Abstract

Background

Rapid and effective airway management is a priority for major trauma patients. Advanced airway interventions are necessary for a small subgroup of severely injured patients [1], in whom basic airway interventions are inadequate to maintain oxygenation and ventilation. Pre-hospital emergency anaesthesia (PHEA) is required to facilitate tracheal intubation and ventilation.

Adverse events associated with intubation occur more frequently during emergency airway management particularly when repeated attempts at laryngoscopy are required [2–4]. Hypoxia is one of the more commonly occurring adverse events and has been demonstrated to occur in 9.2% of patients during the first attempt at intubation in an emergency setting, increasing to 37.8% of patients where there are repeated intubation attempts [4]. Pre-hospital data suggests that between 10.9 and 18.3% of patients undergoing PHEA experience episodes of hypoxaemia [5–7], and these episodes are associated with an increase in morbidity and mortality [8].

Preoxygenation is a universally accepted method of reducing hypoxia during the drug-induced apnoeic phase of induction of anaesthesia. Achieving peripheral oxygen saturations above 93% extends the time taken before the onset of hypoxia during induction. At lower values, the dissociation of oxygen from haemoglobin takes place on the steep portion of the oxyhaemoglobin dissociation curve and oxygen saturations drop rapidly [9]. Standard practice for pre-oxygenation typically involves use of a reservoir bag supplying a high concentration of inspired oxygen. The benefit of additional apnoeic oxygenation has been widely debated but has been reported to provide benefit in terms of increased peri-intubation oxygen saturation, decreased rates of hypoxia, and increased first-pass intubation success without hypoxia [10]. Nasal oxygenation using low-flow nasal prongs is a recognised low-risk and easily administered procedure for providing passive apnoeic oxygenation in the pre-intubation and peri-intubation phases of emergency anaesthesia. This intervention has previously been reported to reduce desaturation rates by 6% [6].

This study aims to investigate whether the introduction of apnoeic oxygenation would reduce the frequency of desaturation in a population of trauma patients undergoing PHEA. The null hypothesis states that there is no difference in median oxygen saturations observed between the two study groups (before and after intervention) in the peri-RSI period, defined as 2 minutes pre-intubation to 2 minutes post-intubation.

Methods

Results

In total, 725 patients were included in the study; 188 patients were included in the standard treatment group and 537 in the intervention group. The overall incidence of hypoxia prior to pre-oxygenation and intubation (defined as initial SpO₂ reading <90%) was 16.7% (121 of 725 patients); 79 patients (10.9%) had SpO₂ less than 85%. 98 of 725 patients (13.5%) were hypoxic post-intubation (defined as final SpO₂ reading <90%, observed at 10 minutes post intubation); 70 of these 98 patients (9.7%) were in the group of 79 patients who were initially hypoxic with SpO₂ less than 85% prior to intubation (i.e. the group who could not be pre-oxygenated).

Median SpO₂ in the standard group was 100% (95% CI (99,100), the median SpO₂ in the intervention group was 99% (95% CI (98,100), p=0.0001. The incidence of hypoxia, defined as SpO₂ values of 90% or less, in the 2min before and 2min after intubation was 106/653, 16.2% in the standard group and 500/3181, 15.7% in the intervention group, p=0.74 The incidence of hypoxia, in the period from intubation until 10 minutes post intubation was 177/1461, 12.1% in the standard group and 959/8037, 11.9% in the intervention group, p=0.84. The results from the subgroup analysis are reported in Table 1 below.

