Editorial

Anaesthesia 2013, 68, 791–803

Editorial Sugammadex to rescue a ‘can’t ventilate’ scenario in an anticipated difficult intubation: is it the answer? In this issue of Anaesthesia, Paton et al. [1] describe a case in which sugammadex was used successfully to rescue a ‘can’t ventilate’ scenario. The patient presented with an anticipated difficult airway, previous awake intubation using a flexible fibrescope having failed. Following induction of anaesthesia and neuromuscular blockade with rocuronium, mask ventilation proved to be difficult. An early decision was made to ‘bail out’ by reversing rocuronium-induced neuromuscular blockade – without attempting tracheal intubation. A back-up plan of oxygenation through a narrow-bore cannula cricothyroidotomy was also unsuccessful during this ‘waking up’ period. Paton et al.’s patient had no fewer than five warning signs of difficult airway: carcinoma of the tongue base treated with radiotherapy; difficult neck anatomy; previous failed awake fibreoptic intubation due to large epiglottis and narrow glottis; severely restricted movement of the cervical spine; and limited mouth opening. The anaesthetic team formulated a structured airway management plan in which prophylactic cannula cricothyroidotomy and reversal of neuromuscular blockade with sugammadex were the key rescue elements. Strict adherence to their airway management plans resulted in successful

recovery from general anaesthesia, albeit with a period of upper airway obstruction in the immediate recovery phase. Although many aspects of their decision-making and management plans could be equally commended and criticised [2], there are at least two important issues that merit further discussion: firstly, the failed mask ventilation following neuromuscular blockade; and secondly, the use of sugammadex to rescue failed ventilation in a patient with anticipated difficult intubation.

Failed mask ventilation Before induction of general anaesthesia, the anaesthetist must be confident in his/her ability at least to deliver oxygen effectively to the patients’ lungs. Soon after induction of general anaesthesia, this is normally achieved using ventilation via a facemask. Therefore, the ability to maintain a patent airway and ventilate the lungs using a facemask is an essential skill. Successful mask ventilation requires first, the presence of a patent airway (through either the oral or the nasal route, or both, supported when necessary by an oro- or nasopharyngeal airway device), achieved with appropriate positioning of the head and neck, and second, a tight seal between the mask and the face. Although mask ventilation is usually successful in

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clinical practice, it may rarely fail. Whilst in some patients difficult mask ventilation can be predicted based on certain clinical features [3–6], this is not always the case in reality. If unanticipated failed mask ventilation follows induction of anaesthesia and neuromuscular blockade, oxygenation can still be maintained if either a quick tracheal intubation or successful insertion of a supraglottic airway device (SAD) is possible [6]. However, if neither of these can be achieved, patient safety can be compromised. Some anaesthetists may find it reassuring to demonstrate mask ventilation after induction of anaesthesia but before administration of neuromuscular blocking drugs (NBDs), in case laryngoscopy and intubation prove to be unexpectedly difficult, though this practice is controversial [7–10]. Those who check the ability to mask ventilate may choose to administer a short-acting NBD or decide to wake the patient up when difficult mask ventilation is encountered [11]. Traditionally, suxamethonium has been used as a short-acting NBD, but since rocuronium-induced neuromuscular blockade can now be reversed possibly faster than spontaneous recovery from suxamethonium [12, 13], it can be considered as an equivalent short-acting NBD. 795

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Although some studies have demonstrated improved facemask ventilation following administration of NBDs [14, 15], the case scenario described by Paton et al. is an example of how mask ventilation can become impossible despite neuromuscular blockade. These studies evaluated the effects of NBDs on mask ventilation in patients mostly with normal airways, suggesting that one should exercise caution when applying such results into clinical practice when anaesthetising patients with head and neck pathology and predicted difficult airways [16]. When mask ventilation is attempted after induction of anaesthesia but before administering a NBD, there may be some initial resistance to ventilation, particularly if the dose of induction agent is suboptimal. Reduced chest wall compliance [17] and increased muscle tone, coughing and breath-holding associated with light anaesthesia may result in inefficient mask ventilation [6]. In addition, airway manoeuvres (e.g. insertion of an airway device and/or jaw thrust) in the presence of partially obtunded airway reflexes may lead to laryngospasm and impossible mask ventilation. This situation can be improved by administering a NBD with a rapid onset of action. Bennett et al. demonstrated that sufentanil-induced difficult mask ventilation is caused by vocal cord closure and improves following administration of NBDs [18]. The assumed benefit of withholding the NBD until mask ventilation is confirmed is the possibility to wake up the patient in case mask ventilation proves to be difficult. Nevertheless, other studies have demonstrated the contrary: 796

