinephrine in patients with septic shock. Critical care, 2014, 18:532
Monnet, Xavier; Jabot, Julien; Maizel, Julien; Richard, Christian; Teboul, Jean-Louis. NA increases cardiac preload and reduced preload dependency assessed by passive leg raising in septic shock patients. Critical Care Medicine. 2011 Vol 39, 4.
Olfa Hamzaoui, Jean-François Georger, Xavier Monnet, Hatem Ksouri, Julien Maizel, Christian Richard, Jean-Louis Teboul. Early administration of NA increased cardiac preload and cardiac output in septic shock patients with life-threatening hypotension. Critical Care. 2010; 14:R142.

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Assessing fluid status; USS and the IVC

Fluid resuscitation represents the bedrock of initial treatment in the critically ill and injured patient with shock. In septic shock, fluid loading as part of early goal directed therapy was shown to confer a huge mortality benefit.

It seems intuitive that shocked patients require fluid loading however, numerous studies in critically ill patients have demonstrated that only around 50% respond to a fluid challenge.  Are we over-resuscitating these patients and if so, what are the consequences?  Evidence is accumulating that over-resuscitation is associated with increased morbidity and mortality.

Since clinical determination of fluid status in the haemodynamically unstable patient is unreliable, how do we assess volume status reliably to ensure those who need fluid get it?

The Frank-Starling principle predicts that as cardiac filling pressures go up so the cardiac output (and therefore the blood pressure) increases.  However, surrogate markers for these filling pressures, – including CVP – have consistently demonstrated no utility in identifying fluid responders.  So what tools do we have in our armoury to better assess whether a shocked patient would benefit from fluid loading?

In this podcast we look at whether the change in IVC diameter with respiration, as assessed by ultrasound, can be used to reliably identify patients who would benefit from volume loading versus those who would not.

Central Venous Pressure and fluid responsiveness

Download Central Venous Pressure and fluid responsiveness powerpoint

Since Rivers’s publication of Early Goal Directed Therapy (EGDT) at the turn of the century clinicians have talked about aggressive resuscitation for septic shock. One of the goals underpinning this technique is the insertion of a central line with targeted goals of CVP and central venous oxygen saturations.

This model of care for patients with septic shock had an NNT of 6 to save a life which is pretty phenomenal! Try to think of another therapy that has been proven to have such a dramatic effect on patients……

So why is it that most of you reading this won’t have followed EGDT in your patients with septic shock? How heavily should this guilt be weighing on your shoulders?

Over the past few months the treatment of septic shock has hit the journal headlines, firstly with the Process Trial and latterly the Arise Trial. These studies looked at EGDT vs alternative treatment strategies (both structured and completely at the discretion of the treating clinician). If you’re not familiar with the papers be sure to have a listen to those podcasts before listening to this episode. Keep a look out for the third paper due for publication this year on the same topic; the Promise trial.

In essence the results of the 2 trials were surprising and leave you wondering where EGDT belongs, it has undoubtedly informed our practice over the last decade but hasn’t been universally implemented. We need to break down the individual goals from EGDT and assess their utility in treating our patients in resus, specifically with septic shock.

Our previous podcast on lactate clearance looked at the idea of exchanging the goal of central venous oxygen sats for lactate clearance. In this episode we take a look at the use of CVP as a goal, specifically in the assessment of fluid responsiveness in the shocked patient.

Have a listen and get in touch with your thoughts!


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