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Introduction Healthcare professionals, due to the nature of their work, have always experienced occupational stress, depression and low quality of life, which have been aggravated during the COVID-19 pandemic. Aim A large-scale cross-sectional descriptive correlational study aimed to investigate the impact of the COVID-19 pandemic on Greek healthcare professionals’ psychological status and quality of life. Material and Methods The study was conducted at “Attikon” General University Hospital and the 2nd Health Region in Athens, Greece. An assessment of anxiety and depression was carried out using the Zung’s Self-Rating Anxiety and Depression Scale (SAS/SDS). To assess the participants’ Quality of Life (QoL) the Short Form Survey-36 (SF-36) was used. Results 147 healthcare professionals were enrolled in the study. 70.7% experienced normal stress levels, 23.8% mild, 4.8% moderate and 0.7% severe. Mild depression was experienced by 34.7%, moderate by 10.2% and severe by 1.4%, with a 53.7% showing no depressive symptoms. Women experienced higher levels of anxiety and depression (p=0.001 & 0.001 respectively), and were 5.4 times more at risk to develop anxiety [Odds Ratio (OR) 5.357, 95% Confidence Interval (CI), 1.95-14.72: p=0.001] and 3.4 depression (OR, 3.365, 95% CI, 1.59- 7.12: p=0.002). Nurses and other professionals experienced higher stress and depression levels (p=0.004 & 0.040 respectively) than doctors. Participants reporting more exhaustion exhibited higher anxiety and depression levels (p=0.001). Compared to the pre-COVID-19 era, women (p=0.001), other health professionals (p=0.001) and those experiencing more physical burnout during COVID-19 (p=0.005) reported worse physical health. Anxiety and depression were negatively correlated with most sub scales of SF-36 except social functioning and bodily pain (p=0.001). Conclusions Healthcare professionals’ QoL has been affected by the COVID-19 pandemic and they experience higher levels of anxiety and depression. There is a need to develop strategies to address the negative psychological impact of this pandemic on healthcare professionals.

We report a case of phlegmonous gastritis in a 70-year-old woman without any predisposing factors, presenting with high fever, epigastric pain, and vomiting complicated by septic shock and multi-organ failure. The ultrasound and the computed tomography scan showed thickening of the stomach wall. Streptococcus pyogenes was isolated in the blood, thereby establishing the diagnosis of streptococcal toxic shock syndrome. An exploratory laparotomy excluded the need for a gastrectomy, and the patient was successfully treated with antibiotics. A short review of phlegmonous gastritis caused by S. pyogenes during the last 12 years is also presented. How to cite this article: Elisabeth P, Cornelia M, Athinna S, Anastasia A, Apostolos A, George D. Phlegmonous Gastritis and Streptoccocal Toxic Shock Syndrome: An Almost Lethal Combination. Indian J Crit Care Med 2021;25(10):1197–1200.

Accumulating data has shown a contribution of the renin‐angiotensin system in COVID‐19 pathogenesis. The role of angiotensin‐converting enzyme (ACE) insertion (I)/deletion (D) polymorphism as a risk factor in developing COVID‐19 disease comes from epidemiological data and is controversially discussed. We conducted a retrospective case‐control study and assessed the impact of ACE I/D genotype in COVID‐19 disease prevalence and severity. In 81 COVID‐19 patients explicitly characterized and 316 controls, recruited during the first wave of COVID‐19 pandemic, ACE I/D genotype, and ACE activity were determined. A generalized linear model was used and Poisson regression analysis estimated the risk ratios (RRs) of alleles and genotypes for disease severity. DD patients had almost 2.0‐fold increased risk (RR: 1.886, confidence limit [CL] 95%: 1.266–2.810, p = 0.0018) of developing a more severe disease when contrasted to ID and II individuals, as did D allele carriers compared to I carriers (RR: 1.372; CL 95%: 1.051–1.791; p = 0.0201). ACE activity (expressed as arbitrary units, AU/L) was lower in patients (3.62 ± 0.26) than in controls (4.65 ± 0.13) (p

