It’s 4:30pm on a Friday afternoon. You still haven’t finished your notes from clinic, there are scripts waiting to be signed, and you’re hoping to get through it all before handover. But your pager goes off:

“Please review Mrs Smith in bed 16, complaining of 8/10 pain.”

Mrs Smith has been in and out of the hospital for weeks; a complex polytrauma patient with severe left foot pain in the context of newly diagnosed CRPS. She’s known to multiple teams, has a well-documented pain plan from the pain service, and you’ve already reviewed her twice today for pain.

Before you even walk into the room, there’s a familiar thought:  What am I actually going to do that hasn’t already been done?

These reviews are incredibly challenging – not because we don’t know the medications, but because we’re often unclear on what success even looks like. We vaguely understand that managing these patients isn’t just about adjusting analgesia. It’s about how we approach the conversation: how we listen, what we validate, and how we set expectations in a situation where there often isn’t a simple fix. So what do you do next?

Step 1. Do not ignore the page and wait for the nurses to page again (hopefully when the cover resident takes over).
It’s tempting to delay this review and hope it gets handed over. Clinical inexperience and workload both push us in that direction. But delaying these reviews rarely helps. 

Recently on the paediatrics ward, I started a cover shift to a parent-initiated MET call for pain in a patient on a PCA who had lost IV access. While re-siting the cannula was already the priority for the evening medical team, the parent had no clear sense of when (or if) this might happen and was left watching their child in pain. What should have been a straightforward procedural review quickly escalated into a more complex situation requiring longer discussions, additional documentation, and increased nursing support.

When a patient familiar with chronic pain asks for help, it usually means the current plan isn’t working. Leaving it escalates the situation and signals to the patient that no one is listening. 

Step 2. Enter with an open mind. 

We are not strangers to cognitive bias in medicine. It is easy to get bogged down by the things we think we know. It is far too easy to rule out important differentials before we have all the clinical evidence and, as uncomfortable as it is to admit, it is easy to dismiss a patient before we have even entered the room. At times, I find it helpful to approach the interaction as a blank slate. 

In practice, this can be as simple as letting the patient speak uninterrupted for a couple of minutes. Evidence suggests that up to 78% of patients do not speak for longer than 2 minutes when allowed to speak without interruptions, and often, what they say in this time can reframe the entire objective of the review (Kreijkamp-Kaspers & Glasziou, 2012, pg909).

I’ve found open ended questions can help reset the conversation:

• “What’s different about today?”
• “What were you hoping I could help with?”

Additionally, taking a moment to ask “what if it’s something else?” has changed my management more than once. I once revisited a non-English speaking patient’s abdominal pain, previously attributed to chronic constipation, with a formal interpreter service and uncovered a urinary tract infection on a day she would have otherwise been discharged.

Step 3. Don’t be afraid to treat your patient, and escalate early if you think you can’t.

Severe pain can make history taking and examination tricky. In some situations, it may be more helpful to offer a stat or PRN dose of rapid-onset analgesia before attempting a detailed assessment. This can create enough space for a more meaningful review, rather than trying to assess a patient who is too distressed to engage.

At the same time, consider whether you may be walking into a pain crisis that requires early escalation with an urgent clinical review or MET call. Managing acute pain in patients already on significant multimodal regimens can be daunting, and it’s not something you need to manage alone.

Step 4. Acknowledge, reassure, and validate. 

Managing acute on chronic pain challenges our ability to troubleshoot complex clinical dilemmas, which often do not have satisfying solutions. It’s uncomfortable to acknowledge a symptom without being able to offer a quick fix, but this is often a hidden barrier to a meaningful and productive conversation. Simple acknowledgements such as “It sounds like today has been particularly difficult” can go a long way in letting someone know you are seeing them, that you believe them. Validation doesn’t have to mean agreeing with everything said, but rather reassuring a patient that their lived experience is an important part of the equation too.

Step 5. Set expectations!

The best pain reviews I’ve seen have been honest and a bit humble. These conversations can go either way. I’ve seen them escalate into full-blown arguments (and even a code grey once!), and I’ve also seen a single conversation completely change how the rest of the admission goes. A lot of that comes down to expectations.

One thing I’ve taken from discussions with various pain specialists is to avoid overpromising. Most of the time, we’re not going to make someone pain-free, and not all patients know what the end point of inpatient treatment may look like without a transparent discussion. The NICE guidelines for shared decision-making recommend early discussion of the patient’s goals for treatment and clarification of any misconceptions they might hold (NICE, 2021). 

Simple things like:

• “We might not be able to get rid of the pain completely, but we’ll try to make it more manageable.”

It also helps to be upfront about the longer-term plan:

• “We can try these medications to settle things over the next few days, but we’ll need to start weaning them before you go home.”

In my experience, having this conversation early saves you or an unsuspecting colleague from having a much harder one later.

Step 6. Come up with a plan, knowing that it may fail. 

I find it helpful to frame each management plan as a trial run: all possible options are weighed collaboratively, but only one distinct route is chosen by the end of the review. For example, many patients tend to insist on premature escalation of opioids. While this is not necessarily always appropriate in the first instance, especially for patients being overseen by a pain service, it can be reassuring to let them know that there will be a plan for staged assessment of effect and that medication changes are still on the table for discussion depending on how things progress. 

One situation where this negotiation process comes up often is when I’m reviewing patients that have declined simple analgesia, and usually this is followed by a “paracetamol never works for me.” While I’ve come across the odd patient or two who are receptive to explanations around the analgesic ladder and multimodal analgesia, most patients just prefer simplicity. One phrase I tend to reuse often is:

• “Worst case scenario, the paracetamol won’t do anything. Best case, it takes the edge off while we figure out what else we can do, while giving me more information to work with.”

In my experience, setting it up this way makes the next review easier, for both you and the patient. It turns the interaction into a shared process that they understand, rather than a single moment where you’re expected to get everything right.

In summary,

In 2020, the IASP revised their definition of pain as being “an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage”, taking into account the subjective and personal nature of pain that is influenced by not only biological factors, but also psychosocial factors (IASP, 2020). Patients in pain present in vastly different ways. 

The above suggestions won’t suit every patient’s communication style, but it is not possible to communicate without first starting a conversation. And it is not possible to hold a conversation without listening to what the person in front of you needs.  

Some days it will feel like your patient hates you and the entire hospital no matter what you try. Many patients will find these discussions frustrating, while some need you to acknowledge that their experience is real and difficult. Some patients like to know about every piece of the puzzle, while others are just waiting for someone who can subtract all the medical jargon from the details that matter. Regardless, all patients deserve to be spoken to in a language they can understand.

References

IASP Announces Revised Definition of Pain – International Association for the Study of Pain. (2020, July 16). International Association for the Study of Pain. Retrieved April 1, 2026, from https://www.iasp-pain.org/publications/iasp-news/iasp-announces-revised-definition-of-pain/

Kreijkamp-Kaspers, S., & Glasziou, P. (2012, November). A is for aphorism. The power of silence. Australian Family Physician, Volume 41(11), 909. https://www.racgp.org.au/afp/2012/november/a-is-for-aphorism

NICE. (2021, June 17). National Institute for Healthcare and Excellence. Shared decision making. https://www.nice.org.uk/guidance/ng197/chapter/Recommendations#putting-shared-decision-making-into-practice

Overview

Regional anaesthesia is an important component of modern perioperative care, providing effective analgesia while reducing opioid use and improving recovery. The use of ultrasound guidance has significantly improved the safety and accuracy of nerve blocks by allowing clinicians to visualise anatomical structures in real time. However, identifying nerves on ultrasound can still be challenging due to complex anatomy, variable image quality, and operator experience.

I have had the pleasure to experience new groundbreaking AI technologies that are emerging in the area of regional ultrasound guided anaesthesia. AI-assisted ultrasound systems analyse images in real time and highlight key anatomical structures such as nerves and vessels. Early research suggests these tools may improve anatomical recognition, support trainee learning, and enhance scanning performance.

Healthcare in Europe – “A breakthrough in real-time ultrasound guidance for regional anesthesia.”https://healthcare-in-europe.com/en/news/a-breakthrough-in-real-time-ultrasound-guidance-for-regional-anesthesia.html

Why Nerve Localisation Is Difficult

Ultrasound-guided regional anaesthesia has dramatically improved the safety and accuracy of nerve blocks. However, identifying nerves and anatomical landmarks on ultrasound remains challenging, particularly for inexperienced practitioners.

Several factors contribute to this difficulty. First, ultrasound images often provide limited contrast between nerves and surrounding tissues, making structures difficult to distinguish. Additionally, technical factors such as poor needle visibility, deep anatomical targets, or patient characteristics such as obesity can further complicate image interpretation.

Ultrasound-guided blocks require clinicians to simultaneously interpret sonographic anatomy, manipulate the probe, and guide the needle toward the target structure. This complex visuospatial task demands significant experience and pattern recognition. As a result, the learning curve for regional anaesthesia can be steep, and incorrect interpretation of anatomy may lead to complications such as vascular puncture, nerve injury, or block failure.

What Is AI-Assisted Ultrasound?

AI-assisted ultrasound refers to the use of machine learning algorithms to analyse ultrasound images and identify anatomical structures in real time.

Most systems rely on deep learning neural networks trained on large datasets of annotated ultrasound images. These algorithms learn to recognise visual patterns associated with nerves, vessels, muscles, and fascial planes. Once trained, the system can analyse live ultrasound images and overlay colour highlights on key anatomical structures, helping clinicians interpret the image more easily.

In regional anaesthesia, AI tools may assist clinicians by:

• Identifying nerves and surrounding anatomy
  

• Highlighting critical safety structures such as vessels or pleura
  

• Improving ultrasound image interpretation
  

• Assisting with needle localisation and trajectory planning.
  

AI-assisted systems function as decision-support tools, augmenting the clinician’s interpretation rather than replacing clinical judgement. Their goal is to enhance anatomical recognition and improve procedural accuracy during nerve blocks.

Br J Anaesth. 2022 Aug 18;130(2):217–225. doi: 10.1016/j.bja.2022.06.031

What Does the Evidence Show?

Emerging research suggests that AI-assisted ultrasound may improve ultrasound scanning performance, particularly among less experienced clinicians.

A prospective study evaluating an assistive AI ultrasound device found that non-expert anaesthetists were more likely to obtain the correct block view when using AI assistance. In this study, the correct block view was obtained in 90.3% of scans with AI compared with 75.1% without AI assistance.

Similarly, correct identification of sonographic anatomical structures was significantly higher when AI support was used (88.8% vs 77.4% without AI).

These findings suggest that AI may enhance both image acquisition and interpretation, two critical steps in ultrasound-guided nerve blocks.

Broader reviews of the literature have also identified several potential benefits of AI-assisted ultrasound. These include improved identification of anatomical landmarks, enhanced visualisation of needle advancement, and optimisation of ultrasound image interpretation. AI tools may therefore help reduce complications such as injury to surrounding structures or incorrect needle placement.

However, despite promising early results, the current body of evidence remains relatively limited, and further large-scale clinical trials are required to confirm whether these technologies improve patient outcomes.

Expert global rating score. Distribution of all expert global rating scores, showing a breakdown of scans performed with or without ScanNav Anatomy Peripheral Nerve Block. PNB, Peripheral Nerve Block.

How AI Could Transform Regional Anaesthesia Training

One of the most exciting potential applications of AI-assisted ultrasound is in education and training.

Learning regional anaesthesia requires the development of strong sono-anatomy recognition skills, which traditionally develop through repeated scanning and expert supervision. AI tools could accelerate this learning process by providing real-time anatomical guidance during ultrasound scanning.

For trainees, AI systems may:

• Help identify correct anatomical landmarks during scanning
  

• Reinforce recognition of normal sonographic anatomy
  

• Improve confidence during early learning stages
  

• Provide immediate visual feedback.
  

Studies have suggested that AI assistance may help non-expert clinicians improve their ability to acquire correct ultrasound views and recognise anatomical structures, which could shorten the learning curve for ultrasound-guided blocks.

More broadly, AI-assisted ultrasound could become an important component of technology-enhanced regional anaesthesia training, alongside simulation, augmented reality, and ultrasound-guided training platforms.

Limitations and Concerns of AI-Assisted Ultrasound

Despite the enthusiasm surrounding AI-assisted ultrasound, several limitations and concerns remain.

First, the current evidence base is still developing. Reviews of the literature highlight that many studies involve small sample sizes or experimental settings, and high-quality randomised controlled trials are still lacking.

Another important concern is over-reliance on AI systems. While AI can assist with image interpretation, clinicians must still possess a strong understanding of ultrasound anatomy. Incorrect AI identification of anatomical structures could potentially mislead inexperienced users if they rely too heavily on the technology.

Technical limitations also remain. AI systems may struggle in cases with unusual anatomy, poor image quality, or deep anatomical structures, and their performance may vary depending on the ultrasound machine or scanning conditions.

Finally, there are broader issues related to regulation and standardisation of AI devices. Different AI systems may be evaluated using different datasets and performance metrics, making it difficult for clinicians to compare their accuracy and clinical utility.

Addressing these challenges will require collaboration between clinicians, engineers, and regulatory bodies to ensure that AI technologies are implemented safely and effectively in clinical practice.

Conclusion

Artificial intelligence is beginning to reshape how clinicians interpret ultrasound during regional anaesthesia. Early studies suggest that AI-assisted systems can improve the identification of anatomical structures and help clinicians obtain optimal ultrasound views, particularly among less experienced users. By highlighting nerves, vessels, and surrounding anatomy in real time, these technologies have the potential to enhance procedural accuracy and support the learning process for trainees.

However, AI should be viewed as a clinical decision-support tool rather than a replacement for anatomical knowledge or ultrasound expertise. The current evidence base remains limited, and further research is needed to determine whether these systems translate into improved patient outcomes and reduced complications. As the technology continues to evolve, AI-assisted ultrasound may become an increasingly valuable adjunct in regional anaesthesia practice and education.

References

Bowness JS, Burckett-St Laurent D, Hernandez N, Keane PA, Lobo C, Margetts S, et al. Assistive artificial intelligence for ultrasound image interpretation in regional anaesthesia: an external validation study. Br J Anaesth. 2023;130(2):217-225. doi:10.1016/j.bja.2022.06.031.

Bowness JS, Burckett-St Laurent D, Margetts S, Pawa A, Noble JA, Higham H, et al. Evaluation of the impact of assistive artificial intelligence on ultrasound scanning for regional anaesthesia. Br J Anaesth. 2023;130(2):226-233.

