Emergency tracheal intubation in patients with COVID-19: is it any different? Comment on Br J Anaesth 2020; 125: e28–e37

Editor—We read with interest the correspondence by Yao and colleagues¹ on emergency tracheal intubation in patients with coronavirus disease 2019 (COVID-19). We thank the authors for sharing their valuable experience in this constantly evolving crisis encompassing the globe, with guidelines on managing the disease being published daily. However, there are several interesting points in the article that we believe warrant further clarification.

The authors recommend the use of a fluid bolus as a strategy to combat haemodynamic compromise during tracheal intubation. However, at the same time, they acknowledge a lack of clear evidence regarding the efficacy of this intervention. Fluid management in patients with acute respiratory distress is an area of uncertainty. Competing priorities (e.g. hypoxaemia and arterial hypotension) co-exist, thereby making its management difficult. In an RCT (PrePARE), administration of an i.v. fluid bolus did not decrease the overall incidence of cardiovascular collapse during tracheal intubation in critically ill patients in comparison with no fluid bolus.² In the absence of the need for restoration of depleted intravascular volume, the recommendation is to minimise fluids.³ Interestingly, no patients received a fluid bolus in the authors' cohort of patients. It would be helpful if the authors had clarified the evidence base or experience to support use of a fluid bolus despite not having implemented the strategy themselves.

There appears to have been considerable heterogeneity in practice between the two centres. Despite the presence of clinical parameters signifying impending haemodynamic compromise, there was no use of prophylactic vasopressors in Hospital B as opposed to nearly 30% in Hospital A. Despite this, there was only a slightly higher incidence of hypotension after intubation in Hospital B in comparison with Hospital A, which was not statistically significant. Considering this a comparison of a control group (no vasopressor) vs vasopressor administration, an inference can be drawn that administration of a vasopressor provided no advantage over the control group. We must therefore question the basis upon which the authors recommend prophylactic administration of a vasopressor before airway management in critically ill patients. Interestingly, propofol was the induction agent of choice for nearly all the patients. In light of the availability of etomidate, the near universal use of propofol in this critically ill group of patients (with a very high likelihood of haemodynamic compromise) is surprising.

Four patients suffered cardiac arrest during tracheal intubation. It would be interesting to know the underlying rhythm during these episodes, whether shockable or non-shockable. It would also be helpful to know whether cardiopulmonary resuscitation was required and what precautions were taken to avoid cross-contamination. Hypotension per se is a common occurrence during tracheal intubation in critically ill patients,² and severe hypotension can be misinterpreted as pulseless electrical activity in the absence of invasive haemodynamic monitoring. Management of both these conditions is different, as are the outcomes.

The low incidence of hypotension (7.9%) before securing the airway reflects timely intervention by the operators. However, nearly a quarter of the patients were tachycardic, implying underlying potentially significant haemodynamic derangement. However, we failed to understand the substantial number of unconscious patients (12.9%). Was it haemodynamic compromise leading to impaired cerebral perfusion, or were there any other contributory factors (with metabolic derangement) responsible?

Tracheal intubation was facilitated in all cases by ‘modified’ rapid sequence induction (RSI). Mask ventilation after induction was performed in the majority (93.1%) of patients. Historically, manual ventilation before tracheal intubation was considered an integral component of RSI.^{4 , 5} Wylie⁶ proposed the concept of ‘not inflating’ the patient's lungs with oxygen until tracheal intubation had been accomplished in 1963. This view was subsequently reinforced by Stevens⁷ in 1964. Both these authors hypothesised that positive pressure ventilation before intubation increases the risk of gastric inflation and the potential for regurgitation.^{6 , 7} Incorporation of these changes into practice led to the origin of the concept of ‘modified’ RSI. Thus, we believe that the authors performed ‘traditional’ RSI and not the ‘modified’ RSI technique.

Manual ventilation in this cohort of patients could be counterproductive for three reasons. Firstly, it might increase the risk for regurgitation and aspiration in patients who necessarily could not be ensured to be fasting. Secondly, the underlying condition was necessarily attributable to a shunt or ventilation–perfusion (VQ) mismatch. Administration of supplemental oxygen would not increase the arterial partial pressure of oxygen in the presence of a shunt or VQ mismatch. The operators had done their best by ensuring thorough pre-oxygenation with 100% oxygen in all patients. Bag-mask ventilation would not have contributed anything more to enhance oxygenation apart from losing critical time. Lastly, and most importantly, bag-mask ventilation is an aerosol-generating procedure.^{8 , 9} In light of this, its use in the current context should consider the risk-benefit ratio, keeping in mind the safety of all operators involved. The same rationale applies to the high (70.8%) number of patients subjected to noninvasive ventilation. Given that noninvasive ventilation is also considered an aerosol-generating procedure,⁹ we feel that restraint should have been exercised in its implementation in the current context. Protection of healthcare workers is not just about protective equipment; it encompasses all the principles of infection prevention and control.¹⁰

Declarations of interest

The authors declare that they have no conflicts of interest.