Background: Nosocomial pneumonia in the critical care setting is associated with increased morbidity, significant crude mortality rates and high health care costs. Ventilator-associated pneumonia represents about 80% of nosocomial pneumonia cases in intensive care units (ICUs). Wide variance in incidence of nosocomial pneumonia and diagnostic techniques used has been reported, while successful treatment remains complex and a matter of debate. Objective: To describe the epidemiology, diagnostic strategies and treatment modalities for nosocomial pneumonia in contemporary ICU settings across multiple countries around the world. Design, setting and patients: PneumoINSPIRE is a large, multinational, prospective cohort study of adult ICU patients diagnosed with nosocomial pneumonia. Participating ICUs from at least 20 countries will collect data on 10 or more consecutive ICU patients with nosocomial pneumonia. Site-specific information, including hospital policies on antibiotic therapy, will be recorded along with patient-specific data. Variables that will be explored include: aetiology and antimicrobial resistance patterns, treatment-related parameters (including time to initiation of antibiotic therapy, and empirical antibiotic choice, dose and escalation or de-escalation), pneumonia resolution, ICU and hospital mortality, and risk factors for unfavourable outcomes. The concordance of ventilator-associated pneumonia diagnosis with accepted definitions will also be assessed. Results and conclusions: PneumoINSPIRE will provide valuable information on current diagnostic and management practices relating to ICU nosocomial pneumonia, and identify research priorities in the field. Trial registration: ClinicalTrials.gov identifier NCT02793141.

Interferon (IFN)-β has been classified as a drug that is possibly associated with development of pulmonary arterial hypertension (PAH), a devastating disease that can lead to right heart failure and premature death [1]., The possible causal relationship between interferon-β exposure and pulmonary arterial hypertension development requires close follow-up of patients on treatment with interferon-β http://bit.ly/2OPGSVP

Background and Aim: Feeding interruptions in critical care patients are often unjustified. We aimed to determine the causes, duration, and frequency of enteral nutrition interruptions (ENIs) and to assess macronutrients and antioxidant deficits according to European Society of Parenteral Enteral Nutrition (ESPEN) guidelines. Methods: We prospectively enrolled Intensive Care Unit (ICU) patients admitted for more than 48 h with an inability to orally eat from April to December 2019. The type of enteral nutrition, the number of calories administered, the time of feeding initiation, the reasons for delaying feeding, and the causes for ENI were recorded. Results: 81 patients were enrolled, with a median duration of ENIs of 5.2 (3.4–7.4) hours/day. Gastric residual volume (GRV) monitoring—a highly controversial practice—was the most common cause of ENI (median duration 3 (2.3–3) hours/day). The mean energy intake was 1037 ± 281 kcal/day, while 60.5% of patients covered less than 65% of the total energy needs (1751 ± 295 kcal/day, according to mean Body Mass Index (BMI)). The median daily protein intake did not exceed 0.43 ± 0.3 gr/kg/day of the actual body weight (BW), whereas ESPEN recommends 1.3 gr/kg/day for adjusted BW (p < 0.001). The average administration of micronutrients and antioxidants (arginine, selenium, zinc, vitamins) was significantly less than the dietary reference intake (p < 0.01). Conclusion: ENIs lead to substantial caloric, protein, and antioxidant deficits.

