WCIM 2014 SEOUL KOREA 449
Poster Session
The Korean Journal of Internal Medicine Vol. 29, No. 5 (Suppl. 1)
PS 1567 Critical Care
The Failure of High Flow Nasal Cannula Therapy May Cause Delayed Intubation and Mortality
Byung Ju Kang1, Younsuck Koh1, Chae-Man Lim1, Jin Won Huh1, Myongja Han2, Hyun- Suk Seo2, Sang-Bum Hong1
Department of Pulmonary and Critical Care Medicine, University of Ulsan College of Medicine, Asan Medical Center, Korea1, Medical Emergency Team, University of Ulsan College of Medicine, Asan Medi- cal Center, Korea2
Background: High fl ow nasal cannula (HFNC) provides a high fl ow of humidifi ed and heated oxygen. The use of HFNC allows respiratory failure patients required mechan- ical ventilation a chance to delay intubation. We compared the hospital outcomes of critical ill patients with HFNC therapy, early failure or late failure.
Methods: We performed a retrospective observational study of patients receiving HFNC therapy in a tertiary hospital between January 2013 and March 2014. We se- lected intubated patients for the failure of HFNC therapy and classifi ed the patients into two groups depending on the timing of intubation, intubation before and after 48 hours.
Results: A total of 615 patients receiving HFNC therapy were enrolled in our study.
Among them, 175 patients clinically deteriorated despite HFNC therapy and fi nally re- ceived endotracheal intubation. Before 48 hours, 130 patients (74.3%) were intubated and after 48 hours, 45 patients (25.7%) were intubated. There were no signifi cant differences in baseline characteristics between two groups except higher diabetes mellitus (33.85% vs. 15.56%, p=0.02) and Sequential Organ Failure Assessment (SOFA) score day 1 (9.81±3.82 vs. 8.07±3.85, p=0.009) in the patients with intubation before 48 hours. The patients with intubation before 48 hours had higher extubation (37.69%
vs. 15.56%, p=0.006) and ventilator weaning rate (55.38% vs. 28.89%, p=0.002), lower ICU mortality (39.23% vs. 66.67%, p=0.001), and longer ventilator free days (8.58±10.06 vs. 3.62±7.48, p=0.011).
Conclusions: In a patient with clinically deterioration during HFNC therapy, delayed failure may cause bad outcome and harmful.
PS 1568 Critical Care
Does the Mean Arterial Pressure in the First 24 Hours Affect Mortality in Patients with Acute Hypoxemic Respiratory Failure Under Mechanical Ventilation
Hyun Jung Kim1, Juarda Gjonbrataj2, Hye In Jung1, Won Il Choi1
Department of Internal Medicine, Keimyung University School of Medicine, Korea1, Department of Inter- nal medicine, Mother Thereza University Hospital, Albania2
Background: In sepsis patients, the target mean arterial pressure is recommended to be more than 65 mmHg. However, there was no recommendation of mean arterial pressure target on mechanical ventilation patients. We aimed to evaluate the infl uence of mean arterial pressure during the fi rst 24 hours on 60 days mortality in patients with acute hypoxemic respiratory failure under mechanical ventilation.
Methods: This is a prospective, multicenter study that includes 22 intensive care units.
We compared the mortality and clinical outcomes in acute hypoxemic respiratory failure patients with mean arterial pressure 65-74.9 mmHg and mean arterial pressure 75-90 mmHg in the fi rst 24 hours of admission in intensive care unit.
Results: Among 844 patients with acute hypoxemic respiratory failure, 338 cases had a maintaining mean arterial pressure between 65 to 90 mmHg in the fi rst 24 hours of admission in intensive care unit. At 60 days, there was no signifi cant mortality dif- ference between 50 patients out of 191 in low mean arterial pressure group (26.2%) and 36 out of 147 patients in high mean arterial pressure group (24.5%). The intensive care unit days, hospital days, and 60 days mortality did not differ between two groups.
Conclusions: Mean arterial pressure of 65 to 74.9 mmHg, as compared with 75 to 90 mmHg in patients with acute hypoxemic respiratory failure under mechanical ventila- tion may not result in signifi cant difference in 60 days mortality.