Table 1

Subgroup analysis for study groups

Peri intubation phase 2min pre to 2min post intubation		Standard	Intervention	P value
Median SaO2 (IQR)	All patients	100 (96,100)	99 (96,100)	p=0.0001
	No hypoxia	100 (98,100)	100 (98,100)	p=1.00
	Mild Moderate hypoxia	94 (83,97.75)	94 (88,99)	p=1.00
	Severe hypoxia	79 (66.5,86)	83 (77,95)	p=0.28
Total post intubation values / total 90 or less (% difference)	All patients	106/653 (16.2)	560/3659 (15.3)	0.546
	No hypoxia	24/380 (6.3)	54/1492 (3.6)	0.02
	Mild Moderate hypoxia	28/72 (38.9)	131/386 (33.9)	0.947
	Severe hypoxia	41/51 (80.4)	118/177 (66.7)	0.195
Total post intubation values / total 85 or less (% difference)	All patients	65/653 (10.0)	340/3659 (9.3)	0.864
	No hypoxia	7/380 (1.8)	20/1492 (1.3)	0.466
	Mild Moderate hypoxia	11/71 (15.3)	61/386 (15.8)	0.947
	Severe hypoxia	34/51 (66.7)	100/177 (56.5)	0.195
Post intubation phase (intubation - 10min)	All patients	177/1464 (12.1)	959/8037 (11.9)	0.864
Total post intubation values / total 90 or less (% difference)	No hypoxia	43/1126 (3.8)	254/5928 (4.3)	0.476
	Mild Moderate hypoxia	39/164 (23.8)	377/1424 (26.5)	0.458
	Severe hypoxia	93/160 (58.1)	384/759 (50.6)	0.084
Recovery phase (2min post intubation to 10min post intubstion	All patients	139/1221 (11.4)	728/6396 (11.4)	0.998
Total post intubation values / total 90 or less (% difference)	No hypoxia	33/941 (3.5)	204/5121 (4.0)	0.488
	Mild Moderate hypoxia	31/138 (22.5)	280/1128 (24.2)	0.544
	Severe hypoxia	73/133 (54.9)	234/746 (31.4)	3.06E-07
Median SpO2 (IQR)	All patients	100 (96,100)	99 (96,100)	p=0.0001
	No hypoxia	100 (98,100)	100 (98,100)	p=1.00
	Mild Moderate hypoxia	94 (83,97.75)	94 (88,99)	p=1.00
	Severe hypoxia	79 (66.5,86)	83 (77,95)	p=0.28
Total 90 or less / total peri intubation values (% difference)	All patients	106/653 (16.2)	560/3659 (15.3)	0.546
	No hypoxia	24/380 (6.3)	54/1492 (3.6)	0.02
	Mild Moderate hypoxia	28/72 (38.9)	131/386 (33.9)	0.947
	Severe hypoxia	41/51 (80.4)	118/177 (66.7)	0.195
Total 85 or less / total peri intubation values (% difference)	All patients	65/653 (10.0)	340/3659 (9.3)	0.864
	No hypoxia	7/380 (1.8)	20/1492 (1.3)	0.466
	Mild Moderate hypoxia	11/71 (15.3)	61/386 (15.8)	0.947
	Severe hypoxia	34/51 (66.7)	100/177 (56.5)	0.195
Post intubation phase (intubation - 10min)	All patients	177/1464 (12.1)	959/8037 (11.9)	0.864
Total 90 or less / total post intubation values (% difference)	No hypoxia	43/1126 (3.8)	254/5928 (4.3)	0.476
	Mild Moderate hypoxia	39/164 (23.8)	377/1424 (26.5)	0.458
	Severe hypoxia	93/160 (58.1)	384/759 (50.6)	0.084
Recovery phase (2min post intubation to 10min post intubation)	All patients	139/1221 (11.4)	728/6396 (11.4)	0.998
Total 90 or less / total post intubation values (% difference)	No hypoxia	33/941 (3.5)	204/5121 (4.0)	0.488
	Mild Moderate hypoxia	31/138 (22.5)	280/1128 (24.2)	0.544
	Severe hypoxia	73/133 (54.9)	234/746 (31.4)	p<0.0001

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Table 1 shows the 2 study groups (standard and intervention) subclassified by the degree of hypoxia was subclassified according to the pre-induction SpO2 value (taken at 0min) as:

• No hypoxia: SpO2>95%

• Mild / moderate hypoxia: SpO₂ 85–95%

• Severe hypoxia: SpO₂<85%

The median SpO₂ is the median value of all values recorded for the all patients during the peri-intubation phase

The categories reporting ‘total 90 or less’ and ‘total 85 or less’ refer to the number of patients who desaturated in the peri-intubation, post intubation, or recovery phase to an SpO₂ or 90% or less, or 85% or less. This figure is reported as a proportion of the number of SpO₂ values recorded for all patients in this group and subclassification

Discussion

This is the first reported prospective study of the use of apnoeic oxygenation during PHEA in trauma patients. Hypoxia is a relatively common problem in patients undergoing emergency intubation; 16.7% of patients in this study were hypoxic prior to induction of anaesthesia. This is comparable to previous studies which report that up to 18% of trauma patients are hypoxic prior to airway intervention [7, 12, 13]. A single episode of hypoxia may worsen patient outcome, particularly in traumatic brain injury [8, 14, 15]. Reducing the time spent with low oxygen saturations may translate into an improvement in morbidity and mortality. Patients who have a SpO₂ less than 93% prior to intubation, and multiple or prolonged intubation attempts are much more likely to desaturate [3]. A reduction in hypoxic episodes may be achieved using simple reproducible techniques such as apnoeic oxygenation. The physiology of apnoeic oxygenation is well-described; in the presence of a patent airway, there is a difference between the uptake of oxygen and the excretion of carbon dioxide at an alveolar level [16]. This discrepancy creates a negative pressure gradient that promotes the movement of oxygen into the lungs. Alveoli will continue to take up oxygen even without diaphragmatic movements or lung expansion. The presence of a continuous infusion of oxygen to the upper airways during drug-induced apnoea can supplement oxygenation levels [17].