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mask ventilation may improve following administration of NBDs [5, 14, 15]. In a series of 22 660 mask ventilations, 37 cases of impossible mask ventilation were identified. In all except one, tracheal intubation was performed following a NBD and only one required cricothyroidotomy [4]. Therefore, adequate doses of induction agent and NBD should facilitate both mask ventilation and tracheal intubation [19]. In certain circumstances, administration of NBDs can make mask ventilation more difficult. At induction of general anaesthesia, following loss of consciousness, inhibition of upper airway neural and muscle activity leads to increased collapsibility of the upper airway [20]. Further loss of skeletal muscle tone induced by the NBD may worsen airway obstruction. A similar situation may arise in the presence of undiagnosed upper airway lesions, leading to difficult mask ventilation and intubation. In these scenarios, reversing the NBD may allow the patient to breathe spontaneously and regain airway muscle tone, and facilitate recovery, provided an appropriate NBD such as rocuronium has been administered. Although one of the options available to rescue difficult mask ventilation includes tracheal intubation [6], the incidence of difficult intubation is higher in patients with difficult, compared with easy, mask ventilation [3]. Both difficult intubation and difficult mask ventilation have shared predictors such as sleep apnoea, snoring, abnormal neck anatomy, severely limited mandibular protrusion and obesity [4]. In addition, radiotherapy for head and neck cancer, male sex, sleep

apnoea, Mallampati score 3–4 and the presence of a beard are independent predictors of impossible mask ventilation [5]. Mask ventilation may be difficult because there is failure to achieve a good seal between the face and the mask (e.g. presence of a beard, absence of teeth), but the airway can easily be secured with a SAD or tracheal tube. Alternatively, both mask ventilation and insertion of a SAD or tracheal intubation may be difficult. When unexpected difficulty progresses to an inability to ventilate, patient safety may be compromised unless immediate oxygenation is achieved using a surgical airway. Patients with obstructing lesions at the tongue base and supraglottic region may be in danger of airway obstruction on induction of general anaesthesia due to loss of skeletal muscle tone [21]. Attempts at laryngoscopy, insertion of a SAD or airway adjuncts and any forceful airway manoeuvres may cause bleeding and oedema, leading to complete airway obstruction. Clinical signs in patients with chronic oropharyngeal lesions may be unreliable in quantifying the severity of airway obstruction, as some of them can be asymptomatic until a critical stage is reached [22]. A pre-operative endoscopic airway examination on the day of the procedure may provide valuable information and aid in making decisions regarding airway management plans [23].

Use of sugammadex Sugammadex at a dose of 16 mg.kg 1 rapidly reverses the most profound neuromuscular

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block produced by rocuronium [12, 13]. The implication of this in rescuing a ‘can’t intubate, can’t ventilate’ (CICV) scenario has resulted in case reports with divided opinion. In addition to the report from Paton et al. [1], I am aware of two further case reports where sugammadex has rescued a CICV scenario [24, 25]. However, in two other reports, although sugammadex aided reversal of neuromuscular blockade, airway obstruction secondary to upper airway pathology necessitated a surgical airway [26, 27]. It is of interest to note that in three of these reports [1, 24, 27], the dose of sugammadex used has been variable and lower than the recommended dose of 16 mg.kg 1 [13]. This problem, along with other practical issues such as availability of the drug, the time taken to draw it up and administer it, and human errors have been identified by Bisschops et al. [28] using a simulated CICV scenario. In such a situation, the main fear is severe hypoxia and death. Therefore, a technique that facilitates rapid re-oxygenation of the patient takes priority. Besides immediate reversal of neuromuscular blockade and restoration of spontaneous ventilation, a patent airway is essential. Ideally, we need an induction agent and NBD that reliably abolish all airway reflexes and paralyse the upper airway muscles, whilst allowing both of these effects to be reversed immediately in case of severe difficulty in airway management. It should be remembered that sugammadex only reverses the neuro-