PS 1569 Critical Care
Clinical Differences of the Rapid Response System between Patients Admitted to the Medical and Non- Medical Services
Yeon Joo Lee1,2, Ji soo Park1,2, Jin su Min1,2, Se Joong Kim1,2, Jong Sun Park1,2, Young- Jae Cho1,2, Ho Il Yoon1,2, Choon-Taek Lee1,2
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Seoul National Uni- versity Bundang Hospital, Korea1, Department of Internal Medicine, Seoul National University College of Medicine, Korea2
Background: Few evidences were revealed about the need of different approach in rapid response system (RRS) for specifi c patients’ department.
Methods: We reviewed patients who admitted to 1300-bed tertiary, academic hospital and detected by the RRS from October 2012 to February 2014. We compared the trig- gers, interventions, and clinical outcomes between patients admitted to the medical and non-medical services.
Results: Overall, 21,415 alert lists were generated from 11,271 patients. The RRS was ac- tivated in 460 patients, with the incidence of activation being almost three times higher in the non-medical service (74.3%) than in the medical service (25.7%). The triggers for RRS activation signifi cantly differed between the medical and non-medical groups(p = 0.001), which were in order as abnormal respiratory rate (27.1%), abnormal blood gas analysis (23.7%), and low blood pressure (22%) in the medical group, as compared with low blood pressure (30.1%), low oxygen saturation (19.6%), and abnormal heart rate (16.7%) in the non-medical group. In the case of interventions performed following RRS activation, patients were more likely to be classifi ed as do not resuscitate (DNR) or require intensive care unit admission in the medical group than the non-medical group (65.3% vs. 54.7%; p = 0.045). Difference of individual interventions was also statistically significant. Although the majority of patients were alive at discharge from the hospital in both groups, the number of alive patients was signifi cantly greater in the non-medical group than the medical group(86.8% vs. 60.2%; p < 0.001).
Conclusion: We found that the triggers, interventions, and clinical outcomes associated with the RRS greatly differed between the medical and non-medical services. Further research is needed to evaluate the effi cacy of a tailored approach to specifi c groups in the RRS.
PS 1570 Pulmonary Infection
SIRT1 Contributes to the Pathogenesis of LPS-Induced Lung Injury through the Modulation of PI3K-HIF-VEGF Pathway
So Ri Kim1, Yong Chul Lee1, Hee Jung Kim1, Yang Keun Rhee1, Heung Bum Lee1, Seoung Ju Park1, Yeong Hun Choe1, Seung Yong Park1
Chonbuk National University Hospital, Korea1
Background: SIRT1 has been known to deacetylate several transcription factors that govern metabolism, endocrine signaling, and infl ammation. Moreover, there are very recent studies in which SIRT1 is required for hypoxia inducible factor (HIF)-1a acti- vation and stabilization. In addition to the oxygen-dependent regulation of HIF-1a activity, HIF-1a expression is regulated by a variety of cytokines and growth factors in oxygen-independent pathway and that HIF-1a plays an important role in infl ammatory responses. However, to date, it is still controversial whether SIRI1 plays a pro-infl am- matory role or an anti-infl ammatory role in various pulmonary disorders.
Methods: In this study, using LPS-instilled mice, we aimed to investigate the role of SIRT1 in the pathogenesis of LPS-induced lung infl ammation focusing on the integrat- ed signaling network, HIF-1a pathway.
Results: Our results showed that SIRT1 was signifi cantly increased in lung tissues of LPS-inhaled mice compared with control mice and that inhibition of SIRT1 attenuated typical features of lung injury, including pulmonary neutrophilia, vascular leakage, and increased phosphorylation of Akt thereby improving LPS-induced lung infl ammation.
Moreover, sirtinol also reduced LPS-induced HIF-1a activation and expression of VEGF.
Intriguingly, increased expression of SIRT1 and HIF-1a was observed in LPS-stimulated airway epithelial cells. Lastly, our results also revealed that LPS-induced increases of nuclear translocation of NF-κB, infi ltration of DCs, and TLR4 expression in the lung were signifi cantly reduced by inhibition of SIRT1.
Conclusions: These fi ndings indicate that SIRT1 plays an important pro-infl ammatory role in the pathogenesis of LPS-induced infl ammation through the modulation PI3K- HIF-VEGF axis.