Oxidative stress is considered pivotal in the pathophysiology of sepsis. Oxidants modulate heat shock proteins (Hsp), interleukins (IL), and cell death pathways, including apoptosis. This multicenter prospective observational study was designed to ascertain whether an oxidant/antioxidant imbalance is an independent sepsis discriminator and mortality predictor in intensive care unit (ICU) patients with sepsis (n = 145), compared to non-infectious critically ill patients (n = 112) and healthy individuals (n = 89). Serum total oxidative status (TOS) and total antioxidant capacity (TAC) were measured by photometric testing. IL-6, -8, -10, -27, Hsp72/90 (ELISA), and selected antioxidant biomolecules (Ζn, glutathione) were correlated with apoptotic mediators (caspase-3, capsase-9) and the central anti-apoptotic survivin protein (ELISA, real-time PCR). A wide scattering of TOS, TAC, and TOS/TAC in all three groups was demonstrated. Septic patients had an elevated TOS/TAC, compared to non-infectious critically ill patients and healthy individuals (p = 0.001). TOS/TAC was associated with severity scores, procalcitonin, IL-6, -10, -27, IFN-γ, Hsp72, Hsp90, survivin protein, and survivin isoforms -2B, -ΔΕx3, -WT (p < 0.001). In a propensity probability (age-sex-adjusted) logistic regression model, only sepsis was independently associated with TOS/TAC (Exp(B) 25.4, p < 0.001). The AUCTOS/TAC (0.96 (95% CI = 0.93–0.99)) was higher than AUCTAC (z = 20, p < 0.001) or AUCTOS (z = 3.1, p = 0.002) in distinguishing sepsis. TOS/TAC, TOS, survivin isoforms -WT and -2B, Hsp90, IL-6, survivin protein, and repressed TAC were strong predictors of mortality (p < 0.01). Oxidant/antioxidant status is impaired in septic compared to critically ill patients with trauma or surgery and is related to anti-apoptotic, inflammatory, and innate immunity alterations. The unpredicted TOS/TAC imbalance might be related to undefined phenotypes in patients and healthy individuals.

Purpose Despite significant progress achieved in the management of pulmonary arterial hypertension (PAH), the prognosis remains poor. Sudden cardiac death is one main cause of death in advanced disease. It is already known that in pts with PAH there is an alteration in cardiac autonomic nervous activity. Heart rate turbulence (HRT) is an ECG–related autonomic marker, helpful in risk stratification of proarrhythmia and sudden cardiac death. Aim of the study was to examine HRT in patients with severe idiopathic PAH (IPAH) and its relation to disease's progress. Methods The study population consisted of 46 pts, (32 men and 14 women), mean age 50±9 years, Group A 20 pts: NYHA III, III–IV diagnosed as severe IPAH and Group B 26 pts: NYHA II, II–III diagnosed as moderately severe IPAH. They underwent 24h Holter monitoring-HRT analysis with calculation of 2 parameters, turbulence onset (TO) and turbulence slope (TS) (Abnormal values: TO>0, TS Results Initially abnormal HRT was found in 12 out of 20 pts (n=12, 60%) in group A and in none out of 26 (n=0, 0%) in group B (p=0,001). In 5 pts out of 8 with clinical improvement and 4 pts with clinical deterioration who had HRT reassessed, significant positive correlation was found between TS and change of clinical status (r=0,64, p=0,04). There was a tendency to greater normal TS mean values with clinical improvement even in group where TS was already normal (6,95±4,5 vs 3±0,3 p=0.077). Conclusion In severe IPAH cardiac autonomic system impairment was demonstrated mainly as abnormal TS in HRT. Significant positive correlation between normalization of TS and clinical improvement was revealed and that raises promises for use of HRT optimization as adjuvant index to guide optimal IPAH therapy and efficacy. Funding Acknowledgement Type of funding sources: None.

