Postextubation Stridor in COVID-19: Should We Be Worried?

The reported incidence of postextubation stridor ranges from 1.5–26.3%.¹ Often, re-intubation is necessary, which increases the likelihood of morbidity and mortality.¹ Independent risk factors for postextubation stridor include endotracheal tube diameter, morbid obesity, prolonged intubation, elevated endotracheal cuff pressures, incidences of traumatic intubation, and in some reported anesthesia cases prone position therapy.^2-4

Among these risk factors, some are more prevalent in patients with coronavirus disease 2019 (COVID-19) pneumonia, including prolonged intubation, prone position, and morbid obesity, which suggests that postextubation stridor might be more prevalent in this population.^5-7 If there is in fact a higher rate of postextubation stridor in patients with COVID-19, then the question is what risk factors are prominent? Scarce evidence exists exploring the rate of stridor and risk factors related to this novel disease, including the COVID-19 virus itself. Only case series have been reported surrounding this novel topic and, therefore, calls for a better understanding to delineate preventive treatment.

In the current issue of the Journal, Abdallah and colleagues⁸ looked to answer these questions. Their single-center, retrospective study examined 96 subjects with severe COVID-19 pneumonia requiring mechanical ventilation and were compared to a historical control of non-COVID-19 subjects admitted to the same ICU between 2016–2019. Their primary outcome was to distinguish the rate of stridor between the 2 groups within 2 hours of extubation. The secondary outcome was to assess the risk of postextubation stridor in the presence of a high viral load. Their rationale was that laryngeal swelling may be caused by the virus’s ability to infect both the upper and lower respiratory tracts.⁹ Furthermore, a higher viral load is associated with greater severity of inflammation,⁹ which raises concern about a potentially increased risk for postextubation stridor in a disease where the intubation rate is 28–51%.^10-13

What is unique about this study was that Abdallah and colleagues⁸ tested for viral load levels from tracheal samples prior to extubation. The investigators found that postextubation stridor was significantly higher in COVID-19 subjects compared to the control group with females, a positive diagnosis of COVID-19, tube mobilization, re-intubation, or prone positioning being the highest risk factors. Positive reverse transcriptase-polymerase chain reaction (RT-PCR) samples collected prior to extubation were significantly associated with postextubation stridor. Although the incidence of stridor correlated with a higher viral load, it did not reach statistical significance.

A shorter mechanical ventilation duration was significantly associated with postextubation stridor in comparison to those with a longer duration. Although at first this might seem to be an atypical finding, it is important to note that the relationship between mechanical ventilation duration and postextubation stridor remains controversial.¹⁴ Moreover, both cohorts had a prolonged course so that the clinical relevance of this particular finding remains uncertain.

The findings of Abdallah and colleagues⁸ are consistent with associated case series¹⁵ and confirm the higher risk rate of stridor compared to the non-COVID-19 control group. This signals the need to be more aware of preemptive measures such as preventive corticosteroids, especially in the presence of risk factors including females, a positive RT-PCR prior to extubation and tube mobilization, and the need for re-intubation or prone positioning. In a disease where mechanical ventilation duration tends to be longer than the non-COVID-19 population, it is likely that the frequency of tube mobilization and prone positioning increases as well. In this study, the authors reported that their COVID-19 subjects not only had an average duration of mechanical ventilation 3 times longer than control subjects but more than half also received prone position therapy compared to < 4% in the non-COVID-19 control subjects.

Although the results did not reach statistical significance, there was a clear trend toward higher viral load in COVID-19 subjects. Because the higher incidence of postextubation stridor was associated with a briefer duration mechanical ventilation, the investigators reasoned continued viral shedding may have been a contributing factor. This, however, conflicts with other studies related to mechanical ventilation duration and postextubation stridor.^2,4,16 For example, Moran et al¹⁵ found a 45% postextubation stridor rate among COVID-19 subjects and attributed this to female sex and prolonged intubation duration.

Furthermore, Abdallah and colleagues⁸ acknowledged that during the first wave those with a longer mechanical ventilation duration often had a higher severity of illness, leading to the administration of corticosteroids prior to extubation. Twelve of the 13 subjects who received corticosteroids during the first wave did not experience postextubation stridor, which leaves uncertainty as to whether the overall risk rate of stridor in COVID-19 may have been underestimated. However, the investigators further acknowledged that during the second wave, among those who received corticosteroids prior to extubation, there was no significant difference in postextubation stridor rate. Moreover, administration of corticosteroids prior to extubation did not reduce the RT-PCR viral load count, further suggesting that viral shedding may in fact be the source of laryngeal inflammation.

Although the authors make a good point, there are substantial factors that call into question whether the presence of viral shedding influences the incidence of stridor in patients with COVID-19. First, differences in viral loads were not statistically significant during either the first or second wave of the pandemic. Second, (and very importantly) not all subjects underwent RT-PCR testing prior to extubation. Third, the sample size during the second wave was more limited (n = 33).

Irrespective of these factors, the evidence presented by Abdallah and colleagues provides ample reason to study whether viral shedding found in tracheal samples is a signifier for the laryngeal edema in larger prospective studies. If this can be confirmed, it would suggest that routine measurements of viral load levels in the airway secretions of patients with COVID-19 may help in assessing the risk of postextubation stridor regardless of mechanical ventilation duration.

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