This patient had quite noticeable pulmonary edema, easily fixed with suction prior to intubation.
Neurogenic pulmonary edema is said to occur rapidly post injury while pulmonary contusions typically evolve over time peaking over hours. These two entities have different etiologies but both will benefit from supportive care and positive pressure if needed. Once the initial insult has been attended, the pulmonary edema will usually resolve within 3 to 7 days.
Neurogenic pulmonary edema is said to be triggered broadly by neurohumoral sympathetic surge… however whilst animal models show some benefit with alpha and beta blockade, this is not as yet recommended due to issues with cerebral perfusion and cardiac arrhythmias.
Source: Wemple, M., Hallman, M., Luks, A. Neurogenic Pulmonary Edema In: UpToDate, Post, TW (Ed), UpToDate, Waltham, MA, 2014
Thank you to Dr. Ben Porter for this summary:
The CRASH-3 trial was published in October 2019 and along with collaboration from Prof. Toni Belli (co-investigator on the CRASH-3 trial) we discussed its relevance and applicability to Sydney HEMS operations at our recent education day.
The paper had been widely circulated amongst staff through internal communications as well as being widely circulated through social media and FOAMed sources prior to the education day.
A brief discussion about the study aims, recruitment and methodology started the discussion with a general consensus that that study was well conducted, pragmatic and the results were likely to be reliable given the large recruitment population and study size. Discussion was had over the number of patients recruited from middle income countries where trauma systems that are organised differently to ours as it was felt that the standard of care may differ from that in Australia limiting the applicability of the results.
Discussion then moved onto the results, with focus on the meaningfulness of the subgroup analyses given the overall headline result of no benefit between treatment groups (TXA vs Placebo). There were mixed feelings about the best way to interpret the subgroup analyses (as has also been shown by the wide ranging reviews on many of the FOAMed websites). Some groups feeling that due to the large numbers in each subgroup that there could be some meaningful results extracted, and that the width of some of the confidence intervals suggest there may be potential for some benefit, with low risk of adverse events. Others felt that use of sub-group analysis to guide changes in practice was not best practice and felt like further work needed to be done before changing Sydney HEMS protocols. It was questioned as to why the authors had not published the all-cause mortality data, given this was the primary outcome in the clinical trials registry, which several audience members said would have made them more comfortable looking at the sub-group data. (Further discussion with the authors following the education day has suggested this data may be made available during 2020.)
The overall felling of the group was that even if there was the possibility of benefit to giving TXA in traumatic brain injury the results were difficult to generalise to the Australian population given the large number of patient’s recruited from countries with significantly different healthcare arrangements to our own. If further data is realised containing the all cause mortality and the sub-groups by country of recruitment, then this would be more likely to lead to a change in our practice for a some specific sub-groups sustaining traumatic brain injury.