750 likes | 758 Views
Dr. Helen Wu from Pamela Youde Nethersole Eastern Hospital in Hong Kong shares key insights from the symposium, including advancements in mechanical ventilation and controversies in CPR.
E N D
Highlights of The 31st International Symposium on Intensive Care and Emergency Medicine in Brussels By Dr Helen Wu Pamela Youde Nethersole Eastern Hospital, Hong Kong 15 April 2011
31st International Symposium on Intensive Care and Emergency Medicine BRUSSELS MEETING CENTER (SQUARE) March 22-25, 2011
Belgium Hong Kong
Pre-symposium courses MECHANICAL VENTILATION: INTERACTIVE WORKSHOPS AND REVIEW
The Future • Greater use of computerized algorithms to control ventilation/weaning • Improved ventilator/patient interface • PAV/NAVA • Novel anti-inflammatory therapies for VILI • IL-6 • NIV/Extracorporeal gas exchange
Proportional assist ventilation (PAV) Ventilator generates pressure in proportion to the patient’s instantaneous effort No pre-selected target of pressure, flow or volume Requires measurement and monitoring of respiratory mechanics to determine degree of unloading
The Future • Greater use of computerized algorithms to control ventilation/weaning • Improved ventilator/patient interface • PAV/NAVA • Novel anti-inflammatory therapies for VILI • IL-6 • NIV/Extracorporeal gas exchange
Organized by Fresenius Medical Care CITRATE ANTICOAGULATION
34.2mol/L 119.7mol/L
Conclusion Citrate anticoagulation in patients with liver failure is possible. Measure and observe signs of citrate accumulation React immediately in case of citrate accumulation Be careful in patients with high lactate/hypoxia/shock Stop citrate in case of ongoing accumulation
The hyperoxia group had significantly higher in-hospital mortality (732/115663%; 95% confidence interval CI, 60-66%) compared with the normoxia group (532/1171 45%; 95% CI, 43%-48%; proportion difference, 18% 95% CI, 14%-22%) and the hypoxia group (2297/3999 57%; 95% CI, 56%-59%; proportion difference, 6% 95% CI, 3%-9%)
"Reperfusion after an ischemic insult is associated with a surge of reactive oxygen species, which may overwhelm host natural antioxidant defenses. The oxidative stress from the reactive oxygen species may lead to increased cellular death by diminishing mitochondrial oxidative metabolism, disrupting normal enzymatic activities, and damaging membrane lipids through peroxidation.”
The Australian and New Zealand (ANZ)Adult Patient Database (ANZ-APD)
- We used exactly the same inclusion criteria as the EMShockNet investigators - It involved more than 12000 patients from 125 ICUs in Australia and New Zealand, making it the largest study of its type conducted so far and making its findings reflective of all ICUs in ANZ. - The assessment of oxygenation in the first 24hours was based on the worst possible arterial blood gas result, while the EMShockNet study used the first ICU arterial blood gas measurement for evaluation. - Thus patients may have been exposed to hyperoxia and may not have been identified in our study. However, we found that the measurement used in our study was more closely representative of overall mean oxygenation status in ICU in the first 24 to 48 hours after admission (when reperfusion injury occur) than the first set of blood gas measurements obtained in ICU.
Hyperoxia • PaO2 >=300mmHg • Hypoxia • PaO2 <60mmHg • PaO2/FiO2 <300 • Normoxia • Not classified as hyperoxia or normoxia
Results • The hyperoxia group had higher mortality (754 (59%) of 1285 patients; 95%CI, 56% to 61%) than the normoxia group (911 (47% of 1919 patients; 95%CI, 45% to 50%) with a proportional difference of 11% (95%CI, 8% to 15%), but not higher than the hypoxia group (5303 (60% of 8904 patients; 95%CI, 59% to 61%).
Results • In a multivariate model controlling for some potential confounders, including illness severity, hyperoxia had an odds ratio for hospital death of 1.2 (95%CI, 1.1 to 1.6). • Once we applied Cox proportional hazards modelling of survival, sensitivity analyses using deciles of hypoxaemia, time period matching and hyperoxia defined as PaO2>400mmHg, hyperoxia had no independent association with mortality.
Key findings • The proportion of living patients with hyperoxia (PaO2>400) was 5% (n=280). • However, hypoxaemia was associated with increased mortality. (p=0.03) • 492 (42%) of patients with hypoxaemia had an FiO2<0.8 at that time. • Patients with a higher PaO2 did not have a greater adjusted risk of mortality.
Summary • 1. Hyperoxia was relatively uncommon • 2. Weak relationship with risk of death • 3. Relationship decreased once APACHE scores considered • 4. Relationship no longer significant if one applies Cox proportional hazards modelling, decile analysis, time-period matching, different definitions of hypoxia to match animal experiments
Placebo versus Adrenaline in Cardiac Arrest – The PACA Trial EPINEPHRINE
Placebo versus Adrenaline in Cardiac Arrest – The PACA Trial • Double-blind randomised placebo controlledtrial • Perth,Western Australia between August 2006 and November 2009 • Background survival 5% • Target sample size 5000 (enabling detection of absolute difference of 2%) • All non-traumatic, EMS-treated-out-of-hospital arrests
Placebo versus Adrenaline in Cardiac Arrest – The PACA Trial
Placebo versus Adrenaline in Cardiac Arrest – The PACA Trial
Placebo versus Adrenaline in Cardiac Arrest – The PACA Trial
Adrenaline reduces cerebral microcirculatory flow during CPR • Pig study • Cerebral oxygen tension (PbO2) and microcirculatory imaging • Adrenaline increased arterial pressure but reduced microcirculatory flow
Adrenaline for cardiac arrestSummary • Good theoretical rationale • Clinical studies showed improved ROSC but long term survival is no better • Reduced cerebral microcirculation
Ready for the next pandemic? Lessons learned from H1N1
During 3 months in 2009 (Jun to Aug) • 722 patients with influenza admitted to ICU • ~ 93% <65 years of age • ~ 30% had a BMI >35 • ~ 9% were pregnant • Median duration ICU treatment 8 days • Mortality at least 14.3%