AAGBI Seminar: Anaesthetic Dilemmas and Cervical Spine Injury

This is a copy of the slides I used during a talk I gave at the AAGBI (@AAGBI) seminar entitled Anaesthetic dilemmas and peri-operative conundrums in patients with neurological disease. The full programme of the meeting can be found here.

The talk aimed to review the evidence of the risks and benefits of cervical immobilisation and different tracheal intubation techniques in trauma patients and those with RA.

The pdf of my presentation can be downloaded by clicking the link below.





Cervical Spine Injury: Immobilisation and Airway Management

This is a copy of the slides I used during a talk I gave at the Grand Rounds Presentation of the Department of Anesthesia, Pain Management and Perioperative Medicine, Halifax, Nova Scotia.

This (updated) talk was designed to provide an update for anaesthetists in the management of acute spinal cord injury, with a particular focus on cervical spine trauma. I have focused particularly on the evidence (or lack of it) relating to spinal immobilisation techniques and how to safely undertake tracheal intubation in the patient who has proven, or suspected, cervical spine instability.

The pdf of my presentation can be downloaded by clicking the link below:

SCI Canada 2017


RCoA/RCEM Trauma Study Day: Session 3

Summary of the first session at the RCEM/RCoA Trauma Study Day. The full programme of the meeting can be found here.This is a summary (with references) of the talks I was able to attend.

Pelvic fracture management. Dr Gareth Davis, London. [2A02, 2A05, 2A12]

<5% of ED # with majority from RTCs & 50% have associated long bone #.

Mortality 15-50%; risk greatest if hypotensive.

Classification system of most practical use is Young & Burgess [http://www.orthobullets.com/trauma/1030/pelvic-ring-fractures]

Screen Shot 2015-11-24 at 14.50.44

Lateral compression # (LC): usually visceral rupture rather than pelvic bleeding.

Vertical shear # (VC): venous plexus injuries common.

AP compression (APC): “open book”, common in motorcyclists. Ligament rupture and venous bleeding +++

Blood goes into retroperitoneal or intraperitoneal spaces. Majority is venous from venous plexus (90%); only 10% from internal iliac artery. VS > APC > LC in terms of blood loss.

USS suffers with intra-observer variability. CT + angiography is diagnostic and therapeutic.

Treatment – movement of patient (log rolls, packaging for transfer) associated with hypotension secondary to clot disruption and loss of tamponade. Scoops can reduce this movement significantly, especially if used in the prehospital setting. Don’t rock & roll!

Pelvic binders work a bit but not a lot! REBOA can be used in zone 3 (base of bifurcation) in the prehospital setting but not as easy to insert as you think.

Manage coagulopathy as per any major trauma. Try to maintain normothermia.

RCoA/RCEM Trauma Study Day: Session 2

Summary of the second session at the RCEM/RCoA Trauma Study Day. The full programme of the meeting can be found here. This is a summary (with references) of the talks I was able to attend.

Management of traumatic bleeding. Prof Karim Brohi, London [2A02, 2A05, 2C04]

  • Major trauma haemorrhage associated with 50% mortality at 1 year. Early deaths – you didn’t stop the bleeding, late deaths you didn’t resuscitate them well enough.
  • People are still dying from early exsanguination.
  • Early goal is to stop bleeding and maintain haemostatic competence. Maintain basal cerebral & coronary perfusion only. Not targeting base deficit, lactate or a target SBP.

Four pillars of management

  1. Early haemorrhage control: rapid transit to DCS/IR/tourniquets/REBOA
  2. Permissive hypotension
  3. Limit fluid infusions: all fluids inc. PRC dilute coagulation factors. Avoid all crystalloids/colloids whilst bleeding.
  4. Target coagulopathy: fibrinogen, fibrinogen, fibrinogen….
  • Two types of coagulopathy: traumatic & iatrogenic.
  • 25% of patients have a traumatic coagulopathy (ATC) with associated 25% mortality. By the time the PT is elevated you are already miles behind the disease process.
  • ATC is not a deficiency in coagulation factors but rather fibrinogen loss due to fibrinolysis. Trauma patients present with fibrinogen levels at 50%.
  • After 8 units PRC, you will have no fibrinogen! Keep fibrinogen > 2.0. TXA to minimise fibrinolysis.
  • Give 1:1:1 to avoid the administration of crystalloid. Crystalloid undoes all the beneficial effects of major trauma packs.
  • iTACTIC study on the use of TEG/ROTEM awaited [http://www.tacticgroup.dk/%5D]