Bowness JS, Lobo C, Burckett-St Laurent D, Noble JA, Pawa A, Higham H, et al. Variability between human experts and artificial intelligence in identification of anatomical structures by ultrasound in regional anaesthesia: a framework for evaluation of assistive artificial intelligence. Br J Anaesth. 2024;132(5):1063-1072.

Healthcare in Europe. A breakthrough in real-time ultrasound guidance for regional anesthesia [Internet]. Healthcare in Europe; [cited 2026 Mar 17]. Available from: A breakthrough in real-time ultrasound guidance for regional anesthesia

Purpose of the pre-anaesthetic assessment:

• Identify patients who have increased peri-operative risk;
• Diagnose, assess, and optimise patient comorbidities to minimise peri-operative risk;
• Plan and prepare for the patient’s perioperative journey;
• Encourage patient-centred discussion regarding risk and benefit of surgery and to reach a decision on whether to proceed or delay/cancel.

The structure and depth of the preoperative anaesthesia assessment will vary depending on the severity and stability of the patient, the urgency (elective versus emergency) and risk profile (low risk vs high risk) of the surgery. However, a general structure is always required to encapsulate the key domains imperative for perioperative planning. There is no fixed method, and juniors are encouraged to observe different styles used by perioperative clinicians and adopt one’s own. Here we present the key areas that should be explored during a pre-operative assessment:

1. Detailed History
   1. Anaesthetic history
   2. Past medical history, with specific focus on cardiovascular and respiratory systems
   3. Medication history
   4. Social history & functional status
2. Targeted examination
   1. Airway assessment
   2. Vital signs
   3. CVS exam
   4. Respiratory exam
3. Relevant investigations
4. Surgical considerations
5. Risk stratification

Detailed History

1. Anaesthetic history

• Any issues with prior anaesthetics. Any difficulties encountered with regional/neuroaxial anaesthesia.
• Family history of GA issues -> malignant hyperthermia (MH), sux apnoea (SA) due to pseudocholinesterase deficiency.
• Previous difficult airway.
• Anaphylaxis & other adverse drug reactions.
• Any unplanned HDU/ICU admission following anaesthetic?

The best predictor of intraoperative anaesthetic complications is previous complications and patterns.

Reviewing the previous anaesthesia chart can be a wealth of information. Aside from reviewing major complications and airway grade, note induction medications and doses, vasopressor, analgesics, and antiemetic use. For example, a patient with stable looking blood pressure recordings but needing large doses of metaraminol and ephedrine would be a red flag for any future inductions. Was this a mild case of anaphylaxis, or a sign of decreased cardiac function and undiagnosed heart failure?

Patients with previous anaesthetic issues such as difficult airway, anaphylaxis, MH or SA often carry letters or have electronic record prompts to alert clinicians. Any family members who have undergone genetic or allergy testing after an anaesthetic should prompt the clinician to chase further correspondences of the nature, indications and results of the investigations.

Any unplanned admission to an intensive care setting post-operatively should be reviewed, particularly if the admission was anaesthesia-related:

• Airway trauma / oedema preventing safe extubation.
• Refractory bronchospasm / aspiration event / unexplained oxygenation & ventilation defects requiring ongoing invasive positive pressure ventilation (IPPV).
• Delayed emergence requiring prolonged airway/respiratory support.
• Intraoperative haemodynamic compromise / cardiac event.
• Intraoperative neurologic event.

Etc.

2. Past medical history (PMHx)

With the advancement of perioperative medicine and minimally invasive interventions, clinicians are faced with growing numbers of multimorbid patients who are considered for surgery. This requires a succinct structure to identify and review pertinent PMHx that is relevant for the perioperative setting. Of the body systems, cardiovascular and respiratory conditions are the biggest contributors to perioperative morbidity and mortality.

With any condition that is identified, the following acronym developed by Dr. Lahiru Amaratunge can be used to elucidate important details of the condition:

SSCCT

Severity: how severe is the condition

Stability: is there any acute change recently

Cause: why has this condition occurred

Complications: has this condition led to other disease

Treatment: what is the management, is it working, what is the follow-up

Based on this, one can quickly determine the level of attention you need to pay for a particular condition.

For example, an asthmatic with 2 previous ICU admissions requiring IPPV, with an FEV1/FVC of 0.5, who has presented with new wheeze and cough, on the background of newly diagnosed pulmonary hypertension despite regular preventers and biologics, presents far greater perioperative risks than another mild but otherwise fit asthmatic who barely uses salbutamol PRN with no previous hospital admissions.

Cardiovascular disease:

-Enquire about: chest pain, syncope, orthopnoea, paroxysmal nocturnal dyspnoea, leg swelling, syncope

-Cardiac comorbidities:

• Acute coronary syndrome (ACS)/ ischaemic heart disease

• Cardiac arrhythmias

• Congestive heart failure (CCF)

• Valvular disease, in particular aortic stenosis (AS) / mitral stenosis (MS)

• Pulmonary hypertension (pulmHTN)

• Congenital heart disease

-Current management, such as coronary stenting and/or bypass, AICD/pacemaker

-Patient exercise tolerance, using validated scoring systems. E.g. Duke activity status index (DASI), metabolic equivalent tasks (MET)

-Recent cardiac investigations: ECG/Holter/TTE/stress TTE/CT cardiac/angiogram

Respiratory disease:

-Enquire about: exertional tolerance, requirement for home oxygen, hospitalisations in the past 12 months due to respiratory illness, current or former smoker?

-Recent respiratory function tests

-Illnesses of note: COPD, asthma, pulmonary hypertension, OSA

-Consider the STOP-BANG questionnaire to detect undiagnosed OSA (see below)

Other:

-Diabetes: T1 vs T2? Insulin dependent? Recent HbA1c? Recent hypo/hyperglycaemic episodes?

-Thyroid, renal, liver disease

–GORD, conditions affecting lower oesophageal sphincter function and/or delayed gastric emptying (poorly controlled reflux poses increased intra operative aspiration risk and may affect induction technique)

-Fasting status, GLP-1 agonist use?

-Conditions which may affect the cervical spine e.g. rheumatoid arthritis, ankylosing spondylitis

-In women of reproductive age, ask about possibility of pregnancy

3. Patient medications

-Medications of note include

• Anticoagulants, antiplatelets

• Cardiac, including ACEi/ARB, beta blockers

• Diabetes medications (in particular insulin, SGLT-2 inhibitors and GLP-1 agonists) [Check ANZCA’s latest guidelines https://www.anzca.edu.au/safety-and-advocacy/standards-of-practice/clinical-practice-recommendations-regarding-patients-taking-glp-1],

• DMARDs, steroids and other immunosuppressive medications

• Opioids and other long-acting opioid replacement therapies

-Consider the need for peri operative anticoagulation bridging for patients on warfarin

-Patient allergies – clarify type of reaction e.g. anaphylaxis vs medication side effect )

4. Social History & functional status

–Smoking and alcohol intake

-Other illicit drug use

-Activities of daily living, whether patient is requiring assistance with basic or complex tasks, fatigue and overall frailty

Examination

The physical exam should include a thorough airway, cardiovascular and respiratory assessment, but may include other systems depending on the patient.

Airway assessment

-Modified Mallampati score

-Thyromental distance (note if less than 6cm from thyroid notch to chin when head is extended)

-Inter-incisor distance (should be able to fit approximately 3 fingers when mouth is fully opened)

-Dentition

-Patient body habitus

-Facial hair

-Freedom of neck movements

-Jaw protrusion

The best predictor of a difficult airway is a history of a difficult airway. Recent anaesthetic charts should therefore be reviewed for previous airway grades, ease of BMV, and size of well-seated supraglottic airways.

The above are useful to identify patients with potentially difficult airways, but none in isolation provide the sensitivity nor specificity to confirm one. Nevertheless, the greater the presence of difficult airway risk factors, the more preparation is required in our airway planning. Importantly, if a genuine difficult airway is anticipated, such as those with fixed flexion deformity, extremely limited mouth opening, or retrognathia with limited jaw protrusion, an awake fibreoptic technique should be discussed with the patient and the anaesthetic team looking after the patient.

Cardiovascular

–Key vitals: BP, HR

-Chest auscultation, noting any cardiac murmurs or added heart sounds, bilateral added lung sounds

–Fluid status, noting any pedal oedema

Respiratory

-SpO2, RR, work of breathing, presence of adventitious breath sounds

Investigations

Further investigations depend on the individual patient’s comorbidities, type of surgery and time available for optimisation before their operation

Young patients undergoing low risk elective surgery may not require any investigations prior to surgery.

Bloods:

1. FBE (anaemia or thrombocytopenia, or if having major surgery)
2. EUC (eGFR, electrolytes, creatinine)
3. LFT (if known or suspected liver disease e.g. Hepatitis)
4. HbA1c (elective surgery will often be postponed for patients with poorly controlled HbA1c e.g. > 9)
5. TSH (known or suspected thyroid illness)
6. Coagulation profile (if patient takes anticoagulant medications (particularly warfarin) or haematological disease/ high bleeding risk)
7. Group and hold +- crossmatch (if blood loss anticipated)

Bedside:

1. ECG (particularly for older patients, those with cardiovascular disease or those having high risk surgery)
2. Pregnancy test: for women of reproductive age

Imaging:

1. TTE (may be considered on basis of ECG, unexplained dyspnoea, or if known or suspected CCF or valvular disease, see below)
2. CXR (not routine but may be done if suspected cardiovascular/pulmonary disease)

Other:

1. Respiratory Function Tests: to quantify airways disease (COPD/ asthma/ ILD) or if underlying respiratory illness suspected
2. Cardiac stress test: may be considered for patients with cardiovascular disease (see below)
3. Dental clearance: if concerns on airway assessment (false teeth, poor dentition etc)

Surgical Considerations

Many surgeries present their own unique challenges that anaesthetists must prepare for in our perioperative planning. As junior trainees build up their volume of practice and gain experience in the specific considerations of particular surgeries, it is often helpful to discuss with our surgical colleagues to better understand their special requirements. As always, a general structure helps to encapsulate broad surgical factors that should be included in our planning:

Space: Patient and Surgery

• How is the patient positioned? Supine, lithotomy, lateral, prone, Tredelenburg?
  • Each position is associated with cardiovascular, respiratory changes and specific pressure injury risks.
• How is the patient oriented? Head away from anaesthetic machine? Is our airway close to operative site?
  • These will present logistical challenges that need to be navigated on the day.
• Do I have access to my IV?
  • This is absolutely imperative in cases where access will be restricted, such as when arms are fully tucked or during robotic cases. Make sure you are confident with your IV, and have at least two if total intravenous anaesthesia is used.
• Where and how big is the operative site?
  • Certain regional techniques are extremely useful as a sole method of providing anaesthesia or as an adjunct to perioperative analgesia, especially in high-risk multimorbid patients or in patients where opioid minimisation is ideal. Knowing where the incisions are will help determine the best block technique.

Time: Duration and special timepoints

• How long is the surgery?
  • Duration of surgery often correlates with the complexity, degree of physiological insult, and risk of perioperative complications, such as MACE, hypothermia, major fluid shift, delayed emergence, post-operative nausea & vomiting etc.
• Are there critical moments that require special attention? Some examples include:
  • Laparoscopic surgery: pneumoperitoneum
  • Limb surgery: tourniquet tightening & release
  • Major vascular: vessel clamping & release
  • Neurosurgery: head pin, aneurysm clamping

Bleeding

Major cardiac, hepatic, vascular, obstetric and orthopaedic surgeries often carry significant bleeding risk, and appropriate perioperative management should be in place:

• Preoperative:
  • Up-to-date group and hold, with option for 2x crossmatched blood ready
  • Management of anaemia through combination of iron supplementation, optimisation of comorbidities, and blood loss minimisation (withholding of antiplatelet/anticoagulants)
• Intraoperative:
  • 2x large bore IV, hot fluid line, rapid infuser device, cell saver, blood available, ROTEM/TEG available

Special cases

• Nerve monitoring e.g. thyroidectomy, plastics reconstruction, nerve repair
  • Intraoperative avoidance of neuromuscular blockers to ensure nerve can be monitored

Risk stratification:

There are several tools which are very useful in assessing patient anaesthetic/ surgical risk. These can be used to make decisions about pre-operative optimisation and predict care requirements in the post operative period.

American Society of Anaesthesiologists Physical Status Classification System (ASA):

Useful to assess and communicate a patient’s medical comorbidities.

ASA 1 – A normal healthy patient – e.g. healthy non smoking patient

ASA 2 – A patient with mild systemic disease – e.g. current smoker, obesity, pregnancy

ASA 3 – A patient with severe systemic disease – e.g. poorly controlled diabetes, hypertension

ASA 4 – A patient with severe systemic disease that is a constant threat to life – e.g. MI or stroke < 3 months ago

ASA 5 – Moribund patient, not expected to survive the next 24 hours, with or without surgery – e.g. ruptured aortic aneurysm

ASA 6 – Declared brain dead, entering theatre for organ retrieval purposes

Major adverse cardiovascular events (MACE) represent one of the most significant complications contributing to perioperative morbidity and mortality. The presence of major cardiovascular conditions, such as ACS, CCF and arrhythmias, as well as any new, acute-on-chronic, or untreated conditions, all disproportionally increase the risk of MACE. Clinicians must consider the benefit-risk profile of delaying surgery for optimisation of these conditions.