BackgroundUrine output is widely used as one of the criteria for the diagnosis and staging of acute renal failure, but few studies have specifically assessed the role of oliguria as a marker of acute renal failure or outcomes in general intensive care unit (ICU) patients. Using a large multinational database, we therefore evaluated the occurrence of oliguria (defined as a urine output 16 years) patients in the ICON audit who had a urine output measurement on the day of admission were included. To investigate the association between oliguria and mortality, we used a multilevel analysis.ResultsOf the 8292 patients included, 2050 (24.7%) were oliguric during the first 24 h of admission. Patients with oliguria on admission who had at least one additional 24-h urine output recorded during their ICU stay (n = 1349) were divided into three groups: transient—oliguria resolved within 48 h after the admission day (n = 390 [28.9%]), prolonged—oliguria resolved > 48 h after the admission day (n = 141 [10.5%]), and permanent—oliguria persisting for the whole ICU stay or again present at the end of the ICU stay (n = 818 [60.6%]). ICU and hospital mortality rates were higher in patients with oliguria than in those without, except for patients with transient oliguria who had significantly lower mortality rates than non-oliguric patients. In multilevel analysis, the need for RRT was associated with a significantly higher risk of death (OR = 1.51 [95% CI 1.19–1.91], p = 0.001), but the presence of oliguria on admission was not (OR = 1.14 [95% CI 0.97–1.34], p = 0.103).ConclusionsOliguria is common in ICU patients and may have a relatively benign nature if only transient. The duration of oliguria and need for RRT are associated with worse outcome., 0, info:eu-repo/semantics/published

BACKGROUND Leptin, the prototype adipokine, exerts immunomodulatory actions being implicated in inflammatory responses during sepsis. Clinical evidence regarding its role in sepsis has been contradictory, while free leptin has not been studied. The aim of this study was to jointly investigate circulating total leptin, its soluble receptor (sOB-R), and free leptin, as well as their kinetics in critically ill patients with sepsis regarding their diagnostic and prognostic value. METHODS In a prospective study, serum total leptin, sOB-R and free leptin index (FLI) were determined in 102 critically ill patients with sepsis within 48 hours from sepsis onset and one week after enrollment, and in 102 age and gender-matched healthy controls. RESULTS Upon enrolment, total leptin, sOB-R and FLI were significantly higher in septic patients compared to controls and they were positively correlated with sepsis severity scores, while they presented a significant decrease during the first week (P