Trauma Team Leadership. Dr Caroline Leech, Coventry [1I02, 1I03, 2C01]

  • What can trauma teams (which are unique) learn form other teams.
  • One key element is practice; in situ simulation may be the answer to practice and develop marginal gains. A 1% improvement becomes significant over time. Also develop shared mental models and implicit knowledge.
  • From the prehospital environment we have learnt that task completion increases with the use of names. Why not add names to the trauma tabbards?
  • Avoid individual briefings prior to trauma calls and do not get complacent – you will lose the mental model and shared goal.
  • Checklists are really helpful!
  • Tiered responses help avoid fatigue for recurrent trauma call attendance when not needed.
  • Make attendees to the trauma call welcoming. Introduce, check names etc.
  • Ensure that we have a shared mental model – update with briefings.
  • What makes a good trauma team leader? Common themes include excellent communication, directive with orders and good briefings.
  • Closed communication: Call out, check back, closed loop. Precise instructions with clear directions.
  • Need to reflect on your leadership style as a trauma team leader.
  • Video debriefing useful to review leadership style.
  • Peer review also of value for both technical and non-technical skills.

RCoA/RCEM Trauma Study Day: Session 1

Summary of the first session at the RCEM/RCoA Trauma Study Day. The full programme of the meeting can be found here.This is a summary (with references) of the talks I was able to attend.

The trauma airway and the trauma anaesthetic. Dr Steve Rowe, Sheffield. [1B02, 2A01, 2A08, 2F01]


  • How to write checklists? Read the Civil Aviation Authority Guidance [http://www.caa.co.uk/application.aspx?catid=33&pagetype=65&appid=11&mode=detail&id=158]
  • PPPPPP: local simulation is of great value; the more realistic the better.

DAS ASM Ascot 2013: Key Points

A colleague (Dr Bisanth  Batuwitage) recently attended the Difficult Airway Society Annual Scientific Meeting, in Ascot, November 2013.

In order to allow those who were unable to attend the meeting to gain a flavour of the topics covered by the speakers he has kindly created a summary of the key points of each talk.

The RCOA Matrix Codes for each talk are shown along with the details of the speaker.

How we cause and treat airway stenosis (2A01, 3A02): Mr Guri Sandhu, Imperial College/UCL

  • More than 50% of cases of adult laryngotracheal stenosis are due to a period of ventilation on ICU.
  • Incidence is unknown, risk factors: size of tube, cuff pressures, immunity, infection and natures of patients healing biology.
  • The remainder of cases is due to disorders such as Wegener’s granulomatosis, idiopathic subglottic stenosis and sarcoidosis.
  • Nearly two thirds of tracheal reconstructions can be managed endoscopically, the surgeon and anaesthetist need to work closely and utilize shared airway techniques.
  • They usually perform IV induction, give muscle relaxant and ventilate with positive pressure down an LMA.
  • They use a technique of suspension laryngoscopy and supraglottic jet ventilation at high frequency (100 breaths per minute) delivered by an automated device (Mistral/Monsoon, Acutronic systems). This device alarms if the delivered jet or return of gas is obstructed.
  • They prefer this technique as it employs an open breathing system, so there is no need for an airtight connection between the airway and the breathing system. Thus, the trachea can be open with good surgical access and ventilation still maintained

Gas induction for critical airways in adults is pointless (2A01, 2A06): Dr Anil Patel, Royal National Ear, Nose and Throat Hospital

  • When an inhalational induction is commenced in a patient with a severely obstructed airway, despite the application of CPAP and PEEP, induction is slow there are apnoeic periods and the patient often becomes hypoxic and hypercarbic, there are long periods of instability, arrhythmias and episodes of total airway obstruction.
  • Following airway obstruction the patient often does not awaken and relieve the obstruction, apnoea continues and the hypoxia worsens.
  • If this continues in clinical practice the use of positive pressure is required to relieve the hypoxia. Positive pressure ventilation following IV induction and muscle paralysis is physiologically superior to spontaneous respiration in adult stridulous patients with airway compromise due to laryngotracheal stenosis.