The 2024 AAHA/ACC Guideline for Perioperative Cardiovascular Management for Non-cardiac Surgery provides a detailed flowchart to assist clinicians in deciding the most appropriate actions for patients presenting with significant cardiac comorbidities for non-cardiac surgery. To summarise:

Table 1. Adaptation of Figure 1 of 2024 AAHA/ACC Guideline for Perioperative Cardiovascular Management for Non-cardiac Surgery

Is it emergency surgery	If YES -> Proceed with surgery If NO -> Move to step 2
Does patient have either ACS (within 60 days) Unstable arrhythmias Decompensated CCF	If YES -> consider postponing surgery for management of acute cardiac condition If ACS is managed with drug-eluding stent (DES) PCI requiring cessation of 1 or more antiplatelet therapy Delay for 12 months Delay for 3 months for time sensitive surgery Also consider if any new or undiagnosed/untreated cardiac conditions If NO -> Move to step 3
Does the patient have Elevated risk for MACE based on validated risk calculators and/or Have any risk modifiers? Validated risk scores include: Revised Cardiac Risk Index (RCRI) American College of Surgeons NSQIP Surgical Risk Calculator (ACS-SRC) Risk modifiers are: Severe valvular heart disease Severe pulmHTN Elevated risk congenital heart disease Prior coronary stent/coronary bypass Recent stroke AICD or pacemaker Frailty	If Low risk score AND no modifiers -> Proceed with surgery Represents low risk procedure / low clinical risk If elevated risk score but no modifiers: Consider ECG for asymptomatic patients with no established CVD Commence or optimise guideline-directed medical therapy (GDMT) Once complete, move to step 4 If any risk modifier present: TTE for evaluation of left ventricular function, valvular pathology, or new symptoms Commence and optimise guideline-directed medical therapy And For valvular pathology, consideration of corrective intervention (valve repair/replacement) Once complete, move to step 4
Does the patient have reduced or unknown functional capacity, MET <4 or DASI <32	If NO -> Proceed to surgery If YES -> move to step 5
Will further testing change management	If NO* -> Proceed to surgery OR consider non-operative options If YES -> move to step 6
Does patient have elevated risk based on cardiac biomarkers: NT-proBNP / BNP Troponin	If NO -> Proceed to surgery If YES: Consider TTE or stress testing, and follow-up with Low risk findings -> Proceed Elevated risk -> GDMT and consideration of non-operative options Proceed w/ post-op cardiac biomarker surveillance

The 2024 AHA/ACC guideline provides a structured framework that can be adapted for any medical condition that may pose increased perioperative risk to patients. A useful mnemonic by Dr. Lahiru Amaratunge distils the steps of the 2024 AHA/ACC guideline that can be universally applied:

“Every Anaesthetist Loves Morning Coffee”

1. Emergency surgery -> proceed, with as much optimisation as possible;
2. Active condition -> if new condition or acute decompensation/deterioration, consider postponing;
3. Low risk -> if low risk procedure / low clinical risk -> proceed
4. MET >4 -> proceed
5. Cardiac investigations (or investigations relevant for the condition) -> further risk stratification and optimisation

Conclusion:

The preoperative anaesthesia assessment aims to minimise a patient’s intra and post operative risk. It encompasses a focused history, examination and select investigations. The assessment is influenced by the patient’s comorbidities, the risk of the operation, and the urgency of the operation.

Useful links:

Peri operative medication management – UpToDate

https://www.uptodate.com/contents/perioperative-medication-management

STOP-BANG Questionnaire

https://www.mdcalc.com/calc/3992/stop-bang-score-obstructive-sleep-apnea

Mallampati Score – LITFL

https://litfl.com/mallampati-score/

NSQIP Risk Calculator Tool

https://riskcalculator.facs.org/RiskCalculator/index.jsp

DASI – MDCalc

https://www.mdcalc.com/calc/3910/duke-activity-status-index-dasi#evidence

References:

Ng ACC, Kritharides L. Preoperative assessment: a cardiologist’s perspective. Aust Prescr 2014;37:188-91.https://doi.org/10.18773/austprescr.2014.079

Pang, C. L., Gooneratne, M., & Partridge, J. S. L. (2021). Preoperative assessment of the older patient. BJA education, 21(8), 314-320.

Lamperti, M., Romero, C. S., Guarracino, F., Cammarota, G., Vetrugno, L., Tufegdzic, B., … & Afshari, A. (2025). Preoperative assessment of adults undergoing elective noncardiac surgery: Updated guidelines from the European Society of Anaesthesiology and Intensive Care. European Journal of Anaesthesiology| EJA, 42(1), 1-35.

Hendrix, J. M., & Garmon, E. H. (2025). American Society of Anesthesiologists Physical Status Classification System. In StatPearls. StatPearls Publishing.

Writing Committee Members, Thompson, A., Fleischmann, K. E., Smilowitz, N. R., de Las Fuentes, L., Mukherjee, D., Aggarwal, N. R., Ahmad, F. S., Allen, R. B., Altin, S. E., Auerbach, A., Berger, J. S., Chow, B., Dakik, H. A., Eisenstein, E. L., Gerhard-Herman, M., Ghadimi, K., Kachulis, B., Leclerc, J., Lee, C. S., … Williams, K. A., Sr (2024). 2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Journal of the American College of Cardiology, 84(19), 1869–1969. https://doi.org/10.1016/j.jacc.2024.06.013

Key reference:

Chua MJ, Lersch F, Chua AWY, Kumar CM, Eke T. Sub-Tenon’s anaesthesia for modern eye surgery-clinicians’ perspective, 30 years after re-introduction. Eye (Lond). 2021;35(5):1295-1304. doi:10.1038/s41433-021-01412-5

Demonstration of sub-Tenon block can be found on ABCs of Anaesthesia Youtube channel:

https://www.youtube.com/watch?v=k_bxA9GiGNs

Quick Summary

• Contemporary ophthalmic surgeries are increasingly being performed under regional and local anaesthesia with non-inferior analgesia, akinesia, safety profile and improved efficiency in list turnover.

• The sub-Tenon block (STB) presents an effective modality to achieve ocular analgesia and akinesia with superior safety profile compared to needle-based peribulbar and retrobulbar techniques.

• STB is associated with common but self-limiting complications including chemosis and subconjunctival haemorrhage.

• Nevertheless, retrobulbar haemorrhage (RBH), a sight-threatening ocular emergency resulting from rapid increases in intraocular pressure (IOP) from accumulated retrobulbar blood, remains a rare complication of STB.

• Prompt recognition of RBH is essential to expedite definitive lateral canthotomy decompression and minimise long-term sight impairment.

Preamble

You are a junior anaesthetic trainee on your first busy ophthalmology list. Your next patient is Mrs. CS, a 70 year old lady who has arrived for her elective left eye cataract surgery. She had her right eye cataract completed 2 months ago without any issues.

Her history is significant for ischaemic heart disease and atrial fibrillation, for which she is on aspirin 100mg daily and apixaban 2.5mg BD. Her preoperative visual acuity (VA) was 6/6 for right eye and hand movements-only for left eye. Both eyes had deep anterior chamber depths. Baseline IOP was 26mmHg for the right eye. After an unremarkable preoperative assessment, the patient was consented for a sub-Tenon block (STB).

What is a sub-Tenon Block (STB)?

STB is a regional eye block technique developed in 1884 and popularised in the 1990s. In contrast to needle-based peribulbar and retrobulbar blocks, STB utilises blunt-end cannula to deliver local anaesthetics into the episcleral potential space, targeting both sensory ocular nerves and all 6 extraocular muscle sheaths to produce anaesthesia and akinesia.

Tenon’s capsule is the fascial sheath that surrounds the globe. Anteriorly, it merges with the conjunctiva at the limbus, and posteriorly fusing with the meninges and sclera of the optic nerve. Between the Tenon’s capsule and the sclera contains the episcleral potential space, which is transverse by:

To access the sub-Tenon space, the infero-nasal quadrant is favoured as it is least likely to be traversed by the vortex veins or other neurovascular and muscular structures.

Once administered, the local anaesthetic hydro-dissects the episcleral space and creates a circumferential collection bathing the ciliary nerves. With larger volumes (>3mls), local anaesthetic spreads along the extraocular muscle sheath, as well as anteriorly to the facial plane of the lid to provide akinesia of the globe and eyelid muscles.

Steps to completing a STB

1. Patient consent

2. Position patient supine position

3. WHO block timeout

4. Standard ANZCA monitoring

5. IV access +/- anxiolysis/sedation if necessary, with IV midazolam/low dose propofol/ fentanyl

6. Hat/mask/sterile glove

7. 2-3 drops of topical anaesthetics of choice to target eye (e.g. 0.4% oxybuprocaine)

8. Skin prep with iodine-based antiseptic (e.g. betadine 1% solution), followed by sterile drape

9. Apply eye speculum

10. Ask patient to look superotemporally with the target eye to expose the inferonasal quadrant

11. Create a small tent of conjunctiva 5-7mm from the limbus using a conjunctival forceps (e.g. Moorfield’s), and make a small incision using Wescott spring scissors

    1. Non-snip techniques are also available using pencil point cannula or other plastic probes

12. Insert the blunt-end sub-Tenon cannula through the incision and up to the globe equator in depth, always hugging the sclera during the insertion

13. Slowly inject 3-5ml of local anaesthetic solution of choice into the sub-Tenon space (e.g. 2% lidocaine with 30 units/ml hyaluronidase), avoiding injecting if high resistance or discomfort encountered

    1. Hyaluronidase hydrolyses part of the extracellular matrix, improves local anaesthetic dispersion and penetration, reduces volume of LA required, and reduces time for onset of akinesia

14. Perform a post-block assessment, noting any immediate complications (e.g. chemosis, subconjunctival haemorrhage), pain, discomfort, periorbital swelling, proptosis etc.)

Sub-Tenon Block set up and equipment

Who is suitable for STB?

STB and other needle-based regional techniques are allowing patients to undergo low-risk ophthalmic procedures who would otherwise be at significant high risk for general anaesthetics. While STB is considered safe and effective for vast majority of patients, certain patient populations have relative and absolute contraindications to a STB:

Complications of STB

STB is a favoured eye block technique due to its superior safety profile. Two prospective studies in Australia and New Zealand with combined 8688 STBs observed no sight-threatening complications related to STBs. While STB is associated with higher rates of benign and transient complications such as chemosis and subconjunctival haemorrhage, sight and life-threatening complications are exceedingly rare and are 2.5 times less common than needle blocks. A Cochrane review of 605 patients undergoing cataract surgery found no evidence STB had a higher rate of intraoperative complications compared to non-invasive topical anaesthesia, albeit with limited statistical power.

…………………………..

Returning to Ms CS:

You successfully complete the STB for Mrs. CS in the holding bay. You note the patient’s bleeding risk whilst on both anticoagulant and antiplatelet therapy, but are reassured by your consultant of the low risk of sight threatening haemorrhage.

As you are waiting for the surgeons to prepare, Mrs CS reports increasing discomfort of the operative eye. You note that the eye has become tense with onset of periorbital swelling and resistance to retropulsion. Examination revealed proptosis of the right eye, with increased IOP up to 45mmHg. Your consultant immediately suspects a retrobulbar haemorrhage and reports to the ophthalmologist.

What is retrobulbar haemorrhage?

Retrobulbar haemorrhage (RBH) is a sight-threatening ophthalmic emergency, characterised by raised intraocular pressure (IOP) secondary to accumulating blood within the tight intraconal space, causing extrinsic compression of neurovascular structures, impairing orbital venous drainage and arterial supply, ultimately resulting in retinal ischaemia and optic nerve injury. RBH can be spontaneous, or through iatrogenic trauma such as with regional anaesthesia, which has a prevalence of 0.04% to 0.43%.

RBH is an extremely rare complication of STB, with isolated cases described in a small number of case reports and retrospective studies. The pathophysiology is attributed to iatrogenic injury to the vortex veins that traverses through the sub-Tenon space, causing slow ooze and gradual intraocular pressure rise. The use of metal cannulas, transient intraocular pressure rise from cough/Valsalva reflex, posterior vessel crowding from increased axial length, and use of antithrombotic therapy were respectively implicated as possible contributing factors. Due to the lack of case numbers, there is insufficient statistical power to-date to validate these risk factors.

Minimising RBH risk during STB

Using standard inferonasal approach

The inferonasal quadrant avoids the majority of neurovascular and muscular structures. Specifically, the vortex vein in the temporal region commonly loops around into the inner surface of the Tenon’s capsule, posterior to the insertion of the inferior rectus muscle. Thus, the inferonasal approach is usually preferred over inferotemporal to reduce the risk of vortex vein injury and RBH.

Using shorter, non-metal, blunt cannula

The vortex veins and ciliary vessels are concentrated in the posterior quadrant. As such, it is advisable to avoid cannula over-advancement beyond the globe equator and endangering posterior vascular structures. Anaesthetists should pay extra attention to the orbit’s axial length during their pre-operative assessment, which informs the required needle depth, as well as the risks of scleral thinning and irregularities. The use of shorter, flexible cannulas in favour of rigid metal cannulas has been suggested to avoid inadvertent vessel injury.

Using smaller local anaesthetic volume

Further risk minimisation through reducing volume (and speed of injection) of local anaesthetics to prevent shearing of sclerotic vessels and rise of intraocular pressure must be balanced with patient discomfort and suboptimal akinesia conditions associated with incomplete block.

Avoidance of “orbital massage”

Orbital massage is a technique used to disperse local anaesthetic throughout the sub-Tenon space by firm rocking pressure applied against the orbit. This has been shown to increase intraocular pressure abruptly to 400mmHg, significantly increasing shear stress on posterior vessels.

Management of RBH

Management of RBH requires early recognition of intraocular pressure, which may present as eye pain, proptosis, periorbital swelling, visual disturbance, impaired eye movements, or increased IOP. Immediate surgical decompression via lateral canthotomy/cantholysis, with adjunct medical management to reduce IOP is the first line of management, and is associated with only 0.14% rate of blindness if instituted promptly. Medical management commonly involves administration of acetazolamide, corticosteroids, and topical timolol to decrease aqueous humor production in the eye to further reduce IOP.

Returning to Ms CS

The ophthalmologist immediately sets up and performs a lateral canthotomy and cantholysis in theatre, with you administering procedural sedation. A small pocket of blood is evacuated.

Within minutes, Ms. CS’s symptoms improved, and proptosis is visibly reduced. Reassessment of the IOP showed a pressure of 15 mmHg.

You arrange for Ms. CS to be transferred to a tertiary eye centre for overnight observations. You instruct her to withhold her apixaban and aspirin for today. You commence her on acetazolamide (500 mg IV) and topical timolol to control her IOP. Immediate post-procedure monitoring noted no further signs of rebleeding or worsening of symptoms.

Ms. CS is discharged the next day. She returns 1 week later to complete her cataract surgery under general anaesthesia without complication, and fully recovers her VA.

Conclusion

STB continues to be a popular, safe and effective regional technique for ophthalmic surgery. While major complications are extremely rare, anaesthetists must be vigilant of signs and symptoms and follow techniques that minimise their risk. In the case of suspected RBH, prompt action must be taken to prevent permanent vision loss through surgical and medical management.

References

Chua MJ, Lersch F, Chua AWY, Kumar CM, Eke T. Sub-Tenon’s anaesthesia for modern eye surgery-clinicians’ perspective, 30 years after re-introduction. Eye (Lond). 2021;35(5):1295-1304. doi:10.1038/s41433-021-01412-5

Clarke JP, Plummer J. Adverse Events Associated with Regional Ophthalmic Anaesthesia in an Australian Teaching Hospital. Anaesthesia and Intensive Care. 2011;39(1):61-64. doi:10.1177/0310057X1103900109

Ernest JT, Goldstick TK, Stein MA, Zheutlin JD. Ocular massage before cataract surgery. Trans Am Ophthalmol Soc. 1985; 83: 205–217.

