CRITICALLY ILL PATIENTS ARE DIFFERENT

Why airway assessment is so crucial in critically ill patients

Critically ill patients present unique and formidable challenges, frequently necessitating emergency airway management under suboptimal conditions. Unlike elective surgical settings, these patients often exhibit profound physiological derangements that can precipitate rapid and catastrophic complications during the process of tracheal intubation.

Consequently, a thorough, albeit frequently time-limited, assessment becomes paramount. Such an assessment is crucial for anticipating potential difficulties, formulating robust contingency plans, and ultimately optimizing patient outcomes.

This module underscores that effective airway assessment extends far beyond merely predicting anatomical challenges; it critically encompasses the patient’s dynamic physiological state and the broader clinical context in which airway intervention is required.

These problems can helpfully be separated into anatomical and physiological difficulties: the Anatomically Difficult Airway and the Physiologically Difficult Airway.

THE ANATOMICALLY DIFFICULT AIRWAY

Assessment of anatomical difficulty should address past and potential problems with all four airway management techniques: facemask ventilation (FMV), supraglottic airway devices (SADs), tracheal intubation and neck rescue. It is essential to review records of previous airway management.

To maximise the utility of airway assessment, it is important to understand how anatomical variations affect airway management and the choice of airway management technique.

Assessment includes history, airway examination and investigations. Clinical examination can include a variety of validated tests which are outlined in the table below. Individually, they all have sensitivity and specificity values that limit their use in the prediction of difficulty. This can be ameliorated to some extent by combining test into scoring systems, such as the Wilson risk sum score and the Arne Risk Index (see table below).

Summary of the sensitivity, specificity and positive predictive value of the commonly used airway assessment tests. Adapted from ANZCA – Airway Assessment

THE MACOCHA SCORE

THE THREE AIRWAY COLUMNS

This section should be read in conjunction with the section on Two Curve Theory in Plan A

An alternative approach to airway assessment divides the airway into three anatomical airway columns, abnormalities or variations within which can cause difficult airway management.
The Posterior Column
The posterior column (comprised of structures posterior to the airway, particularly the cervical spine) is managed during positioning of the head and neck before attempts at airway management. The ability to optimally position the head and neck is dependent on the range of movement of the occipito-atlanto-axial complex.
Pathologies affecting the posterior column include rheumatoid arthritis, previous surgical fixation and external stabilisation such as halo fixation or manual in-line stabilisation.
The Middle and Anterior Columns
Abnormalities of the middle column (the air passage) include foreign bodies, tumours and infections, such as abscesses or epiglottitis.
The anterior column is important during laryngoscopy, where anterior column tissues are moved to obtain a view of the glottis. The anterior column contains the submandibular space and glossal muscles. Anything that reduces the size of this column (such as retrognathia or a narrow jaw) or the compliance of the tissues within it (such as infection, haemorrhage or radiotherapy) can affect how easily the tissues can be displaced during laryngoscopy.

 

Thinking about the patient in terms of the three anatomical airway columns can help to predict which airway devices might be of use for each problem.

THE PHYSIOLOGICALLY DIFFICULT AIRWAY

Assessment of physiological difficulty should address physiological derangements that affect airway management, namely: hypoxaemia, cardiovascular instability, right ventricular dysfunction, increased intracranial pressure and the physiological alterations that occur in obesity and pregnancy.

Hypoxaemic respiratory failure is a frequent indication for TI in critical care. Shunt physiology can result in rapid desaturation which in turn can lead to haemodynamic instability, and cardiac arrest.

Management Considerations:
  • Pre-oxygenation is paramount to extend the safe apnoea time.
  • There is emerging evidence that non-invasive ventilation may be superior for pre-oxygenation
  • High-flow nasal oxygen can also be used while the team is preparing for tracheal intubation
  • A non-rebreather (NRB) mask is often inadequate in critically ill patients due to ambient air entrainment, especially with higher minute ventilation.
  • Supraglottic Airway Devices (SADs) are an option for preoxygenation in patients with significant mask leaks or when higher pressures are needed, such as in pulmonary oedema or morbid obesity.
  • Routine pre-oxygenation should comprise:
    • Head-up position, ramping for obese patients
    • A tight-fitting facemask with added PEEP and waveform capnography
    • Careful ventilation during the onset of neuromuscular blockade
  • Pharmacological assistance (Delayed Sequence Intubation – DSI): For patients who are intolerant of optimal techniques, sedation with agents like ketamine can allow for better preoxygenation before administering a neuromuscular blocking agent.
  • There is no evidence to support the use of apnoeic oxygenation during attempts at TI

Cardiovascular instability is common during TI in critically ill patients: with an incidence of 43% in the INTUBE Study.

Venous return to the heart is driven by the pressure difference between mean systemic pressure and right atrial pressure. While spontaneous respiration augments this gradient, the conversion to positive pressure ventilation during intubation increases intrathoracic pressure and right atrial pressure, thereby decreasing venous return.

Patients with pre-existing conditions such as volume depletion, capillary leak, or loss of systemic vascular resistance have reduced mean systemic pressure, making them particularly susceptible to positive pressure ventilation-induced hypotension.