Despite multiple previous studies, the clinical benefit of apnoeic oxygenation remains unproven. A positive association between apnoeic oxygenation and lower rates of hypoxaemia during emergency intubation has been demonstrated [10, 13, 18–20] but these findings are not universally reproducible. The application and delivery of apnoeic oxygenation varies between the studies, with some using 15L/min via nasal cannulae and some studies using high flow oxygen at 50–60L/min; endpoints also vary between studies. Results from two randomised controlled trials performed in the emergency setting could not demonstrate a benefit of apnoeic oxygenation [21, 22]. Studies conducted using pre-hospital data are retrospective; two studies have demonstrated a reduction in the incidence of hypoxia, but this has not reached statistical significance [6, 23]. This study provided apnoeic oxygenation at a rate of 15L/min using nasal prongs but did not show a significant overall benefit in reducing the frequency of episodes of hypoxia during the drug-induced apnoeic phase of intubation. Apnoeic oxygenation may be beneficial where intubation is difficult and time to ventilation is prolonged. It can increase time to desaturation which reduces the incidence of desaturation and the frequency of hypoxic episodes in difficult or prolonged intubations [24–26].

Overall, the results of this study did not demonstrate a significant reduction in the incidence of hypoxia using apnoeic oxygenation during PHEA. It is likely that where pre-oxygenation has been adequately performed and the intubation is uncomplicated, minimal benefit will be observed with the addition of apnoeic oxygenation [24]. The intubation success rate for the services in which the study was conducted has previously been demonstrated to be 99.1 and 99.3% [27] with a first pass success rate of 93 and 87.5% [28]. There was a statistically significant difference in the median peri-intubation oxygen saturations between the two study groups in favour of the standard group, but this does not translate into any clinically relevant difference as neither result demonstrates clinically significant hypoxia.

Subgroup analysis was performed to assess the effect of apnoeic oxygenation on different categories of pre-intubation hypoxia. There was a statistically significant benefit from apnoeic oxygenation in the frequency of peri-intubation hypoxia (SpO₂ of 90% or lower) for patients who started with normal oxygen saturations (>95%) as shown in Table ​Table1.1. The other significant benefit was observed in the recovery phase for the group of patients who were severely hypoxic prior to induction of anaesthesia.

Apnoeic oxygenation is a simple low-cost intervention with a low complication rate. The intervention currently lacks a firm evidence base but may be helpful in a difficult intubation or where intubation takes longer than usual. The ongoing controversy surrounding use of this technique does not necessarily mean that apnoeic oxygenation is ineffective in reducing the incidence of hypoxaemia associated with emergency intubation. This study used a pragmatic approach to try and investigate the effect of apnoeic oxygenation in a cohort of severely injured patients undergoing pre-hospital intubation. Although apnoeic oxygenation is unlikely to make a difference to the majority of trauma patients who are straightforward to oxygenate and easy to intubate, it has the potential to reduce the frequency, incidence, and duration of hypoxia in the minority of patients who are already hypoxic or require a longer time to intubate. Difficult pre-oxygenation is a risk factor for subsequent hypoxia, and up to 30% of patients can remain hypoxic, defined as SpO₂<90%, after 5min of pre-oxygenation [29], so apnoeic oxygenation is potentially very beneficial in the group of patients most vulnerable to hypoxia. A recent study comparing bag-mask ventilation to no ventilation during intubation of critically ill patients reported higher oxygen saturations and a lower incidence of severe hypoxemia in the bag-mask ventilation group [30]. This positive finding may be relevant to this study population because an alternative strategy to providing supplemental oxygenation in the apnoeic phase of induction might be to avoid the apnoeic phase altogether with bag-valve-mask ventilation.

Conclusions

In this study apnoeic oxygenation did not influence peri-intubation oxygen saturations but it did reduce the frequency and duration of hypoxia in the post-intubation period in specific patient groups. Given that apnoeic oxygenation is usually a safe and simple technique and that hypoxia can be detrimental to outcome, application of nasal cannulas during the drug-induced phase of emergency intubation may benefit a small subset of patients undergoing emergency intubation.

Acknowledgements

Authors’ contributions

KC: Data collection and co-author of first and subsequent drafts. AH: Data collection and co-author of first and subsequent drafts. MR: Co-author of first and subsequent drafts, reviewed and constructively criticised the manuscript. SS: Co-author of first and subsequent drafts, reviewed and constructively criticised the manuscript. DL: Conceived the study, co-author of first and subsequent drafts, reviewed and constructively criticised the manuscript. The authors read and approved the final manuscript.

Funding

Not applicable.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

There are no competing interests to declare.

Footnotes

References