Lerch D, Venter JA, James AM, Pelouskova M, Collins BM, Schallhorn SC. Outcomes and Adverse Events of Sub-Tenon’s Anesthesia with the Use of a Flexible Cannula in 35,850 Refractive Lens Exchange/Cataract Procedures. Clin Ophthalmol. 2020;14:307-315. Published 2020 Jan 31. doi:10.2147/OPTH.S234807

Subbiah S, McGimpsey S, Best RM. Retrobulbar hemorrhage after sub-Tenon’s anesthesia. J Cataract Refract Surg. 2007;33(9):1651-1652. doi:10.1016/j.jcrs.2007.04.042

Article Reference: Whately, Y. and Stead, M. (2023) ‘Perioperative management of patients on naltrexone’, Australasian anaesthesia 2023. Edited by B. Cheung. doi:https://doi.org/10.60115/11055/1180.

Key Points

• Naltrexone is a long-acting opioid receptor antagonist, used commonly to manage alcohol use disorder.

• Due to its opioid receptor antagonism, naltrexone presents challenges for managing pain in the perioperative period – making patients both resistant to, and have increased sensitivity to the respiratory side effects of opioids.

• It is recommended to discontinue naltrexone 3 days before surgery to ensure effective and safe use of opioid analgesia.

• In emergency cases, additional post op monitoring may be needed, as higher doses of opioid are required to overcome the naltrexone blockade, making patients vulnerable to respiratory side effects.

• In all cases, an individualised and multi-disciplinary approach is recommended for optimal care.

Case

You are an anaesthetic trainee working in a pre-assessment clinic. You see a 45-year-old male patient scheduled for an elective laparoscopic cholecystectomy. The patient has no significant past medical history besides a history of alcohol use disorder, for which he has been on naltrexone 50mg daily for the past 6 months.

He reports good compliance with his medication and has maintained sobriety.

You remember learning that some extra planning and consideration is required with naltrexone but you can’t remember why.

What is Naltrexone

Naltrexone is a competitive opioid receptor antagonist most commonly used in the treatment of alcohol use disorder. It has high mu opioid receptor affinity but does not activate them and blocks opioids from attaching and mediating their effects.

In the treatment of alcohol use disorder, it works by blunting the opioid receptor-mediated reward pathway and blocking the pleasurable effects of endogenous opioids that are released with alcohol consumption. It is also used in opioid abstinence programmes. In other drug combinations and dose formulation, it can be used in weight loss, chronic pain, and severe constipation.

The most common formulation is the daily oral 50mg tablet, which is used in alcohol and opioid dependence. Other formulations of naltrexone include a long-acting surgical implant, monthly depo injection, a combination drug with bupropion, and a low-dose tablet form.

Relevance for the Anaesthetist

Patients taking naltrexone present a significant challenge in managing perioperative pain because of their competitive blockade of opioid analgesics. It reduces the effectiveness of opioids, often necessitating higher doses to achieve adequate pain relief. However, the increased opioid requirement in turn heightens the risk of opioid-related side effects, such as respiratory depression and sedation.

Due to the homeostatic upregulation of opioid receptors that can occur after long-term naltrexone use, patients who have stopped taking naltrexone pre-op remain at increased risk of opioid-induced adverse effects with conventional analgesic doses.

Careful consideration is needed for these cases and planning between the anaesthetist, surgical team, patient, and naltrexone prescriber is essential to ensure the best outcome. As such, timely detection and referral of these patients to multidisciplinary perioperative teams would allow streamlined optimisation, increase team preparedness, prevent unnecessary delays and improve patient outcomes.

Management of Patients for Elective Procedures

If the patient is presenting for a minor procedure with minimal expected postoperative pain, then it is reasonable to continue naltrexone and use non-opioid analgesia. Examples include minor plastics and general surgical cases where combination of local anaesthetic and simple analgesia may be sufficient.

In most cases, where there is an expected need for opioids, oral naltrexone should be stopped at least 24 hours, and ideally 72 hours, prior to surgery. A longer period may be required in renal or hepatic insufficiency and for long-acting formulations. While naltrexone therapy is temporarily discontinued, extra support is recommended as it is a vulnerable time for potential relapse.

Management in Acute or Emergency Cases

In emergency cases, where discontinuation is not feasible, careful planning and implementing an opioid-sparing strategy is essential.

These patients are prone to variability in their response to opioids and must be monitored in a space with a capacity for airway and ventilation support due to the high risk of respiratory depression. If the last dose of naltrexone was taken within 72 hours of surgery, higher doses of opioids will be required for effective pain management. Prioritising alternative pain management techniques through neuraxial or regional anaesthesia, and non-opioid analgesia is favoured in these cases to minimise unpredictable and harmful effects.

Post-operative planning

In the post-op period, the Acute Pain Service, in liaison with the Addiction Medicine service, should be involved to guide the analgesic regime . Determining the optimal time to resume naltrexone requires an individualised, multi-disciplinary approach. The decision must carefully balance the need for effective pain management with the potential risks of restarting naltrexone too soon, as well as the risks of delaying its use, which could hinder the therapeutic benefits it was initially prescribed for. Once the acute pain has resolved and opioids have been discontinued, it is recommended to have at least a 5 day opioid free interval before restarting naltrexone. If there are any doubts or concerns regarding opioid dependence, a naltrexone challenge can be performed to avoid any precipitated withdrawal.

Conclusion

You sit down with your supervisor to discuss the case. You correctly flag your patient with your institution’s Acute Pain service. They agree with your plan for the patient to discontinue naltrexone 3 days before surgery, and adopt an opioid-sparing anaesthetic and to minimise their use post-operatively. You coordinate with the patient, surgeon, and naltrexone prescriber who are all on board..

The case goes well. The Acute Pain Service are involved post-operatively and manage to avoid excess use of opioids following surgery. The patient experiences no opioid-induced sedation or ventilatory impairment.

The patient is safely restarted on his regular medication.

References

Beauchamp GA, Hanisak JL, Amaducci AM, Koons AL, Laskosky J, Maron BM, McLoughlin TM. Perioperative Management of Patients on Maintenance Medication for Addiction Treatment: The Development of an Institutional Guideline. AANA J. 2022;90(1):50-57. PMID: 35076384.

Lane O, Ambai V, Bakshi A, et al Alcohol use disorder in the perioperative period: a summary and recommendations for anesthesiologists and pain physicians. Regional Anesthesia & Pain Medicine 2024;49:621-627.

Whately, Y. and Stead, M. ‘Perioperative management of patients on naltrexone’, Australasian anaesthesia 2023. Edited by B. Cheung. doi:https://doi.org/10.60115/11055/1180.

By Dr Jessica Spurio

Key reference: Riley, C. and J. Andrzejowski (2018). “Inadvertent perioperative hypothermia.” BJA Education 18(8): 227-233.

Quick Summary

• Hypothermia is defined as a core body temperature below 36°C.

• Perioperative hypothermia is a common consequence of general and regional anaesthesia, occurring due to the effect of anaesthesia on thermoregulatory mechanisms.

• It is associated with adverse outcomes such as increased risk of surgical site infections, increased bleeding, altered drug metabolism and adverse cardiac events.

• Patients undergoing combined general and regional anaesthesia are at greatest risk.

• Active warming using a forced air warming device is a practical technique for preventing or treating perioperative hypothermia and is recommended for all patients at risk.

Preamble

You are a resident starting your first week in anaesthesia. Your next patient is a 67 year old woman undergoing an elective laparoscopic cholecystectomy. Her past medical history includes hypertension and type 2 diabetes. She has a BMI of 35. Whilst reviewing her in the pre-operative bay, you look at her admission observations and notice her temperature is 35.8°C. How will this impact your anaesthetic management?

The Physiology of Thermoregulation

Core body temperature is tightly maintained within strict parameters (36.7°C – 37.1°C) to maintain optimal physiological conditions. Thermoregulation occurs via afferent input, central regulation and efferent responses.

Afferent Input: Heat and cold sensors located both peripherally (in skin and deep tissues) and centrally (in the brainstem, spinal cord and hypothalamus) relay thermal information to the brain via the lateral spinothalamic tract.

Central regulation: The hypothalamus is the primary thermoregulatory controller. It integrates input from sensors, and when a temperature outside of the targeted set point is detected, it triggers effector mechanisms to return the body to normothermia.

Effector mechanisms: These include both behavioural and autonomic responses.

• Behavioural changes: changing clothing, altering ambient temperature or initiating voluntary movement.

• Autonomic responses:

  • The main effectors are skin, skeletal muscle, sweat glands and brown adipose tissue,

  • Cooling mechanisms include vasodilation and sweating,

  • Warming mechanisms include vasoconstriction, non-shivering thermogenesis and shivering.

What are the effects of general and regional anaesthesia on thermoregulation?

Threshold temperature is the temperature at which an autonomic response is triggered.

Inter-threshold range is the range of core body temperatures between which no autonomic thermoregulatory effects are triggered.

Anaesthesia causes a reduced threshold temperature and therefore a widened inter-threshold range. This means that warming mechanisms are only triggered at much cooler body temperatures, in turn impairing the thermoregulatory response to hypothermia. .

In normal circumstances, the threshold temperature is 36.5°C for vasoconstriction and approximately 36°C for shivering. General anaesthesia reduces these thresholds by 2-3°C.

Furthermore, normal behavioural responses are completely eliminated during general anaesthesia, leaving patients reliant on already impaired autonomic responses.

Intraoperative hypothermia typically develops in a triphasic pattern

1. Rapid initial reduction in temperature as vasodilation occurs due to induction agents, leading to redistribution of body heat from core to peripheral tissues. Anaesthesia also reduces the activation threshold for thermoregulatory vasoconstriction.

2. Gradual, linear decline in temperature as heat loss via radiation, convection and evaporation exceeds metabolic heat production. Metabolic heat production is reduced by 15-40% during general anaesthesia.

3. Plateau phase as patients become hypothermic to the point of reaching the altered threshold for vasoconstriction. Maximal vasoconstriction occurs and the body begins to conserve heat.

Figure 1: Characteristic triphasic pattern of intraoperative hypothermia

Measuring temperature: when and how?

Temperature should ideally be measured every 30 minutes in patients undergoing anaesthesia. Various devices may be used to measure temperature and these vary in their ability to provide an accurate estimate of core body temperature.

Most accurate

• Pulmonary artery catheter (provides a highly accurate estimate of core temperature but is very invasive)

• Lower oesophagus

• Nasopharynx

• Intravesical (In-dwelling catheter with temperature probe)

Less accurate

• Tympanic

• Axillary

• Rectal

In modern day practice a nasopharyngeal temperature probe (thermistor) is used to continuously measure core temperature in patients under general anaesthesia.

Risk factors for perioperative hypothermia

Patient factors

• ASA grade 2 – 5

• Low BMI (higher surface area:volume ratio increases heat loss)

• Elderly or paediatric patients

• Pregnancy

• Temperature < 36°C preoperatively

Surgical or anaesthesia factors

• Major or emergency surgery

• Duration of surgery > 30 minutes

• Degree of body exposure

• Theater ambient temperature < 21°C

• Use of cold irrigation fluids

• Combined general + regional anaesthesia

Risks and complications

Prevention and treatment

Before surgery

• Identify high risk patients

• Measure temperature preoperatively

• Encourage patients to walk to theatre where possible

• Ensure majority of patient’s body area is covered

• Actively pre warm patients

During surgery/anaesthesia

• Monitor temperature continuously

• For anaesthesia expected to last >30 minutes, actively warm all high risk patients using forced air warming devices or heated blankets/mattresses

• Ensure an ambient temperature of at least 21°C whilst the patient is exposed

• Use warmed IV fluids and blood products (38-40°C)

After surgery

• Monitor temperature in the PACU

• Keep patients comfortably warm with blankets

• Actively warm patients if their temperature is < 36°C

Conclusion

Let’s return to your next patient in the pre-operative bay. You identify that this patient has multiple risk factors for perioperative hypothermia including her pre-operative hypothermia and ASA grade of 2. You discuss the case with your consultant and propose a plan, which includes actively pre-warming the patient for at least 30 minutes before anaesthesia induction, ensuring warmed IV fluids are available to use during the case, continuing to warm the patient with a forced air warming device during the case and inserting an nasopharyngeal temperature probe to monitor her temperature. You communicate this plan with your anaesthetic nurse and your patient and proceed with the case. After wheeling her to PACU, you preemptively bring the forced air warming blanket together with her to ensure she remains warm until she fully emerges from her anaesthetic..

References

1. NICE guideline 65 Hypothermia: prevention and management in adults having surgery. 2008 [Available from: www.nice.org.uk/guidance/cg65

2. Bindu B, Bindra A, Rath G. Temperature management under general anesthesia: Compulsion or option. J Anaesthesiol Clin Pharmacol. 2017;33(3):306-16.

3. Doufas AG. Consequences of inadvertent perioperative hypothermia. Best Practice & Research Clinical Anaesthesiology. 2003;17(4):535-49.

4. Kirkbride DA, Buggy DJ. Thermoregulation and mild peri‐operative hypothermia. BJA CEPD Reviews. 2003;3(1):24-8.

5. Kurz A. Physiology of Thermoregulation. Best Practice & Research Clinical Anaesthesiology. 2008;22(4):627-44.

6. Riley C, Andrzejowski J. Inadvertent perioperative hypothermia. BJA Education. 2018;18(8):227-33.

Key Reference

Iglesias, I. Kaplan’s Cardiac Anesthesia: Perioperative and Critical Care, 8th Edition.

Can J Anesth/J Can Anesth 71, 1438–1439 (2024)

Background on Cardiac Bypass

Cardiopulmonary bypass (CPB) maintains systemic circulation and oxygenation during cardiac surgeries while the heart is stopped and isolated. In short, venous blood is diverted to an external oxygenator and returned to the body via large cannulae traditionally inserted in the right atrium and ascending aorta. The heart is isolated from systemic circulation via aortic cross clamping, and cardioplegia delivered to achieve cardiac arrest and provide cooling to minimise ischaemic injury for the duration of bypass. These steps allow surgeons to operate on a motionless and blood-free heart in a controlled environment, whilst systemic perfusion and anaesthesia can be maintained via an extracorporeal system.

Cardiac bypass is an essential component of procedures such as

• Coronary artery bypass grafting (CABG).

• Heart valve repair or replacement.

• Repair of congenital heart defects.

• Heart transplants.

By ensuring uninterrupted circulation, CPB allows complex surgeries to be performed safely. However, because blood comes into contact with artificial surfaces in the bypass circuit, anticoagulation is critical to prevent clotting. Heparin, in light of its predictability, reversibility and ease of administration, has become the anticoagulant-of-choice for CPB.

What Is Heparin?