Management Considerations
  • Fluid Resuscitation: Increasing circulating volume can augment mean systemic pressure and venous return. Rapid assessment of volume responsiveness is crucial before intubation.
  • Vasopressors: If patients are not volume responsive, vasopressors like noradrenaline can be initiated to maintain vascular tone and perfusion pressure. Peripherally administered vasopressor boluses can be useful for managing transient hypotension.
  • Choice of Induction Agents: Benzodiazepines, opioids and propofol can cause myocardial depression and decreased vascular tone and dose reduction should be the norm in critically ill patients. Ketamine is the most cardio-stable of the induction agents available in Australia and New Zealand, with the added benefit that it is a useful agent for DSI.

In severe metabolic acidosis, acid-base homeostasis is critically dependent on compensatory respiratory alkalosis achieved through alveolar hyperventilation.

Unlike respiratory acidosis, where PaCO2 can be rapidly reduced, further hyperventilation in metabolic acidosis yields diminishing returns. This implies that patients with severe metabolic acidosis (e.g., diabetic ketoacidosis, salicylate toxicity, severe lactic acidosis) may already be at their maximal respiratory compensation, and even a brief apnoeic period during TI can cause a precipitous drop in pH.

Mechanical ventilation may not be able to match the patient’s pre-existing minute volume, leading to worsened acidosis and subsequent haemodynamic deterioration.

Management Considerations:
  • Delay TI while acidosis is treated, if possible.
  • If TI cannot be postponed, hyperventilation will be required to match the pre-existing minute volume.
  • The administration of bicarbonate may be useful in mineral acidosis (hyperchloraemic metabolic acidosis). In most other cases this treatment is of no benefit.

The right ventricle (RV) is a low-pressure, high-compliance chamber. Intrathoracic pressure changes associated with respiration have an exaggerated effect on haemodynamics in RV failure, worsening cardiopulmonary interactions. After TI, mechanical ventilation causes increased RV afterload and decreased preload, which can result in precipitous cardiovascular collapse in patients with RV failure.

Management Considerations
  • Supportive measures: The work of breathing and gas exchange should be supported with appropriate medications, supplemental oxygen, and NIPPV with low positive end-expiratory pressure (PEEP). These measures aim to decrease the work of breathing, limit atelectasis, and reduce hypoxic vasoconstriction, while allowing spontaneous breathing to limit the rise in intrathoracic pressure.
  • Hemodynamic optimization: Bedside echocardiography is crucial for distinguishing RV dysfunction from overt RV failure. Cautious fluid resuscitation may be considered if there is demonstrable contractile reserve, but volume overloading a pressure-overloaded RV can paradoxically worsen left ventricular filling. RV afterload reduction with inhaled pulmonary artery vasodilators (e.g. inhaled nitric oxide, inhaled epoprostenol) should be considered prior to TI.
  • Preoxygenation: this is essential despite the challenges posed by intracardiac shunt and ventilation-perfusion (V/Q) mismatch in RV failure. Inhaled nitric oxide or epoprostenol can augment oxygenation and reduce pulmonary vascular resistance.
  • Induction agents: cardio-stable sedative and induction agents should be considered to blunt the hypertensive response to laryngoscopy.
  • Vasopressor Support: A continuous noradrenaline infusion should be initiated before induction in hypotensive patients to maintain mean arterial pressure. For normotensive patients, noradrenaline should be prepared and readily available for potential post-intubation hypotension.
  • Mechanical Ventilation Goals: The primary goals of mechanical ventilation in patients with RV failure include maintaining a low mean airway pressure and meticulously avoiding hypoxaemia, atelectasis, and hypercapnia, all of which increase RV afterload.

Obesity significantly alters respiratory mechanics and physiology, posing unique challenges to airway management. Obese patients exhibit increased oxygen demand and carbon dioxide production, which can predispose to respiratory acidosis.

Their altered respiratory mechanics include reduced chest wall compliance and increased airway resistance. The increased abdominal and thoracic tissue mass transmits additional pressure to the pleural space and alveoli, leading to compression atelectasis, predominantly in dependent lung areas, causing shunt. This results in impaired functional residual capacity (FRC) and reduced total lung and vital capacity. Neuromuscular blockade further reduces end-expiratory lung volume (EELV) by about 50%.   Excess fat in the neck and throat can also make difficult mask ventilation more likely.

Management Considerations
  • Positioning and pre-oxygenation: Optimal positioning is paramount. ‘Ramping’ the upper body to 45 degrees (ear-to-sternal notch position) improves FRC. A tight-fitting facemask with PEEP is recommended for preoxygenation.
  • Non-invasive ventilation (NIV) may offer benefit and is considered first-line therapy for postoperative acute respiratory failure in obese patients.

CONCLUSION

Comprehensive airway assessment in critical care extends beyond the traditional focus on anatomical predictors of difficult intubation.

The three-column model elevates airway assessment in that the findings can be carried forward into the choice of airway device used.

The recognition of the physiologically difficult airway represents a critical paradigm shift, highlighting that underlying derangements in physiology can independently or synergistically increase the risk of catastrophic complications during airway management.

No single assessment tool or technique is infallible. The inherent limitations of individual predictive tests highlight the need for a multi-faceted approach to assessment and risk stratification.

Effective airway management in critically ill patients then demands meticulous pre-optimisation of physiological status, a well-coordinated team prepared for all potential contingencies and the application of biomechanical principles (like the three-column model and two curve theory (see module – Plan A).

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