The adipocytokines eNampt and resistin are involved in the regulation of inflammation exerting pro-inflammatory actions. Our aim was to jointly investigate whether circulating eNampt and resistin, and their kinetics predict 28-day mortality of sepsis.In a prospective study, serum eNampt and resistin were determined in 102 critically ill patients fulfilling the diagnostic criteria of SEPSIS-3, at enrollment and one week after, and in 102 healthy controls matched on age, gender and month of diagnosis.Serum eNampt and resistin were significantly higher in septic patients than controls (p 0.001), and higher in septic shock compared to sepsis (p 0.001). Both eNampt and resistin decreased significantly during the first week of sepsis (p 0.001). However, patients with septic shock presented a sustained elevation of eNampt and resistin compared to patients with sepsis. Both adipocytokines were positively correlated with sepsis severity scores and lactate. Baseline eNampt was a better discriminator of sepsis and septic shock compared to C-reactive protein and procalcitonin. Serum eNampt and resistin were higher in nonsurvivors than in survivors during the first week of sepsis. Prolonged and sustained elevation of both eNampt and resistin, as reflected by a lower percentage change from their baseline values, was independently associated with 28-day mortality (HR: 0.05, 95% C.I. 0.01-0.28, p = 0.001; HR: 0.19, 95% C.I. 0.07-0.50, p = 0.001, respectively), after adjustment for significant clinical and laboratory biomarkers.Circulating eNampt and resistin, and their kinetics may represent useful diagnostic and prognostic biomarkers in critically ill septic patients. More prospective studies are needed to elucidate their ontological and pathophysiological role in sepsis.

Purpose: To investigate age-related differences in outcomes of critically ill patients with sepsis around the world., Methods: We performed a secondary analysis of data from the prospective ICON audit, in which all adult ( >16 years ) patients admitted to participating ICUs between May 8 and 18, 2012, were included, except admissions for routine postoperative observation. For this sub-analysis, the 10,012 patients with completed age data were included. They were divided into five age groups - 80 years. Sepsis was defined as infection plus at least one organ failure., Results: A total of 2963 patients had sepsis, with similar proportions across the age groups (80 = 30.9%). Hospital mortality increased with age and in patients >80 years was almost twice that of patients 70 years was independently associated with increased risk of dying., Conclusions: The odds for death in ICU patients with sepsis increased with age with the maximal rate of increase occurring between the ages of 71 and 77 years. (C) 2019 Elsevier Inc. 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Xiaobo, H.] Sichuan Prov Peoples Hosp, Chengdu, Sichuan, Peoples R China., [Ge, H.] Sir Run Run Shaw Hosp, Hangzhou, Zhejiang, Peoples R China., [Yan, T.] Affiliated Guiyang Med Coll, Guiyang, Guizhou, Peoples R China., [Yuhui, C.] Fudan Univ, Peoples Hosp Shanghai 5, Shanghai, Peoples R China., [Zhang, J.] Dalian Med Univ, Affiliated Hosp 1, Dalian, Peoples R China., [Jian-Hong, F.] Suzhou Univ, Affiliated Hosp 1, Suzhou, Peoples R China., [Zhu, H.] Xinjiang Med Univ, Affiliated Hosp 1, Urumqi, Peoples R China., [Huo, F.; Wang, Y.] Jilin Univ, Hosp 1, Changchun, Jilin, Peoples R China., [Li, C.] First Peoples Hosp Kunming, Kunming, Yunnan, Peoples R China., [Zhuang, M.] Gen Hosp Shenyang Mil Reg, Shenyang, Liaoning, Peoples R China., [Ma, Z.] Peoples Hosp Cangzhou, Cangzhou, Peoples R China., [Sun, J.] Jilin Univ, Hosp 2, Changchun, Jilin, Peoples R