Heparin is widely used in medical and surgical settings in the prevention and management of blood clot formation. It is available in two forms, unfractionated heparin (UFH) which contains unfiltered mixture of glycoaminoglycan polymers with molecular weights between 3000 to 30,000D, and low molecular weight heparin (LMWH) with only small-chain polymers with molecular weights ranging 3,000 to 6,000D.

Pharmacodynamics

Heparin exerts its anticoagulant effect through indirect agonism of endogenous antithrombin III (ATIII), causing a conformational change that enhances the affinity and inhibitory activity of ATIII to clotting factor proteases, predominantly thrombin and factor Xa. The anticoagulant effectiveness of UFH demonstrates interpersonal variability partly due to heterogeneity in polymer composition, and must be monitored using laboratory activated partial thromboplastin time (APTT) or point-of-care activated clotting time (ACT) when administered at high doses.

Pharmacokinetics

UFH can be administered intravenously or subcutaneously, with distribution primarily within intravascular space as largely protein-bound molecules. UFH follows a biphasic elimination pattern, combining rapid sequestration by the saturatable reticuloendothelial system with slower non-saturatable first-order renal clearance. As such, UFH half-life is dose-dependent and non-linear. Alternatively, UFH is rapidly bound and reversed with protamine at a 1mg(protamine):100IU(UFH) ratio

Why Do You Need Heparin During Cardiac Bypass?

During CPB, blood comes into contact with artificial non-endothelial surfaces, which activates inflammatory and clotting mechanisms, leading to thrombus formation. Exposure of tissue factor via surgical wound further adds clotting burden. UFH prevents these clots from forming in the extracorporeal circuit, ensuring smooth blood flow and preventing catastrophic complications like embolism or stroke.

How Do We Dose and Measure Heparin?

Dosing:

The standard initial dose is 300–400 units/kg administered intravenously. This may require individualised adjustment given variable dose-responsiveness. As such, clear evidence of anticoagulation through ACT measurement is required before CPB initiation.

Monitoring:

ACT is used to measure heparin’s efficacy. While APTT correlates with heparin concentrations at lower therapeutic concentrations (e.g. for existing thrombus management), APTT demonstrates a logarithmic relationship with poorer sensitivity at higher heparin doses, whereas ACT shows a linear relationship. Moreover, ACT is more logistically feasible as a point-of-care test than laboratory APTT or anti-Xa assays that have substantial time delays. However, ACT becomes unreliable with increasing CPB duration, as ACT is non-heparin specific and prolonged from hypothermia and haemodilution.

An ACT greater than 480 seconds is typically required during bypass to ensure adequate anticoagulation. Close communication is required with the cardiac surgeon to ensure the correct timing of heparin and the correct ACT.

Reversal:

After surgery, the effects of heparin are reversed with protamine sulfate.

• Dose: 1mg of protamine for every 100 units of heparin

• This may be reduced if >1hr since last heparin dose

Anaesthetists must entertain the risk of postoperative bleeding when reversing heparin. Protamine not only neutralises heparin through direct ionic bonding, but also impairs platelet adhesion and aggregation, paradoxically increasing bleeding risk. Patients may exhibit “heparin rebound” with redistribution of heparin from sequestered stores, where patients may require repeated protamine dosing for larger initial heparin boluses. Individualised dosing based on predicted heparin concentration is recommended to reduce bleeding risk.

In addition, protamine is associated with arterial hypotension, pulmonary vasoconstriction and anaphylaxis. These deleterious haemodynamic effects must be considered when managing patients with brittle compensatory reserves intraoperatively during cardiac surgery.

What Happens If Heparin Fails?

Heparin resistance is defined as an inability to achieve ACT > 480s despite adequate heparin dosing (300-400 unit/kg)

Although rare, heparin resistance can result in clot formation in the bypass circuit, potentially leading to severe complications such as

• Blockage of the oxygenator or pump.

• Embolic events causing stroke, myocardial infarction, or organ damage.

Heparin resistance may be due to ATIII deficiency, ATIII-independent mechanisms, or pseudo-resistance.

ATIII deficiency

This can be acquired from impaired production secondary to critical illness or liver injury, and increased ATIII clearance from preoperative heparin use, nephrotic syndrome and sepsis. CPB itself can lead to consumptive reduction in ATIII by activating coagulation cascade, while the patient cohort requiring CPB often presents with vascular endothelial abnormalities and inflammatory states that are prothrombotic.

Congenital ATIII deficiency is a rare autosomal dominant disorder due to mutation of the SERPINC1 gene. These patients invariably develop profound thrombophilia and require haematology input.

ATIII-independent mechanisms

Intravascular heparin concentration may be reduced when there is a greater proportion of positively-charged extracellular molecules present, such as during sepsis when there is an upregulation of pro-inflammatory cytokines, platelets and acute phase reactants. As heparin is highly negatively charged, they bind to heparin and reduce effective heparin concentration.

Pseudo-resistance

Upregulation of factor VIII and fibrinogen in cases of endothelial dysfunction may blunt the apparent effectiveness of heparin through low APTT and ACT without impacting anti-Xa or ATIII levels. This may cause underestimation of heparin effect and lead to heparin overdose,

Management of heparin resistance

Therapeutic options include additional heparin dosing, ATIII supplementation (through fresh frozen plasma (FFP) or ATIII concentrates), and/or use of alternative anticoagulants.

Heparin resistance is commonly overcome with adding further heparin up to 4U/ml, where a ceiling effect is reached corresponding with saturation of ATIII. Care must be taken to appropriately dose protamine to reduce the risk of protamine-induced platelet dysfunction and heparin rebound.

FFP and ATIII concentrates aim to rectify ATIII deficiency and augment heparin effectiveness. The addition of adjunct anticoagulants, such as bivalirudin, has been trialled in isolated case reports with promising results. Emergency interventions, including switching anticoagulants or circuit components, may be necessary.

What Do You Do If Heparin is Contraindicated?

Heparin-Induced Thrombocytopenia (HIT): HIT is an immune-mediated reaction where heparin causes a drop in platelets and paradoxical clotting.

Alternatives: In patients with HIT or allergy, anticoagulants like bivalirudin, argatroban, or fondaparinux are used. These agents provide anticoagulation without cross-reactivity with heparin.

Other Interesting Facts About Heparin?

Origin: Heparin was first isolated in 1916 from liver cells (hence the name, derived from “hepar,” Greek for liver).

Dual Role: Besides anticoagulation, heparin has anti-inflammatory properties, which may reduce complications during surgery.

Re-exposure: Heparin can safely be reused in most patients without HIT, as long as precautions are taken.

Reference

Cartwright B, Mundell N. Anticoagulation for cardiopulmonary bypass: part one. BJA Educ. 2023;23(3):110-116. doi:10.1016/j.bjae.2022.12.003

Deranged Physiology. Unfractionated and low molecular weight heparin. From https://derangedphysiology.com/main/cicm-primary-exam/haematological-system/Chapter-221/unfractionated-and-low-molecular-weight-heparin. Last Accessed 01/01/2025

Iglesias, I. Kaplan’s Cardiac Anesthesia: Perioperative and Critical Care, 8th Edition. Can J Anesth/J Can Anesth 2024; 71, 1438–1439

Key reference:

Athanassoglou V, Rogers A, Hofmeyr R. In-hospital management of the airway in trauma. BJA Educ. 2024;24(7):238-44. Available from: https://www.bjaed.org/article/S2058-5349(24)00031-3/fulltext

Preamble

You are the anaesthetic registrar on-call for a major trauma hospital. After your third morning coffee, your pager buzzes from ED resus for a trauma call.

On the resus bed is an e-scooter rider found unresponsive at the scene after colliding with a lamppost. Paramedics report a transient loss of consciousness and subsequent GCS of 8. Blood trickles from the patient’s nose, and a cervical collar sits snugly around their neck. The trauma team leader orders you to manage the airway.

On your primary survey

Critical haemorrhage

• Nil external exsanguinating haemorrhage identified

A + Cspine

• Partial obstruction with active oropharyngeal haemorrhage and soiling in unprotected airway,

• Nil obvious red flag for aerodigestive / vascular neck injury

• After suctioning, nil major distortion of maxillary-facial or oropharyngeal anatomy identified

• Jaw movements not restricted,

• Neck fixed in collar

B

• Tachypnoea with oxygen saturation 92% on 6L hudson mask

• Right sided consolidation on x-ray suggestive of aspiration, nil obvious pneumothorax

C

• HR 105 bpm, BP 110/60mmHg

D

• GCS 8 (E1 V2 M5)

• Pupils right 3mm, left 5mm, reactive

“How do I manage this trauma airway?”

Airway management in trauma presents a unique challenge due to the critical and dynamic nature of these cases. This blog outlines a structured approach to in-hospital airway management for trauma patients. The focus is on preparation, early assessment, addressing anatomical and physiological complexities; by employing a variety of airway devices and techniques. Special considerations are needed where anatomical distortion and physiological instability add layers of complexity to airway management. While no approach can fully eliminate the unpredictability of trauma care, this exploration aims to aid and highlight tools to equip practitioners with greater confidence when facing these challenges.

Preparation

Managing a difficult trauma airway requires optimal environmental setup and team preparation, coordination and delegation. The team should have a clear, shared understanding of roles, priorities and checkpoints for escalation, with closed-loop communication and dynamic leadership to ensure the team can rapidly respond to deterioration.

Ideally, the trauma team should consist of Emergency physicians, Trauma Surgeons, Anaesthetists, the nursing team, and other teams as required. The trauma team should be assembled prior to the arrival of an injured patient; this allows for gathering of necessary personnel and equipment, role allocation and planning for management. The team leader (most often the Emergency physician) assigns roles, ensures the completion of the primary and secondary survey by coordinating between team members, and directs management priorities by maintaining a “hands-off” end-of-bed overview of the resuscitation.

All airway management in trauma patients should be assumed to be difficult. Therefore, every effort should be made for equipment to be made readily available in the resuscitation area to deal with a soiled airway, difficult oxygenation and difficult laryngoscopy. An airway checklist should be used as a prompt prior to patient arrival to avoid critical omissions. It should also prompt the primary airway operator to verbalise their airway plans to establish a shared mental model and help quickly transition to contingency measures when difficulties are encountered. In most cases, additional personnel are required to provide manual inline stabilisation (MILS) or surgeons skilled in front-of-neck access.

Airway assessment

There may be limited time available for a comprehensive airway assessment before definitive management is required. Patients may be difficult to assess clinically.

Initial Evaluation:

• Ensure a stable and patent airway while considering potential cervical spine injuries.

• Early assessment includes identifying visible obstruction (blood, debris, swelling) and predicting anatomical challenges such as limited jaw mobility or airway distortion caused by maxillofacial and lower-airway trauma.

• Large bore suction should be available to clear any debris.

Tools for Prediction:

• Standardised frameworks like the modified LEMON scoring system (Look, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility) can be utilised to predict difficult laryngoscopy.
  Note: Neck mobility cannot be assessed in patients in C-spine precautions.

Table 1. Modified LEMON assessment for predicting difficult laryngoscopy and tracheal intubation

Dynamic Considerations

• Oxygenation and ventilation are monitored continuously. Any deterioration in these parameters necessitates rapid adaptation of management strategies.

• Predicting complications such as aspiration or airway collapse informs preparation for alternate techniques or emergency surgical airways.

Specialised Techniques

• Flexible Naso-endoscopy (FNE), video laryngoscopy and fiberoptic techniques can be used to overcome limited visibility or anatomical distortion.

• Airway ultrasound by trained operators can provide information such as identification of the depth and position of the cricothyroid membrane, trachea and pre-tracheal vessels as well as any relevant distorting features such as haematoma or other lesions.

Protection of the cervical spine

• Cervical spine injuries (CSI) occur in 2-3% of patients after blunt force trauma.

• There is a risk of exacerbation of CSI during the course of airway management.

• The NEXUS and Canadian C-spine rules can be used to safely rule out C-spine injury without requiring radiographic imaging. (https://www.mdcalc.com/calc/696/canadian-c-spine-rule, https://pmc.ncbi.nlm.nih.gov/articles/PMC6494628/)

It is unlikely that trauma patients who require acute airway management will be able to have their cervical spine cleared without imaging.

• Rigid collars are no longer recommended for in hospital cervical spine immobilisation as there is a lack of evidence of their efficacy and they carry an increased risk of pressure injuries and increase difficulty of airway management.

• In hospital cervical spine immobilisation can be carried out using head blocks/rolls tape and a hard mattress.

Manual in-line stabilisation (MILS) is the recommended technique to stabilise the cervical spine during airway-management.

• A dedicated assistant is required to align the patients head and neck in a neutral position and prevent inadvertent movements.

• The assistant can crouch beside the intubator and cradle the patient’s mastoid processes and occiput.

• MILS can also be done standing in-front of the intubator and beside the patient, with hands placed on the sides of the patient’s head and forearms resting on the patient’s chest.

• Traction is not applied.

• MILS improves the Cormack-Lehane grade in 56% of patients when their hard collar is removed and switched to a MILS technique.

Laryngoscopy:

• Cervical spine immobilisation increases difficulty of laryngoscopy and intubation.

• A Video Laryngoscope with a hyper-angulated blade is recommended as it does not require manual alignment of oral, pharyngeal and laryngeal axes

.

Tracheal intubation

Appropriate timing of intubation is key in trauma patients.

Indications for intubation

Patients can require intubation for a multitude of reasons; below are some common indications for intubation in trauma cases.

Airway

• Unprotected airway

• Airway obstruction (e.g., foreign bodies, bleeding into the mouth)

• Airway trauma/burns

Breathing

• Respiratory failure (e.g., respiratory arrest, poor oxygenation/ventilation)

Circulation

• Severe haemodynamic instability (Intubation/sedation can help control the situation of an unpredictable unwell patient at risk of deterioration)

Disability

• Altered GCS <8 (loss of protective airway reflexes)

• Seizures

Environmental

• Situational control for agitated or uncooperative patients

• Facilitate further investigations or management (diagnostic/therapeutic procedures)

• Stabilisation for transfer

Stabilising haemodynamics prior to intubation

• Peri-intubation haemodynamic instability is common: encountered in up to 42% of critically ill patients undergoing emergency intubations.

• It is essential to optimise resuscitation before induction and having fluids/blood, vasopressors and inotropes running or ready prior to administering induction agents.

• Ensure adequate patient and equipment preparation, including at least 2x large bore IV access, standard monitoring (blood pressure, pulse oximetry, 3 lead ECG, end-tidal CO2), with consideration of invasive blood pressure monitoring and rapid infusion pumps, with blood products ready

Rapid Sequence Intubation (RSI)

Trauma patients undergoing emergency intubation are assumed to be unfasted and at risk of aspiration, warranting a RSI.