Anaesthesia 2013, 68, 791–803

muscular blockade and not the effect of general anaesthetics or other sedative/opioid drugs used during induction of anaesthesia. Stefanutto et al. demonstrated that a combination of remifentanil and propofol (without NBD) resulted in apnoea of sufficient duration to produce significant arterial desaturation despite adequate pre-oxygenation [29]. There is debate as to what constitutes ‘adequate’ preoxygenation [30, 31], and modelling data suggest that even in healthy patients, critical desaturation might supervene before the time taken to reverse neuromuscular blockade [32]. Even after complete reversal of neuromuscular blockade, residual effect of opioids and induction agents may precipitate laryngospasm with any airway manipulation. The obstructed pattern of breathing on return of spontaneous ventilation can also risk the development of negative pressure pulmonary oedema [33]. In the case described by Paton et al. [1], a period of upper airway obstruction was observed in the immediate recovery period despite not administering any opioid. Therefore, the decision to reverse the neuromuscular blockade should be carefully considered as a part of any management strategy, to ensure oxygen delivery. As highlighted in the 4th National Audit Project of the Royal College of Anaesthetists and Difficult Airway Society (NAP4), the outcome of managing an unanticipated difficult airway scenario is significantly influenced by human factors such as leadership with an appropriate level of assertiveness, situation awareness and decision-making [34].

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Awake tracheal intubation remains the gold standard in most cases of anticipated difficult airway. Nevertheless, the practical challenge is accurate prediction of difficulty, as bedside assessment has low sensitivity and positive predictive values [35]. In addition, there are circumstances when awake intubation may not be feasible (e.g. uncooperative patients), when one may have to choose an appropriate technique of tracheal intubation under general anaesthesia. Sugammadex may have a role in such situations, where a tracheal intubation plan fails and neuromuscular blockade can be reversed to facilitate a rapid return of spontaneous ventilation. There is still a paucity of evidence for whether sugammadex will reliably allow one to bail out from a CICV situation. Hence in a patient with anticipated difficult airway, the ability to maintain spontaneous ventilation should not be compromised until an alternative, reliable method of oxygenation following loss of consciousness is established. Although Paton et al. [1] used a prophylactic cannula cricothyroidotomy, it failed to aid oxygenating the patient. This should remind anaesthetists that any technique can fail. As exhalation following inflation of the lungs using high pressure ventilation takes place through the upper airway, some degree of upper airway patency is essential when narrow-bore cannula cricothyroidotomy is used. A higher failure rate with this type of cannula cricothyroidotomy has also been reported in NAP4 [36]. Despite the encouraging outcome described by Paton et al., we 797

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should be cautious about the overenthusiastic use of sugammadex. Using rocuronium in cases of predicted airway difficulty, and relying on sugammadex to guarantee rapid reversal and enable effective oxygenation, can be a potentially dangerous path. Its use should be limited mostly to reversal of rocuronium-induced neuromuscular blockade in an unanticipated difficult airway, following swift and careful decision making. The most important element in airway management remains prevention of failure by anticipation of difficulty and optimal preparation, with well thought-out plans for management and back-up.