China., [Liuqingyue, L.] Second Peoples Hosp Liaocheng City Shandong Prov, Liaocheng, Shandong, Peoples R China., [Yang, M.] Third Xiangya Hosp, Changsha, Hunan, Peoples R China., [Meng, J.] Tongde Hosp Zhejiang Prov, Hangzhou, Zhejiang, Peoples R China., [Ma, S.] Tongji Univ, Shanghai East Hosp, Shanghai, Peoples R China., [Kang, Y.] West China Hosp, Scu, Peoples R China., [Yu, L.] Wuhan Ctr Hosp, Wuhan, Hubei, Peoples R China., [Peng, Q.] Xiangya Hosp, Changsha, Hunan, Peoples R China., [Wei, Y.] Yantai Yuhuangding Hosp, Yantai, Peoples R China., [Zhang, W.] Yantaishan Hosp, Yantai, Shandong, Peoples R China., [Sun, R.] Zhejiang Prov Peoples Hosp, Hangzhou, Zhejiang, Peoples R China., [Yeung, A.] Pamela Youde Nethersole Eastern Hosp, Hong Kong, Peoples R China., [Wan, W.] Princess Margaret Hosp, Hong Kong, Peoples R China., [Sin, K.] Queen Elizabeth Hosp, Hong Kong, Peoples R China., [Lee, K.] United Christian Hosp Hong Kong SAR, Hong Kong, Peoples R China., [Wijanti, M.] Anestesi, Yogyakarta, Indonesia., [Widodo, U.] Pku Muhammadiyah Bantu, Yogyakarta, Indonesia., [Samsirun, H.] Rd Mattaher Hosp Jambi, Jambi City, Indonesia., [Sugiman, T.] Rumah Sakit Pantai Lndah Kapuk, North Jakarta, Indonesia., [Wisudarti, C.] Sardjito Hosp, Yogyakarta, Indonesia., [Maskoen, T.] Sch Med Unpad, Hasan Sadikin Hosp, Bandung, Indonesia., [Hata, N.] Nippon Med Sch, Chiba Hokusoh Hosp, Inzai, Japan., [Kobe, Y.] Chiba Univ Hosp, Chiba, Japan., [Nishida, O.] Fujita Hlth Univ, Sch Med, Toyoake, Aichi, Japan., [Miyazaki, D.] Japanese Red Cross Maebashi Hosp, Maebashi, Gumma, Japan., [Nunomiya, S.] Jichi Med Univ Hosp, Shimotsuke, Japan., [Uchino, S.] Jikei Univ, Sch Med, Tokyo, Japan., [Kitamura, N.] Kimitsu Chuo Hosp, Kisarazu, Japan., [Yamashita, K.] Kochi Med Sch, Nankoku, Kochi, Japan., [Hashimoto, S.] Kyoto Prefectural Univ Med, Kyoto, Japan., [Fukushima, H.] Nara Med Univ Hosp, Kashihara, Nara, Japan., [Adib, N. Nik] Hosp Sultanah Nur Zahirah, Kuala Terengganu, Terengganu, Malaysia., [Tai, L.] Kuala Lumpur Hosp, Kuala Lumpur, Malaysia., [Tony, B.] Queen Elizabeth Hosp 2, Kota Kinabalu, Malaysia., [Bigornia, R.] Cebu Velez Gen Hosp, Cebu, Philippines., [Bigornia, R.] Perpetual Succour Hosp, Cebu, Philippines., [Palo, J.] Med City, Pasig, Philippines., [Chatterjee, S.] Alexandra Hosp, Singapore, Singapore., [Tan, B.] Natl Univ Hlth Syst, Singapore, Singapore., [Kong, A.] Singapore Gen Hosp, Singapore, Singapore., [Goh, S.] Tan Tock Seng Hosp, Singapore, Singapore., [Lee, C.] Natl Taiwan Univ Hosp, Taipei, Taiwan., [Pothirat, C.] Chiaingmai Univ, Maharaj Nakorn Chiangmai Hosp, Chiang Mai, Thailand., [Khwannimit, B.] Prince Songkla Univ, Hat Yai, Thailand., [Theerawit, P.] Ramathibodi Hosp, Bangkok, Thailand., [Pornsuriyasak, P.] Ramathibodi Hosp, Somdech Phra Debaratana Med Ctr, Bangkok, Thailand., [Piriyapatsom, A.] Mahidol Univ, Siriraj Hosp, Bangkok, Thailand., [Mukhtar, A.] Cairo Univ, Giza, Egypt., [Dsicu] Demerdash Surg Intens Care Unit, Cairo, Egypt., [Hamdy, A. Nabil] Ain Shams Fac Med, Cairo, Egypt., [Hosny, H.] Zaitoun Specialized Hosp, Cairo, Egypt., [Ashraf, A.] Gums, Tehran, Iran., [Mokhtari, M.] Sbums, Imam Hossein Hosp, Tehran, Iran., [Nowruzinia, S.] Imamreza Hosp, Mashhad, Razavi Khorasan, Iran., [Lotfi, A.] Laleh Hosp, Tehran, Iran., [Zand, F.] Shiraz Anesthesiol & Crit Care Res Ctr, Shiraz, Iran., [Nikandish, R.] Shiraz Univ Med Sci, Shiraz, Iran., [Moghaddam, O. Moradi] Tehran Med Sci