There is limited consensus over induction medications during a trauma RSI. However, case-specific selection of agents and doses should be carefully made based on haemodynamic state, pre-induction conscious state, comorbidities and suspected injuries.

• IV anaesthetic agents include: Ketamine, midazolam, propofol and etomidate

• Rapid onset Neuromuscular blocking drugs (NMBD) include: rocuronium: 1.2 mg/kg, suxamethonium: 1.5-2 mg/kg

• Propofol is a potent sympatholytic that attenuates compensatory mechanisms and causes profound vasodilation, loss of preload/afterload, and increases the risk of haemodynamic collapse in a shocked patient.

• Drastic dose reduction is often required in patients with altered GCS and haemodynamics to achieve safe anaesthesia.

In contrast to a “classical” RSI, trauma airways may require “modified” RSI techniques to improve patient safety

• Patients with traumatic brain injury are susceptible to worsening intracranial hypertension with laryngoscopy-induced sympathetic reflex, and a neuro-protective induction should be employed.

• There remains controversy over the efficacy of cricoid pressure and concerns of impeding laryngoscopic views. If injury is suspected to the airway or oesophagus then cricoid pressure should be avoided to prevent further damage to structures.

• There is data to suggest that the risk of pulmonary aspiration is relatively lower compared to the risk of cardiovascular instability and severe hypoxaemia.The use of modified or delayed sequence RSI techniques, which allow for pressure limited mask ventilation prior to intubation, can be used to minimise peri-induction critical hypoxaemia and haemodynamic instability.

Pre-oxygenation

• Delayed sequence intubation (DSI) involves a period of sedation to facilitate pre-oxygenation followed by induction dosage of hypnotic and NMBD agents. This approach is considered by weighing the risk of aspiration alongside the risk of failed intubation, agitation, cardiovascular instability and hypoxia.

• If the airway is patent, then modalities for apnoeic oxygenation can be considered which include; high flow nasal oxygen (if not contraindicated), CPAP and pressure limited Bag-Mask-Valve (BMV) ventilation, to prolong safe apnoea time.

Theatre is a more appropriate setting if attempting awake intubation due to the patients’ injuries or pre-existing comorbidities. It requires a co-operative patient (often not the case in trauma patients), experienced anaesthetist and clinicians trained in front of neck access.

Optimisation of first-pass success

Achieving first-pass success is vital in trauma airway management.

• Evidence shows first-pass intubation success is associated with a reduced likelihood of major adverse peri-intubation events

• Each failed attempt increases the risk of hypoxia, aspiration, and haemodynamic instability.

• If difficulty is encountered, oxygenating the patient should remain the priority.

Success is optimised by

• Assigning the most airway experienced person for the first attempt.

• Front loading technology; video laryngoscopy has been shown to increase first pass success and reduce rates of failed intubation.

• Use of airway adjuncts (bougie/stylet) and BURP (if permitted)

• Optimise positioning using 30-degree head up position. This is often difficult in trauma, acknowledging competing restrictions in place for spinal precautions.

• The Difficult Airway Society (DAS) recommends a variety of strategies to enhance team performance including the use of team briefings, verbalising the mitigating strategies if initial management fails, minimising distractions and training team members in human factors such as graded assertiveness.

Managing the soiled airway

Trauma patients can present with heavily soiled airways often with blood, vomit or foreign bodies. Temporising measures may include suctioning, turning the patient lateral and allowing the patient to assume the position of greatest comfort. However, the gold standard for airway protection remains a cuffed endotracheal tube. It is essential to have at least 2 large bore suction catheters prepared when managing these patients.

In the instance that debris in the airway accumulates as soon as suction is removed, the suction assisted laryngoscopy and decontamination (SALAD) technique may be appropriate.

SALAD

• The suction catheter clears the oropharynx and glottis of debris.

• In the case of active regurgitation, the catheter is held in a fixed position on the left side of the laryngoscope, directly in the oesophagus to maintain continuous suction throughout the intubation process.

• The disadvantage of continuous suctioning can include suctioning of oxygen enriched air.

Supra-Glottic Airway Device (SAD)/ Laryngeal Mask Airways (LMA)

• The use of LMAs may aid in oxygenation as well as to tamponade bleeding from the upper airway.

• Second generation LMAs have the added advantages of having higher pressure seals and ports for nasogastric insertion.

• The Intubating LMAs are designed to allow a flexible endoscope to pass through the LMA and allow for rail–roading of an endotracheal tube.

• The disadvantage of these devices is that they require adequate mouth opening and may not function with deformed anatomy.

Special patient groups

Traumatic brain injury (TBI)

Managing the airway in patients with TBI presents a dual challenge: protecting the airway while minimising secondary brain injury.

Core priorities include:

• Maintaining oxygenation: Preventing hypoxaemia and hypotension, as these exacerbate cerebral ischaemia. Effective preoxygenation/apnoeic oxygenation can be crucial in avoiding peri-intubation hypoxaemia.

• Avoiding cerebral hypoperfusion: Ensure adequate volume resuscitation prior to administering opioids and IV agents which can cause hypotension. Use of an arterial line can be instrumental in ensuring stable peri-intubation haemodynamics.

• Avoiding raised Intracranial Pressure (ICP): Reverse Trendelenburg positioning can assist in reducing intracranial pressure and facilitating intubation. Adequate analgesia eg: fentanyl 1.5 mcg/kg or IV lignocaine 1.5mg/kg, and use of video assisted laryngoscope limits ICP surges during intubation. Rocuronium is the preferred agent for RSI in TBI as suxamethonium can cause a transient increase in ICP

• Post-intubation care: Patients should remain well sedated to lower cerebral metabolic demands and prevent seizure due to TBI. Avoid tight-fitting collars and ties or positions that impede venous outflow from the head which can increase ICP.

Facial fractures

Challenges and Risks

• Facial fractures are often high-energy injuries accompanied by bleeding, swelling, and airway obstruction.

• Structural instability, such as malocclusion or posterior displacement of fractured segments, can further obstruct the airway.

• Soft tissue injuries, haematomas, and foreign objects (e.g., teeth or bone fragments) complicate visualisation and access during intubation.

• The risk of aspiration from blood and secretions is heightened, demanding urgent and effective airway management.

Le Fort Classification

The Le Fort classification provides a systematic approach to describing maxillary fractures, based on their severity and anatomical disruption:

Le Fort I: Horizontal fracture separating the maxilla and palate from the midface. Patients may present with dental misalignment or mobility of the upper teeth.

Le Fort II: Pyramidal fracture extending superiorly through the maxilla, involving the nasal and orbital regions. Often results in swelling, bruising, and midface instability.

Le Fort III: Craniofacial disjunction, where the facial skeleton is entirely separated from the cranium. It is often accompanied by dural tears, cerebrospinal fluid rhinorrhoea, and skull base fractures, complicating airway management further.

Examination and Initial Steps

• Assess for stridor, hoarseness, and visible deformities. Stridor suggests airway narrowing, requiring immediate action.

• Suction blood and debris to maintain airway patency.

• Use Magill forceps as necessary to remove larger foreign bodies.

• Maintain neutral cervical spine alignment using MILS if indicated.

Techniques for Airway Management

• Positioning: Patients with unstable midface fractures often prefer sitting upright, as this allows the fractured segment to fall forward, relieving obstruction.

• Adjuncts: Nasopharyngeal airways may be contraindicated due to potential base-of-skull fractures.

• Video Laryngoscopy: Preferred for intubation as it enhances visibility without requiring excessive neck extension.

• Backup Surgical Access: ENT or maxillofacial surgeons should be available for emergency front-of-neck access or other advanced techniques in cases of intubation failure.

Strategies for Intubation

• Plan for a failed intubation, involving a multidisciplinary team. Ensure all necessary equipment, including a bougie and hyper-angulated video laryngoscope, is ready.

• In alert, compliant patients, consider awake fibreoptic intubation to maintain spontaneous ventilation during airway visualization.

• For severe cases, advanced techniques such as retromolar or submental intubation may be required, and these should be performed in a controlled setting ideally in theatre.

Burns

Airway burns and inhalation injuries present significant risks and require close monitoring for signs of deterioration.

Challenges and Risks

• • Rapid progression of airway oedema, particularly after fluid resuscitation.

  • Obstruction from ulceration, soot, and secretions can lead to difficult mask ventilation.

  • Hypoxaemia can be caused by pulmonary injury, carbon monoxide poisoning, or compromised lung compliance.

• Delaying intubation can increase difficulty due to progressive swelling and anatomical distortion.

Signs of Airway Injury

• • Stridor, hoarseness, and deep burns to the face or neck.

  • Soot or blackened secretions in the oropharynx, singed nasal hairs, or visible swelling.

• • FNE is a useful tool in predicting airway compromise by oedema or burns. It is well tolerated and is strongly predictive for the need for intubation and allows targeted decision-making.

Equipment and Techniques

• • ETT: Use a tube with an internal diameter of ≥8 mm to facilitate pulmonary toilet and bronchoscopy for debris and secretion management.

• • Rocuronium is the preferred NMB for intubation. Suxamethonium is considered safe in the first 24 hours after a burn injury. However, after 24-48 hours there is increased risk of hyperkalaemia with suxamethonium due to upregulation of nicotinic acetylcholine receptors at the neuromuscular junction.

Scenario

As the trauma team assembles, roles are assigned, and the necessary equipment is meticulously prepared. You prepare for intubation as your ED colleague administers midazolam, 2mg, ketamine 1mg/kg and rocuronium 1.2mg/kg with metaraminol ready. Your airway assistant prepares for MILS while 2 large suction devices are double checked in anticipation.

Blood and secretions obscure the view. Large-bore suction is deployed, but the airway remains heavily soiled. You adopt the SALAD technique clearing the oropharynx and maintaining a satisfactory view.

Using a hyperangulated video laryngoscope, you avoid unnecessary cervical movements. The first-pass intubation is a success, the endotracheal tube sliding into place with chest rise and fall, misting, ausculatation of breath sounds bilaterally and convincing etCO2 trace for 5 breaths.

The team exhales as the ventilator begins its rhythmic hum. Imaging confirms significant facial fractures, but the airway is secure. You take a step back with the immediate crisis resolved. With the patient’s airway stable and ventilation assured, the team transitions to the next phase of trauma management.

Key lessons in trauma airway management include

• Thorough preparation and assessment are key.

• Having the requisite equipment and expert personnel available ensures that unexpected problems are addressed in an appropriate and efficient manner.

• Special patient populations demand tailored strategies and vigilant monitoring.

• Airway management in trauma requires excellent teamwork and communication skills.

References:

Athanassoglou V, Rogers A, Hofmeyr R. In-hospital management of the airway in trauma. BJA Educ. 2024;24(7):238-44. Available from: https://www.bjaed.org/article/S2058-5349(24)00031-3/fulltext

Australian and New Zealand College of Anaesthetists (ANZCA) (2016) Airway Assessment Resource. Melbourne: ANZCA. Available at: https://www.anzca.edu.au/getattachment/eff1ab5d-46cf-46db-95ef-5e65ecb88c26/PU-Airway-Assessment-20160916v1

Baratloo A, Ahmadzadeh K, Forouzanfar MM, Yousefifard M, Farhang Ranjbar M, Hashemi B, et al. NEXUS vs. Canadian C-Spine Rule (CCR) in Predicting Cervical Spine Injuries; a Systematic Review and Meta-analysis. Arch Acad Emerg Med. 2023;11(1):e66.

Derakhshan P, Nikoubakht N, Alimian M, Mohammadi S. Relationship Between Airway Examination with LEMON Criteria and Difficulty of Tracheal Intubation with IDS Criteria. Anesth Pain Med. 2023;13(6):e142921.

DuCanto J, Serrano KD, Thompson RJ. Novel Airway Training Tool that Simulates Vomiting: Suction-Assisted Laryngoscopy Assisted Decontamination (SALAD) System. West J Emerg Med. 2017;18(1):117-20.

Kelly FE, Frerk C, Bailey CR, Cook TM, Ferguson K, Flin R, et al. Implementing human factors in anaesthesia: guidance for clinicians, departments and hospitals: Guidelines from the Difficult Airway Society and the Association of Anaesthetists: Guidelines from the Difficult Airway Society and the Association of Anaesthetists. Anaesthesia. 2023;78(4):458-78.

McCann C, Watson A, Barnes D. Major burns: Part 1. Epidemiology, pathophysiology and initial management. BJA Educ. 2022;22(3):94-103.

Park L, Zeng I, Brainard A. Systematic review and meta-analysis of first-pass success rates in emergency department intubation: Creating a benchmark for emergency airway care. Emerg Med Australas. 2017;29(1):40-7.

Russotto V, Myatra SN, Laffey JG, Tassistro E, Antolini L, Bauer P, et al. Intubation Practices and Adverse Peri-intubation Events in Critically Ill Patients From 29 Countries. JAMA. 2021;325(12):1164-72.

Saini S, Singhal S, Prakash S. Airway management in maxillofacial trauma. J Anaesthesiol Clin Pharmacol. 2021;37(3):319-27.

Ultrasonography measurement of glottic transverse diameter and subglottic diameter to predict endotracheal tube size in children: a prospective cohort study. Scientific Reports, 12(1).

Key reference:

Karamchandani et al. (2024). Tracheal intubation in critically ill adults with a physiologically difficult airway. An international Delphi study. Intensive care medicine, 50(10), 1563–1579. https://doi.org/10.1007/s00134-024-07578-2

Quick Summary

• The “physiologically difficult airway” (PDA) was first coined by Mosier et al. in 2015, filling a conceptual gap in the management of airways in critically unwell patients.

• Critically unwell patients experience higher rates of peri-induction adverse events (one in five patients) irrespective of first pass intubation success, underscoring PDA as an additional entity to the traditional “anatomical” difficult airway.

• Hypoxaemia, hypotension, increased intracranial pressure, right ventricular failure, obesity and pregnancy present the most common and challenging PDA.

• Complications mostly occur during induction, intubation and transition to positive pressure ventilation.

• Environmental factors (ED, ICU, under-resourced ward) and human factors increase the risk of complications for PDAs

• Recent consensus statements published by Society of Critical Care Anaesthesiologists provide guidance on the management of PDAs

Preamble

You are an overnight anaesthesia registrar. You receive a call from a panicked ICU registrar requesting your assistance with an emergency intubation. The patient is a 60-year-old male admitted to ICU for severe community-acquired pneumonia, who has now deteriorated with respiratory fatigue, respiratory acidosis, and desaturation to 90%, despite an FiO₂ of 60% on non-invasive ventilation. Invasive blood pressure monitoring shows a mean arterial pressure of 67 mmHg and a sinus tachycardia of 110 bpm, supported by 2 mcg/min of noradrenaline. You attend to the patient immediately.