Physiological problems with inhalational induction and maintenance of spontaneous ventilation:

  1. Reduction in airflow
  2. Reduction in respiratory drive as anaesthetic depth is increased
  3. Increased collapsibility of the airway
  4. Increased work of breathing
  5. Critical instability at points of narrowing leading to further airway collapse
  6. Reduction in FRC
  • The only mechanisms to counteract these changes in a gas induction are to provide CPAP and PEEP.
  • For non-obstructed adult airways and children this is often enough but for critically obstructed adults airways the application of CPAP and PEEP is not enough to counteract the physiological principles that impair inspiratory airflow and ultimately obstruct the airway.
  • Positive pressure ventilation however produces positive pressure during both phases of ventilation by positive pressure of the bag during inspiration and elastic recoil of the lungs on expiration.

Ultrasound in Airway management (1A03, 2A12): Dr Michael Seltz Kristensen, Righospitalet University Hospital, Copenhagen, Denmark.

Ultrasound hardly penetrates air: as soon as the beam reaches air a strong echo appears, this is seen as a bright white line, this line delineates the border between tissue and air; everything beyond it is artifact. The airway can be visualised with US from the tip of the chin until the mid-trachea and pleura.

Clinical applications of airway ultrasonography:

  1. Screening of difficult airway management
  2. Diagnosing pathology that can affect airway management
  3. Identification of the cricothyroid membrane
  4. Measuring gastric content prior to airway management
  5. Airway related nerve blocks
  6. Prediction of appropriate diameter of ET tube or tracheostomy tube
  7. Differentiating between tracheal and oesophageal intubation
  8. Differentiating between tracheal and endobronchial intubation
  9. Confirmation of gastric tube placement
  10. Diagnosis of pneumothorax
  11. Differentiating between different causes of dyspnoea/hypoxia and pulmonary oedema
  12. Prediction of successful weaning from ventilator
  13. Localisation of trachea and tracheal ring interspaces for tracheostomy and percutaneous dilatational tracheostomy

Dr Kristensen admits that a lot of these techniques are research based although the two that he thought had real potential to have an impact on clinical practice are localising the trachea/cricothyroid membrane when it cannot be identified easily and the detection of a pneumothorax.

His group’s website is http://www.airwaymanagement.dk/ultrasonography-in-airway-management

Every Obstetric GA does not have to be a Rapid Sequence Induction (2B05, 3B00): Dr Wendy Teoh, KK Women and Children’s Hospital, Singapore

  • Mallampati score has been shown to increase in pregnancy and labour.
  • In obstetric patients Mallampati class 3 and 4 strongly associate with difficult laryngoscopy, with increased relative risks of 7.6 and 11.3 respectively.
  • The use of “Macintosh-like” videolaryngoscopes (eg C-MAC, McGrath) are being used as a first line device for securing the maternal airway on a routine basis in some units.
  • Increasing reports of supraglottic airways not only used as a rescue device but also for elective cesarean sections (may want to avoid intubating e.g Pre-eclampsia).

Declining use of general anaesthesia in obstetrics: implications for training and strategies for improvement (2B02, 3B00): Dr Ashutosh Wali, College of Medicine, Texas, USA

  • The use of general anaesthesia for cesarean section has decreased from 45% in 1981 to 0.7% in 2005 in the United States. A similar decline over the same period has been seen in the UK, 79% to less than 10%.
  • Lack of exposure of GA for caesarean section resulted in a severe lack of exposure amongst US trainees and many residents graduated without having performed a GA in an obstetric patient.
  • Solutions to the decline include use of a structured advanced airway management rotation, formal repetitive training of difficult airway algorithms on manikins and in the operating room on non-obstetric healthy patients and use of simulation based training.

DAS/OAA Obstetric difficult airway guidelines (1H02, 2B05): Dr Mary Mushambi, Leicester Royal Infirmary

  • Update on the DAS/OAA national obstetric difficult airway guidelines. The project is expected to take around 2 years to complete.
  • Needs to be different to standard DAS guideline due to physiological/anatomical changes of pregnancy, presence of foetus and remoteness of delivery suite theatres in many hospitals.
  • There is currently no national airway guideline in the UK and wide variation in practice.
  • The guidelines working party of the OAA published six example guidelines on their website having invited hospitals to submit their local guidelines.