Univ, Tehran, Iran., [Cohen, J.] Rabin Med Ctr, Petah Tiqwa, Israel., [Sold, O.] Sourasky Tel Aviv Med Ctr, Tel Aviv, Israel., [Sfeir, T.] Ctr Hosp Nord, Ettelbruck, Luxembourg., [Hasan, A.] Sohar Hosp, Sohar, Oman., [Abugaber, D.] Specialized Arab Hosp, Nablus, Palestine., [Ahmad, H.] Almana Gen Hosp, Khobar, Saudi Arabia., [Tantawy, T.] KFSHRC, Riyadh, Saudi Arabia., [Baharoom, S.] King Abdulaziz Med City Riyadh, Riyadh, Saudi Arabia., [Algethamy, H.] King Abdulaziz Univ, Jeddah, Saudi Arabia., [Amr, A.] King Saud Med City, Riyadh, Saudi Arabia., [Almekhlafi, G.] Riyadh Mil Hosp, Riyadh, Saudi Arabia., [Coskun, R.] Erciyes Univ, Med Fac, Kayseri, Turkey., [Sungur, M.] Erciyes Univ, Med Sch, Kayseri, Turkey., [Cosar, A.] Gulhane Mil Med Acad, Ankara, Turkey., [Gucyetmez, B.] Int Hosp, Istanbul, Turkey., [Demirkiran, O.] Istanbul Univ, Cerrahpasa Med Sch Hosp, Istanbul, Turkey., [Senturk, E.] Istanbul Univ, Istanbul Med Fac, Istanbul, Turkey., [Ulusoy, H.] Karadeniz Tech Univ, Med Fac, Trabzon, Turkey., [Atalan, H.] Mem Atasehir Hosp, Istanbul, Turkey., [Serin, S.] Pamukkale Univ, Denizli, Turkey., [Kati, I] Yuzuncu Yil Univ, Med Fac, Van, Turkey., [Alnassrawi, Z.] Dubai Hosp, Dubai, U Arab Emirates., [Almemari, A.] Mafraq Hosp, Abu Dhabi, U Arab Emirates., [Krishnareddy, K.] Sheikh Khalifa Med City, Abu Dhabi, U Arab Emirates., [Kashef, S.] Tawam Hosp, Al Ain, U Arab Emirates., [Alsabbah, A.] City Hosp, Dubai, U Arab Emirates., [Poirier, G.] Hop Charles Lemoyne, Longueuil, PQ, Canada., [Marshall, J.] St Michaels Hosp, Toronto, ON, Canada., [Herridge, M.] Toronto Gen Hosp, Toronto, ON, Canada., [Herridge, M.] Toronto Western Hosp, Toronto, ON, Canada., [Fernandez-Medero, R.] San Juan Hosp, San Juan, PR USA., [Fulda, G.] Christiana Care Hlth Syst, Newark, DE USA., [Banschbach, S.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA., [Quintero, J.] El Camino Hosp, Mountain View, CA USA., [Schroeder, E.] George Washington Hosp, Washington, DC USA., [Sicoutris, C.] Hosp Univ Penn, Philadelphia, PA 19104 USA., [Gueret, R.] John H Stroger Hosp Cook Cty, Chicago, IL USA., [Kashyap, R.] Mayo Clin, CCM, Rochester, MN USA., [Bauer, P.] Mayo Clin, PCC, Rochester, MN USA., [Nanchal, R.] Med Coll Wisconsin, Milwaukee, WI 53226 USA., [Wunderink, R.] Northwestern Mem Hosp, Chicago, IL 60611 USA., [Jimenez, E.] Orlando Reg Med Ctr Inc, Orlando, FL USA., [Ryan, A.] Washington Hosp Ctr, Washington, DC 20010 USA., [Ryan, A.] Washington Hosp Ctr, 2H, Washington, DC USA., [Ryan, A.] Washington Hosp Ctr, 2G, Washington, DC USA., [Ryan, A.] Washington Hosp Ctr, 3H, Washington, DC USA., [Ryan, A.] Washington Hosp Ctr, 3G, Washington, DC USA., [Ryan, A.] Washington Hosp Ctr, 4H, Washington, DC USA., [Ryan, A.] Washington Hosp Ctr, CVRR, Washington, DC USA., [Prince, D.] Armadale Hlth Serv, Mount Nasura, WA, Australia., [Edington, J.] Bendigo Hosp, Bendigo, Vic, Australia., [Van Haren, F.] Canberra Hosp, Canberra, ACT, Australia., [Bersten, A.] Flinders Med Ctr, Bedford Pk, SA, Australia., [Hawkins, D. J.] Joondalup Hlth Campus, Joondalup, WA, Australia., [Kilminster, M.] Lismore Base Hosp, Lismore, NSW, Australia., [Sturgess, D.] Mater Adult Hosp, South Brisbane, Qld, Australia., [Ziegenfuss, M.] Prince Charles Hosp, Brisbane, Qld, Australia., [O'Connor, S.] Royal Adelaide Hosp, Adelaide, SA, Australia., [Lipman, J.] Royal Brisbane & Womens Hosp, Brisbane, Qld, Australia., [Campbell, L.] Royal Darwin