You confirm the patient’s previous airway grade as a Grade I with direct laryngoscopy. On examination, he has a thyromental distance of 7 cm, satisfactory mouth opening, and good neck extension. He is adequately fasted.

“Should be an easy airway, right?”

Tracheal intubation remains one of the most specialised and high-risk procedures performed in critical care, requiring the clinician to navigate the technical challenges of airway manipulation, rapid physiological alterations associated with apnoea, induction agents, and initiation of positive pressure ventilation—all within a matter of seconds.

Traditionally, an airway is anticipated to be “difficult” when there are anatomical features that impede the ability to ventilate and oxygenate the patient using bag-mask ventilation, tracheal intubation, or rescue supraglottic airway devices. These limitations prolong apnoea time and increase the risk of peri-intubation complications, including the “can’t intubate, can’t oxygenate” (CICO) scenario. The “anatomically difficult airway” is a well-recognised entity that has driven extensive advances in airway equipment, practice guidelines, and training for its management.

However, improvements in first-pass success rates have uncovered persistent peri-intubation complication rates in the critically ill. Indeed, observational studies have consistently demonstrated serious complication rates—such as hypoxaemia, haemodynamic instability, and cardiac arrest—to be around 20% in critically ill patients undergoing intubation, despite first-pass success. The International Observational Study to Understand the Impact and Best Practices of Airway Management in Critically Ill Patients (INTUBE) found that 45.2% of the 2,964 ICU patients undergoing intubation experienced at least one major adverse peri-intubation event. Specifically, while first-pass success was imperative in avoiding further critical desaturation (p<0.001 for both two attempts and >two attempts), it was not shown to be protective against haemodynamic instability (p=0.416 for first pass vs two attempts, and p=0.572 for >two attempts). As such, pathophysiological alterations not only pose peri-intubation challenges independent of traditional anatomical limitations, but they also exacerbate the negative consequences of a failed first-pass attempt in patients with compromised physiological reserve.

Mosier and colleagues first coined the term “physiologically difficult airway” (PDA) in 2015, recognising that pre-existing physiological derangements increase the rates of serious complications during intubation and the transition to positive pressure ventilation. The concept emphasises the need for critical care specialists to consider specific physiological derangements—beyond airway anatomy—when planning an intubation. Since then, growing recognition and research have improved the understanding and management of the PDA. In 2024, an international Delphi study chaired by the Society of Critical Care Anesthesiologists (SOCCA) Physiologically Difficult Airway Task Force synthesised the best available evidence and expert consensus into practice statements to guide the safe intubation of PDAs.

This article will explore the concept of the PDA, specific physiological derangements we commonly encounter, and key recommendations from the SOCCA Delphi study to aid our management of the critically ill airway.

What is a “Physiologically Difficult Airway (PDA)”

Mosier’s group and SOCCA define PDA as the patient who presents with pre-intubation physiological or pathophysiological factors that increase the risk of peri-intubation adverse events despite one or few intubation attempts, irrespective of (and possibly exaggerate) the effect of an anatomically difficult airway.

Multiple large observational studies have demonstrated pre-intubation haemodynamic compromise, defined as hypotension with mean arterial pressure (MAP) <65mmHg, systolic blood pressure <130mmHg, or sepsis, and requirement for pharmacological augmentation (e.g. need for vasopressor or fluid bolus, diuresis, or avoidance of propofol) to be associated with post-intubation hypotension. Similarly, pre-intubation respiratory failure requiring non-invasive ventilation, emergency or cardiac indication for intubation, and fluid resuscitation are all associated with post-intubation hypoxaemia. Unsurprisingly, age and advanced disease grades are patient factors that increase the risk of both hypotension and hypoxaemia.

Induction, apnoea, intubation and positive pressure ventilation impose drastic physiological changes and demands upon patients’ compensatory reserve, which is evidently diminished and largely exhausted in the critically ill. Hypotension and hypoxaemia commonly ensue due to inability to overcome the haemodynamic effects of anaesthetic agents, impaired oxygenation, hypermetabolic state, and unfavourable cardiopulmonary biomechanics of positive pressure ventilation. An understanding of specific physiological derangements and their effects on peri-intubation physiology is therefore paramount to mitigating these risks.

Understanding specific PDA scenarios

In their first description of PDA in 2015, Mosier and colleagues described 4 commonly encountered PDAs. This has since expanded to 6 in the SOCCA Delphi study. We summarise their pathophysiology, optimisation strategies and their associated evidence below:

Hypoxaemia

Failure to maintain adequate arterial oxygenation and resultant tissue hypoxia is one of the most common indications for intubation, and one that paradoxically carries the most significant risk of peri-intubation desaturation and worsening hypoxia, haemodynamic instability, hypoxic brain injury, and arrest.

Type 1 respiratory failure (hypoxaemic respiratory failure) results from gross ventilation-perfusion (V/Q) mismatch from pulmonary shunting (V/Q <1) where blood passes through alveolar units without adequately participating in gaseous exchange. Common causes include pneumonia, pulmonary oedema and acute respiratory distress syndrome. When intubating, type 1 respiratory failure patients are more prone to desaturation due to impaired gaseous exchange and limited response to pre-oxygenation. For the critically ill, an increased O2 demand may rapidly deplete an already compromised O2 reserve, while patients in physiological extremes such as severe obesity, pregnancy, paediatric and the elderly have diminished functional residual capacity (FRC) to maintain a sufficient O2 reservoir. However, severe Type 2 respiratory failure, particularly from obstructive airway disease, can present far greater challenges in ventilation and oxygenation. Managing these patients requires a delicate balance to mitigate the risks of under-ventilation, barotrauma and dynamic hyperinflation.

Optimisation strategies

The goal for these patients is to ensure optimal pre-oxygenation, appropriate airway assessment, intubation and ventilator setup, to prolong safe apnoea time (time between apnoea to critical desaturation), minimise total apnoea time, and maximise first-pass success rate.

Preoxygenation aims to denitrogenise a patient’s FRC with O2 and create an O2 reserve during apnoea. Standard method of pre-oxygenation using non-rebreather mask or bag-valve mask at maximal O2 flow is often inadequate for the critically ill, as their elevated respiratory rate limits tidal volume, impairs lung recruitment, and increases entrained ambient air which dilutes FiO2. Non-invasive ventilation (NIV) partly circumvents the problem by providing a tighter seal, positive end-expiratory pressure (PEEP) to improve lung recruitment, reduce shunting and improve oxygenation, and pressure support for additional tidal volumes. A randomised controlled trial by Baillard et al. showed patients undergoing intubation with hypoxaemic respiratory failure experienced less adverse events and desaturation <80% (17.8% vs. 41.3%) when pre-oxygenated with NIV compared to bag-valve mask. Pre-intubation anxiolytics and sedation may be required for patients with altered conscious states to improve compliance with NIV.

Once in the apnoeic phase post-induction, one may further prolong safe apnoea time with apnoeic oxygenation or positive mask ventilation. Apnoeic oxygenation involves the continued delivery of low-flow or high flow O2 during apnoea, entraining O2 down the lungs via the diffusion gradient generated by the patient’s alveolar O2 uptake. There is mixed evidence of its efficacy prolonging safe apnoea time and prevention of severe hypoxaemia.

While positive pressure mask ventilation post-induction has been traditionally discouraged (contraindicated in “classic” rapid sequence induction) due to concerns of gastric insufflation and aspiration, it has seen increased adoption by critical care specialists for safely managing critically ill, hypoxic patients with compromised FRC and O2 reserve. Real-time sonographic studies have demonstrated that mask ventilation pressures of less than 15cmH2O can safely improve ventilation without causing significant gastric insufflation. Recent randomised controlled trial investigating 400 intubations in US ICUs showed that mask ventilation not only reduced rates of severe hypoxaemia by 52%, aspiration events were not increased compared to the no-ventilation group. Both strategies can be considered to delay desaturation.

Ultimately, all steps should be taken to maximise first pass success as to minimise total apnoea time. Unsurprisingly, first pass failure requiring multiple attempts is directly related to increased rates of severe hypoxia and haemodynamic instability. Optimal patient positioning with 30 degrees head ramping, careful airway assessment, use of video laryngoscopy, and in cases of predicted “anatomical difficult airway”, use of intubation adjuncts (bougie/stylet), hyperangulated blade, and BURP, are all protocolised practices that are familiar for critical care physicians.

Hypotension

The critically ill patients often display hypotension as a late-stage sign of haemodynamic decompensation and shock. All four types of shock (distributive, hypovolaemic, obstructive, cardiogenic) are worsened to some degree by the venodilation, vasodilation and negative inotropic effects of anaesthetic agents and haemodynamic alterations from the transition to positive pressure ventilation. Unsurprisingly, post-intubation haemodynamic instability is by far the most common adverse event as illustrated by the INTUBE study.

Optimisation strategies

Appropriate pre-induction resuscitation, haemodynamic support with vasopressors, and use of “cardiostable” induction can assist to minimise/prevent peri-intubation cardiovascular collapse.

Volume resuscitation is a common first-line strategy for correcting hypotension, although careful assessment of patient fluid balance and volume tolerance is needed to avoid iatrogenic overload and cardiopulmonary decompensation. The multicentre randomised PrePARE and subsequent PrePARE II trial analysed the effectiveness of initiating a 500ml crystalloid bolus prior to induction for the critically ill and found no effect in reducing rates of cardiovascular collapse. As such, indiscriminate administration of fluid bolus is discouraged. Rather, individualised selection should be made through assessing fluid responsiveness (straight leg raise, pulse pressure variation (PPV), echocardiogram-evident inferior vena cava (IVC) collapsibility and left ventricular dynamic volume assessments) and balancing against risk of overload (through clinical and echocardiogram assessment, chest x-ray etc.)

Vasopressor support may be used to dampen the effects of induction agents and positive pressure ventilation to maintain perfusion pressure. Evidence is mixed around use of prophylactic vasopressor to prevent peri-induction cardiovascular collapse. Nevertheless, patients with distributive and cardiogenic shock are likely to benefit from the reduction in post-induction vasoplegia.

Appropriate choices of induction agents and their dosages are paramount to minimise haemodynamic instability during induction. Propofola nd thiopentone causes loss of vascular tone and bradycardia, leading to reduced preload, afterload and coronary perfusion pressure. These agents are therefore avoided in critically ill patients in favour of more “cardiac stable” agents such as etomidate, midazolam, ketamine, and fentanyl co-induction. There is ongoing debate regarding the superiority of either etomidate or ketamine in the critically ill in reducing cardiovascular instability. Regardless, one should judiciously dose-reduce based on patient factors and severity of illness, or employ an induction strategy to limit doses required of each agent to achieve sufficient anaesthesia.

Right heart failure

In addition to haemodynamic instability, Mosier specifically distinguished moderate-severe right ventricular (RV) dysfunction and failure as a PDA entity. Rightfully so, RV physiology is intimately related and exquisitely sensitive to the physiological alterations caused by anaesthetic induction and positive pressure ventilation.

In normal right heart circulation, the RV is a low pressure, high compliance, flow-based chamber that mobilises venous blood through the pulmonary vasculature. It is preload dependent, reliant on adequate venous return to generate Frank-Starling mediated contractility, and afterload sensitive, where marginal increases in pulmonary pressure in a low-pressure system can cause RV strain and trigger RV compensation. Long-standing pulmonary hypertension (from pulmonary vascular disease, left ventricular dysfunction, chronic airway disease, or chronic pulmonary embolism) leads to pathological RV remodelling, RV dysfunction, and ultimately RV failure, where the RV can no longer overcome excess afterload, resulting in retrograde flow, reduced left heart and coronary perfusion, and cardiovascular collapse.

Unfortunately, induction and positive pressure ventilation can impair RV compensatory mechanisms and add further RV strain

• Vasodilatory effects of induction agents reduce venous pressure and preload;

• Transient hypoxaemia and hypercapnia during apnoea results in pulmonary vasoconstriction and increase in pulmonary vascular resistance;

• Positive pressure ventilation increases intrathoracic pressure with a net effect of impeding venous return and increasing pulmonary vascular resistance, causing both reduced preload and increased RV afterload.

As such, intubating a patient with RV failure can result in RV decompensation and cardiovascular collapse.

Optimisation strategies

Optimisation of these patients requires a multidisciplinary approach and careful assessment. Common ventilatory aims would be to ensure adequate pre-oxygenation with sufficient etO2 using low PEEP NIV strategy, shorten apnoea time with apnoeic oxygenation to avoid hypoxaemia, and ventilate using spontaneous breathing modes to minimise positive pressure. Haemodynamics often needs to be evaluated using bedside echocardiograms to determine RV strain, contractile reserve and likelihood for fluid responsiveness. Use of fluid, vasopressors, and introduction of pulmonary vasodilators such as inhaled nitrous oxide should be guided by an expert team.

Intracranial hypertension

Intracranial pressure (ICP) is modelled by the Monro-Kellie doctrine. During cerebrovascular insults, such as intracranial haemorrhage, malignant ischaemic stroke, traumatic brain injury, and meningoencephalitis, intracranial pressure rises due to excess volume of blood and cerebral oedema within the rigid calvarium, resulting in compromised cerebral perfusion pressure and risk of herniation syndromes.

Laryngoscopy can cause a significant spike in ICP and worsen cerebral insult. Laryngoscopy may directly stimulate the gag/cough reflex in under-anaesthetised patients, in addition to the well-recognised sympathetic reflex that causes drastic spikes in heart rate, blood pressure and consequently raised ICP.

Optimisation strategies:

Key aims in the peri-intubation phase include pre-intubation optimisation, blunting of reflex sympathetic response to laryngoscopy, and post-intubation ventilation strategy.

In addition to standard preparation of pre-oxygenation and haemodynamic stabilisation, patient should be optimised to reduce ICP as much as possible

• Ventilate to etCO2 target that correlate with PaCO2 of 35-40 to limit cerebral vasodilation;

• Manage hypertension with short-acting beta-blockers and/or analgesia;

• Non-pharmacological management (head-up 30 degrees, minimise neck compression, hyperthermia avoidance) and pharmacological (hypertonic saline if clinical evidence of worsening ICP);

• Light sedation may be necessary to manage the agitated/non-compliant patient.

The neurocritical induction is heavily geared to blunting of the sympathetic reflex using large dose opioids. Fentanyl 3-5mcg/kg 1-3min prior to laryngoscopy is most commonly used in the emergent setting, while anaesthetists may have the luxury of accessing faster-onset and titratable opioids such as alfentanil and remifentanil.

Pharmacological strategies should not distract from non-pharmacological steps to minimise laryngoscopy manipulation:

• Maximise first pass success as previously discussed;

• Minimise force used with VL to achieve glottic exposure.

