Non-invasive ventilation immediately after extubation improves weaning outcome after acute respiratory failure: a randomized controlled trial.
Lower Tidal Volume Strategy (3ml/kg) Combined with Extracorporeal CO2 Removal Versus ‘Conventional’ Protective Ventilation (6 ml/kg) in Severe ARDS (Bein et al)
QMC AICU Journal Club, April 2013.
Dr Amit Pancholi
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Originally posted on STH Journal Club:
Myburgh JA, Finfer S, Bellomo R et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. New England Journal of Medicine 2012; 367: 1901-1911.
RHH Journal Club. November 22nd, 2012. Dr Balaji Kasa
No free full-text available
To evaluate the safety and efficacy of 6% HES (130/0.4) in 0.9% saline as compared to 0.9% saline alone for fluid resuscitation in ICU.
Type of Study: Multicentre, Prospective, Blinded, Parallel group, Randomised controlled trial
7000 patients from 32 hospitals in Australia and New Zealand, 18 years or older eligible for admission to ICU and who met the criteria for fluid resuscitation
Exclusions: more than 1000mls of HES is administered to patient before screening, those with impending or current dialysis dependent renal failure and those with intracranial haemorrhage on CT scan.
HES(130/0.4) in 0.9% saline or 0.9% saline
View original 115 more words
Mortality after Fluid Bolus in African Children with Severe Infection. Maitland, K et al. New England Journal of Medicine, May 26th 2011 (epub ahead of print) (DOI: 10.1056/NEJMe1105490)
An interesting paper published in this weeks NEJM will cause substantial comment and concern after it’s headline result showed increased mortality with rapid fluid resuscitation in paediatric sepsis. This surprising result is potentially extremely important as, if verified, undermines much of peadiatric (and adult)emergency care.
Before examining the paper in detail it’s worth making a few comments on what we think we know already….
An interesting editorial published a couple of months ago in Anaesthesia by Neil Soni. It adds to the growing disquiet that our understanding of disease, and attempts to find effective remedies, are being hampered by the tendency to treat all organ failures equally. I agree that there seems little reason to believe that meningococal sepsis in an 18 year old will behave the same as peritonitis in an 80 year old, nor that ARDS following pancreatitis is the same as that following FFP. However, these syndromes were designed partly to make research into rare presentations possible. If we define patients according to causative factor and co-morbidity how are we ever to recruit enough to power even the most basic trial ?
A fascinating study from the NEJM.
This RCT gave a 48 hr infusion of cis-atricurium to early (<24hrs) ARDS patients. It is the first study to show a mortality difference in this condition since ARDSnet a decade ago (although caution is required as it was underpowered). Whilst it is likely that a large proportion of the population included in this study (early, severe ARDS) will already be on NMB to aid ventilation, there has up until now been an assumption that this therapy was a necessary harm (due to the risk of critical illness polyneuropathy and subsequent slow weaning). This study questions that wisdom, showing both a reduction in adjusted mortality at 90 days (although not at 28) and no increase in the risk of CIPN. The results need to be taken with caution, but are certainly interesting and if confirmed may offer an important advance. There is further detailed analysis of the paper in the presentation ‘Atricurium ARDS’ in the blue box. Remember that restrictions on comments have been lifted on Critical Insight, no sign in required – so let us know your opinions.
We’ve known for sometime that high inspired oxygen fractions (>0.8) are associated with atelechasis (and decruitment / shunt) and lung injury and suspected that hyperoxia also leads to the generation of toxic oxygen free radicals, which may have deleterious effects in other pathologies. A recent paper adds to this story;
This paper has been appraised by a colleague, Paul Townsley, and you can download his presentation from the blue box on the right. Although the methodology has some potential flaws (which is probably inevitable), the paper provides evidence of definite harm of hyperoxia in ischemic brain injury.
Of course, there is an alternative weight of evidence of the harm associated with even short periods of desaturation in traumatic brain injury (and presumably also brain injury from poor perfusion). How to square this circle? The devil as always is in the detail. Controlling hyperoxia is probably important, but whether the benefits of avoiding hyperoxia outweigh the additional risk of periods of desaturation, or how often those periods occur within patient populations, is unknown. There is sufficient evidence to warrant a carefully designed RCT in the post resuscitation phase, (and maybe also in ARDS while we’re at it).