Competing interests No external funding and no competing interests declared. C. Mendonca Consultant Anaesthetist University Hospitals Coventry and Warwickshire NHS Trust Coventry, UK Email: [email protected]

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18. Bennett JA, Abrams JT, Van Riper DF, Horrow JC. Difficult or impossible ventilation after sufentanil-induced anesthesia is caused primarily by vocal cord closure. Anesthesiology 1997; 87: 1070–4. 19. Lieutaud T, Billard V, Khalaf H, Debaene B. Muscle relaxation and increasing doses of propofol improve intubating conditions. Canadian Journal of Anesthesia 2003; 50: 121–6. 20. Hillman DR, Platt PR, Eastwood PR. The upper airway during anaesthesia. British Journal Anaesthesia 2003; 91: 31– 9. 21. Patel A, Pearce A. Progress in management of the obstructed airway. Anaesthesia 2011; 66(Suppl 2): 93–100. 22. Patel A, Pearce A, Pracy P. Head and neck pathology. In: Cook T, Woodall N, Frerk C, eds. 4th National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society. Major Complications of Airway Management in the United Kingdom. London: RCoA, 2011: 143–54. 23. Rosenblatt W, Ianus AI, Sukhupragarn W, Fickenscher A, Sasaki C. Preoperative endoscopic airway examination (PEAE) provides superior airway information and may reduce the use of unnecessary awake intubation. Anesthesia and Analgesia 2011; 112: 602– 7. 24. Desforges JC, McDonnell NJ. Sugammadex in the management of a failed intubation in a morbidly obese patient. Anaesthesia and Intensive Care 2011; 39: 763–4. 25. Barbosa FT, da Cunha RM. Reversal of profound neuromuscular blockade with sugammadex after failure of rapid sequence endotracheal intubation: a case report. Revista Brasileira de Anestesiologia. 2012; 62: 281–4. 26. Curtis R, Lomax S, Patel B. Use of sugammadex in a ‘can’t intubate, can’t ventilate’ situation. British Journal of Anaesthesia 2012; 108: 612–4. 27. Kyle BC, Gaylard D, Riley RH. A persistent ‘can’t intubate, can’t oxygenate’ crisis despite rocuronium reversal with sugammadex. Anaesthesia and Intensive Care. 2012; 40: 344–6. 28. Bisschops MMA, Holleman C, Huitink JM. Can sugammadex save a patient in a simulated ‘cannot intubate, cannot ventilate’ situation? Anaesthesia 2010; 65: 936–41. 29. Stefanutto TB, Feiner J, Krombach J, Brown R, Caldwell JE. Hemoglobin desaturation after propofol/remifentanilinduced apnea: a study of the recovery of spontaneous ventilation in healthy

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Editorial The quick and the dead In this issue of the Journal, Lee et al. describe how they observed more postoperative complications in slow people [1]. Speed was measured twice: by the distance walked in six minutes; and by peak oxygen consumption, pedalling a bicycle. In this editorial I consider the following questions. Can you predict peak oxygen consumption from the distance walked in six minutes? Might walking distance be useful, whether or not the prediction holds? And does the association of survival with physical fitness make sense; should the quick die young or old?

Can you predict peak oxygen consumption from distance walked? The short answer is no. Some authors have interpreted small p values for Pearson’s correlation coefficient as indicating good agree-

ment between the two measures [2–4]. Others have observed that, despite this, observed peak oxygen consumptions often differ from predicted values by more than one metabolic equivalent of task (MET), or 3.5 ml O2.kg 1.min 1 [5]. I will use Lee et al.’s data to illustrate this, the authors having kindly forwarded to me individual patient data. I generated predicted values for distance walked [6–11] and peak oxygen consumption [12] and superimposed them in red on the values they observed (Fig. 1). Clearly, equations that generate predicted values for healthy populations work poorly for this colorectal surgical cohort.

A note on regression and agreement So, rather than use inappropriate predictions, what happens if we use

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the regression line that Lee et al. plotted through their own data to generate predicted peak oxygen consumptions from observed walking distances? Two complementary tests can provide us with information on the (dis)agreement between observed and predicted oxygen consumptions: Bland and Altman’s limit of agreement [13]; and Lin’s concordance correlation coefficient [14, 15]. Figure 2 is a plot of the limit of agreement. The mean difference between observed and predicted values was 0.5 ml.kg 1.min 1. However, half of the predicted oxygen consumptions disagreed with those observed by 3.5 ml.kg 1.min 1 (one MET) or more. This variation in peak oxygen consumption is substantially more than that one would expect from repeating the bicycle test in the same cohort [16]: one would expect 95% of repeated measure799