Once transitioned to positive pressure ventilation, neuroprotective ventilation strategy should be adopted:

• Avoid hypoxaemia

• Ventilate to PaCO2 30-35mmHg;

• Minimal PEEP to avoid ICP increases;

• Paralysis may be considered to further reduce ICP

Obesity & Pregnancy

Obesity and pregnancy have been specifically added by the SOCCA Delphi study as two PDAs. The predominant concern surrounds the restricted FRC, increased V/Q mismatch, and reduced O2 reserve due to increased metabolic demand, which limit the effectiveness of pre-oxygenation and make positive pressure ventilation particularly challenging. Haemodynamic effects of induction may be poorly tolerated from diminished compensatory reserve, or underlying cardiomyopathy. Lastly, the obese and parturient patients are at increased risk of aspiration during induction.

Optimisation strategies

While these patients present significant challenges in the peri-intubation setting, a structured approach using strategies outlined in “hypoxaemia” and “hypotension” can be similarly used to limit adverse events. Specifically, adequate pre-oxygenation, optimal patient positioning with ramping and a right wedge to prevent aortocaval compression, and careful haemodynamic monitoring with adequate resuscitation are important considerations.

Human factors in managing PDA

PDA adds additional cognitive and logistical challenges to an already complex procedure. Practitioners are often faced with high-acuity, time-sensitive and hyperdynamic scenarios in managing rapidly deteriorating patients, which can be overwhelming even for the most seasoned, leading to mistakes. Crisis resource management (CRM), which are non-technical skills that allow for optimal organisation and utilisation of available skillset, manpower and equipment in crisis situations, is paramount to enhance teamwork and performance.

Some key principles of CRM include clear role delegation appropriate for level of experience and training, closed loop communication, effective team leadership and shared mental model, all of which have been incorporated in airway management guidelines and simulation training.

The use of an “airway checklist” is common practice in ED and ICUs, providing a cognitive aid to ensure comprehensive patient, personnel, equipment and environmental preparation and minimise critical omissions prior to embarking on induction.

The team should at a minimum compose of a team leader who has overview of patient progress and provide clear decision-making, a primary airway operator, and an airway assistant/second airway operator. Clear verbalisation of airway and medication plan, including explicit checkpoints to enact contingency plans and seek early help, helps to establish a shared mental model of priorities and goals, catch complications early, and prevent task fixation and mobilise help to minimise further deteriorations.

Key SOCCA Statements

The following table summarises the key statements from the Delphi study on the approach to managing a PDA:

Team preparation

Use of airway checklists, Team assignment with at least 3 healthcare workers, Crisis resource management, including clear team roles, communication loops, shared mental model, cognitive aids etc., Simulation-based training.

Patient preparation and optimisation

Routinely perform airway assessment to anticipate difficult anatomical airway, Haemodynamic stabilisation with interventions such as vasopressor or inotrope infusion, Use of point-of-care ultrasound to assess and appropriately manage cardiac-related compromise, Use of non-invasive ventilation pre-oxygenation, apnoeic oxygenation, gentle positive pressure mask ventilation to avoid desaturation.

Performing the rapid sequence induction (RSI)

Use of the “head up” 30 degrees laryngoscopy position Use of a “modified” RSI with dose-adjusted rapid onset hypnotic (propofol, ketamine or etomidate), rapid-acting neuromuscular blocker (suxamethonium or rocuronium), judicious use of positive-pressure mask ventilation to optimise intubating conditions, Use of video laryngoscopy with bougie/stylet should be used routinely during the first attempt.

Post-intubation care

Immediate priorities include confirmation of tube placement (consistent etCO2 pattern over 7 breaths) and management of complications, most commonly cardiovascular instability and hypoxaemia, Use of lung protective ventilation, using Tidal volumes 6-8ml/kg of predicted body weight (PBW) PEEP >= 5 cmH2O Plateau pressure <30 cmH2O FiO2 titrated to SpO2 aims 92-95% Invasive blood pressure monitoring, central venous access to manage persistent haemodynamic instability post-intubation.

Conclusion

Despite the patient having no red flags for difficult laryngoscopy, you recognise the patient has a physiologically difficult airway. Together with your ICU colleagues, you set out to maximise preparations to optimise your attempt

• You organised your team with the ICU reg as the team leader, yourself as the primary airway operator, and the nurse-in-charge as the airway assistant, with the resident performing drug administration.

• Your team contacts your respective consultant-on-call to be readily available to assist if the patient deteriorates.

• You verbalise your plan to the team, with plan A being ETT size 8 with size 4 VL with bougie +/- BURP (max 2 attempts), plan B for second generation size 4 LMA + consultant assistance, with plan C to revert to BMV if plan B fails or saturation <88% at any stage and consider plan D – front of neck access.

• During this time, you positioned the patient to head up 30 degrees, pre-oxygenate the patient with NIV on 100% FiO2 for 5 min and provided a 500ml crystalloid bolus which increased the patient’s MAP to 72mmHg.

• You opted to give a cardiac-stable modified RSI of 1mg/kg ketamine, 2mg midazolam and 1.2mg/kg rocuronium, with gentle positive mask ventilation post induction.

Thankfully, your first pass was successful. The patient’s saturation decreased to 95%, blood pressure was relatively stable on 5mcg/min norad.

While advances in training, guidelines and airway technologies have increased our competencies in managing the anatomically difficult airways, the PDA has only gained recognition over the last decade, unveiling the multidimensional complexities in its management. This recent Dephi study by SOCCA provides guidance on best practice of managing PDAs, and provides a robust foundation for ongoing research regarding their feasibility in clinical practice.

References

Al-Saadi, M. A., Heidari, B., Donahue, K. R., Shipman, E. M., Kinariwala, K. N., & Masud, F. N. (2023). Pre-Existing Right Ventricular Dysfunction as an Independent Risk Factor for Post Intubation Cardiac Arrest and Hemodynamic Instability in Critically Ill Patients: A Retrospective Observational Study. Journal of intensive care medicine, 38(2), 169–178. https://doi.org/10.1177/08850666221111776

Baillard, C., Prat, G., Jung, B., Futier, E., Lefrant, J. Y., Vincent, F., Hamdi, A., Vicaut, E., & Jaber, S. (2018). Effect of preoxygenation using non-invasive ventilation before intubation on subsequent organ failures in hypoxaemic patients: a randomised clinical trial. British journal of anaesthesia, 120(2), 361–367. https://doi.org/10.1016/j.bja.2017.11.067

Bouvet, L., Albert, M. L., Augris, C., Boselli, E., Ecochard, R., Rabilloud, M., Chassard, D., & Allaouchiche, B. (2014). Real-time detection of gastric insufflation related to facemask pressure-controlled ventilation using ultrasonography of the antrum and epigastric auscultation in nonparalyzed patients: a prospective, randomized, double-blind study. Anesthesiology, 120(2), 326–334. https://doi.org/10.1097/ALN.0000000000000094

Casey, J. D., Janz, D. R., Russell, D. W., Vonderhaar, D. J., Joffe, A. M., Dischert, K. M., Brown, R. M., Zouk, A. N., Gulati, S., Heideman, B. E., Lester, M. G., Toporek, A. H., Bentov, I., Self, W. H., Rice, T. W., Semler, M. W., & PreVent Investigators and the Pragmatic Critical Care Research Group (2019). Bag-Mask Ventilation during Tracheal Intubation of Critically Ill Adults. The New England journal of medicine, 380(9), 811–821. https://doi.org/10.1056/NEJMoa1812405

Karamchandani, K., Nasa, P., Jarzebowski, M., Brewster, D. J., De Jong, A., Bauer, P. R., Berkow, L., Brown, C. A., 3rd, Cabrini, L., Casey, J., Cook, T., Divatia, J. V., Duggan, L. V., Ellard, L., Ergan, B., Jonsson Fagerlund, M., Gatward, J., Greif, R., Higgs, A., Jaber, S., … Society of Critical Care Anesthesiologists (SOCCA) Physiologically Difficult Airway Task Force (2024). Tracheal intubation in critically ill adults with a physiologically difficult airway. An international Delphi study. Intensive care medicine, 50(10), 1563–1579. https://doi.org/10.1007/s00134-024-07578-2

Mosier, J. M., Joshi, R., Hypes, C., Pacheco, G., Valenzuela, T., & Sakles, J. C. (2015). The Physiologically Difficult Airway. The western journal of emergency medicine, 16(7), 1109–1117. https://doi.org/10.5811/westjem.2015.8.27467

Mosier, J. (2024). The Physiologically Difficult Airway and Management Considerations. Curr Anesthesiol Rep 14, 446–457 . https://doi.org/10.1007/s40140-024-00629-w

Myatra, S. N., Divatia, J. V., & Brewster, D. J. (2022). The physiologically difficult airway: an emerging concept. Current opinion in anaesthesiology, 35(2), 115–121. https://doi.org/10.1097/ACO.0000000000001102

Nickson, C. (2023). Intubation of the Neurocritical Care Patient. Life In the Fast Lane.URL: https://litfl.com/intubation-of-the-neurocritical-care-patient/, [Last accessed 25/11/2024]

Patel, S. D., & Habib, A. S. (2021). Anaesthesia for the parturient with obesity. BJA education, 21(5), 180–186. https://doi.org/10.1016/j.bjae.2020.12.007

Russell, D. W., Casey, J. D., Gibbs, K. W., Ghamande, S., Dargin, J. M., Vonderhaar, D. J., … & Whitson, M. R. (2022). Effect of fluid bolus administration on cardiovascular collapse among critically ill patients undergoing tracheal intubation: a randomized clinical trial. Jama, 328(3), 270-279.

Russotto, V., Myatra, S. N., Laffey, J. G., Tassistro, E., Antolini, L., Bauer, P., … & Giacomucci, A. (2021). Intubation practices and adverse peri-intubation events in critically ill patients from 29 countries. Jama, 325(12), 1164-1172.

White, L. D., Vlok, R. A., Thang, C. Y., Tian, D. H., & Melhuish, T. M. (2023). Oxygenation during the apnoeic phase preceding intubation in adults in prehospital, emergency department, intensive care and operating theatre environments. Cochrane Database of Systematic Reviews, (8).

In our last article, we were tangled up in the brachial plexus. This time, we are looking at the lumbosacral plexus, a close cousin of the brachial plexus. In a similar vein, the lumbosacral plexus provides motor and sensory supply to the lower limb.

In this article, we will be looking at the anatomy and function of the main terminal branches of the lumbosacral plexus. This will set the backdrop for an article series on regional anaesthesia blocks. Knowing our anatomy for regional blocks helps us to locate the appropriate landmarks for anaesthetic injection.

The Lumbosacral Plexus

Figure 1. Schematic of the lumbosacral plexus, demonstrating relationship of nerve roots, divisions, and terminal branches.

Imagine a busy switchboard connecting calls between your spine and lower limbs. That’s the lumbar and the sacral plexi. Thanks to the lumbosacral trunk (the middleman), there is substantial overlap between the lumbar and sacral plexus, so much so that they are often collectively referred to as the lumbosacral plexus. This networking hub is formed from the ventral rami of L2-S3, making up the motor and cutaneous supply of our lower limbs.

The lumbar component of the lumbosacral plexus, originating from L1-L4, exits the spinal canal through the intervertebral foramen and enters into the psoas major muscle. Within this muscle, the roots split into the anterior and posterior divisions, reuniting to form the individual nerves of the lumbar plexus. Think of it as a nerve-themed family tree! (See image below which shows the branches of the lumbar plexus)

Figure 2. Close-up schematic of the lumbar component of the lumbosacral plexus

The sacral component of the lumbosacral plexus arises from the spinal nerves L4-S4, with some fibres from the lumbar plexus. Among these nerves, the largest is the sciatic nerve, comprising the common peroneal/fibular nerve and the tibial nerve, wrapped in a common sheath.

Due to its relatively deep location, the lumbosacral plexus is protected from acquired injuries. However, temporary deficiencies/ lesions may occur in the setting of pregnancy and childbirth, retroperitoneal pathology, and pelvic malignancies

Figure 3. Close-up schematic of the sacral component of the lumbosacral plexus. Note the close association of the two major terminal branches in forming the sciatic nerve: the common peroneal nerve (AKA common fibular nerve) and the tibial nerve.

Clinically, if there is damage to one of these nerves, the deficiency will be seen within the specific muscles and cutaneous innervation that the nerve supplies. At the spinal nerve level, this is commonly manifested as radiculopathy, which can comprise both positive (such as radicular pain, paraesthesia)and negative symptoms (such as numbness, weakness) that anatomically align with the supplied distribution of the affected nerve or nerve group. One of the most common lumbosacral pathologies is “sciatica”which describes the radicular pain originating from the lower back and hip region, radiating along the posterior thigh in the inferior direction – the very course of the sciatic nerve that is supplied by the lower lumbar and sacral nerve roots.

Additionally, injury of the distal terminal nerve branches can result in peripheral neuropathy with the same positive and negative symptoms and signs. For example, injury to the common fibular nerve, which commonly occurs due to its superficial location at the head and neck of the fibula, results in paresis/paralysis of the anterior and lateral leg muscle compartments, manifesting as foot drop and weakness in ankle eversion. Similarly, injury to the tibial nerve can result in paralysis of the calf muscles, leading to an inability to plantar flex the foot and the development of a shuffling gait.

Now equipped with our knowledge of the anatomy and pathology associated with the lumbosacral plexus, let’s delve a little deeper into the major nerves and their motor and cutaneous innervations.

Femoral nerve (L2-L4): The Overachiever

Obturator nerve (L2-L4): The Quiet Performer

Sciatic nerve (L4,L5, S1-3): The Beast

Tibial (L4,L5, S1-3): The Reliable Sidekick

Common Fibular Nerve (L4,L5,S1,S2): The Wanderer

Gluteal nerves (L4,L5,S1,S2): The Party Starters.

Pudendal nerve (S2,S3,S4)

That’s the introduction in the lumbosacral plexus and its anatomy. In our future articles, we will explore how this anatomy assists with lower limb regional blocks and the anaesthetic considerations of these blocks.

Keep a look out for them!

References:

Davies, K. (April 26, 2024). Lumbar Plexus. Teach Me Anatomy. https://teachmeanatomy.info/lower-limb/nerves/lumbar-plexus/

Davies, K. (July 8, 2024). The Sacral Plexus. Teach Me Anatomy. https://teachmeanatomy.info/lower-limb/nerves/sacral-plexus/

Palastanga, N., Field, D., & Soames, R. (2006). Anatomy and human movement: structure and function (Vol. 20056). Elsevier Health Sciences.