Hosp, Tiwi, NT, Australia., [Mcallister, R.] Royal Hobart Hosp, Hobart, Tas, Australia., [Roberts, B.] Sir Charles Gairdner Hosp, Nedlands, WA, Australia., [Williams, P.] Queen Elizabeth Hosp, Woodville, SA, Australia., [Parke, R.] Auckland Dist Hlth Board, Auckland, New Zealand., [Seigne, P.] Christchurch Hosp, Christchurch, New Zealand., [Freebairn, R.] Hawkes Bay Hosp, Hastings, New Zealand., [Nistor, D.] Palmerston North Hosp, Midcent Hlth, Palmerston North, New Zealand., [Oxley, C.] Middlemore Hosp, Auckland, New Zealand., [Young, P.] Wellington Hosp, Wellington, New Zealand., [Valentini, R.] Cemic, Buenos Aires, DF, Argentina., [Wainsztein, N.] Fleni, Buenos Aires, DF, Argentina., [Comignani, P.] Hosp Aleman, Buenos Aires, DF, Argentina., [Casaretto, M.] Hosp Cent San Isidro, Buenos Aires, DF, Argentina., [Sutton, G.] Hosp Fernandez, Buenos Aires, DF, Argentina., [Villegas, P.] Hosp Francisco Lopez Lima Area Programa Gen Roca, Gen Roca, Argentina., [Galletti, C.] Sanatorio Allende, Cordoba, Argentina., [Neira, J.] Sanatorio Trinidad Palermo, Buenos Aires, DF, Argentina., [Rovira, D.] Sanatorio Julio Corzo Rosario, Rosario, Santa Fe, Argentina., [Hidalgo, J.] Karl Heusner Mem Hosp, Belize City, Belize., [Hidalgo, J.] Belize Healthcare Partner, Belize City, Belize., [Sandi, F.] Hosp Obrero 1, La Paz, Bolivia., [Caser, E.] Cias Unimed Vitoria, Vitoria, ES, Brazil., [Thompson, M.] Evangelical Hosp Cachoeiro De Itapemirim, Cachoeiro De Itapemirim, Brazil., [D'agostino Dias, M.] Hosp 9 Julho, Sao Paulo, Brazil., [Fontes, L.] Hosp Alcides Carneiro, Petropolis, Brazil., [Lunardi, M.] Hosp Clin Luzia De Pinho Melo, Mogi Das Cruzes, Brazil., [Youssef, N.] Hosp Nacoes Curitiba, Curitiba, Parana, Brazil., [Lobo, S.] Hosp Base Famerp, Sao Jose Do Rio Preto, Brazil., [Silva, R.] Hosp Clin Niteroi, Niteroi, RJ, Brazil., [Sales Jr, J.] Hosp Clin Padre Miguel, Rio De Janeiro, Brazil., [Madeira Campos Melo, L.] Hosp Terapia Intens, Sao Paulo, Brazil., [Oliveira, M.] Hosp Trabalhador, Curitiba, Parana, Brazil., [Fonte, M.] Hosp Esperanza, Olinda, PE, Brazil., [Grion, C.] Hosp Evangel Londrina, Londrina, Brazil., [Feijo, C.] Hosp Geral Fortaleza, Fortaleza, Ceara, Brazil., [Rezende, V] Hosp Geral Roraima, Boa Vista, Brazil., [Assuncao, M.] Hosp Israelita Albert Einstein, Sao Paulo, Brazil., [Neves, A.] Hosp Mater Dei, Belo Horizonte, MG, Brazil., [Gusman, P.; Dalcomune, D.] Hosp Meridional, Cariacica, ES, Brazil., [Teixeira, C.] Hosp Moinhos Vento, Porto Alegre, RS, Brazil., [Kaefer, K.] Hosp Municipal Ruth Cardoso, Balneario, Brazil., [Maia, I] Hosp Nereu Ramos, Florianopolis, SC, Brazil., [Souza Dantas, V] Hosp Pasteur, Rio De Janeiro, Brazil., [Costa Filho, R.] Hosp Pro Cardiaco, Rio De Janeiro, Brazil., [Amorim, F.] Hosp Reg Samambaia, Brasilia, DF, Brazil., [Assef, M.] Hosp Reg Hans Dieter Schmidt, Joinville, Brazil., [Schiavetto, P.] Hosp Santa Casa Campo Mourao, Campo Mourao, PR, Brazil., [Houly, J.] Hosp Santa Paula, Sao Paulo, SP, Brazil., [Houly, J.] Hosp Santapaula, Sao Paulo, Brazil., [Bianchi, F.] Hosp Sao Jose Avai, Itaperuna, RJ, Brazil., [Dias, F.] Hosp Sao Lucas Pucrs, Porto Alegre, RS, Brazil., [Avila, C.] Hosp Sao Vicente Paula, Rio De Janeiro, RJ, Brazil., [Gomez, J.] Hosp Sao Vicente Paulo, Rio De Janeiro, Brazil., [Rego, L.] Hosp Saude Mulher, Belem, Para, Brazil., [Castro, P.] Hosp Tacchini, Bento Goncalves, RS, Brazil., [Passos, J.] Hosp Unimed Costa Do Sol Macae Rj, Macae, RJ, Brazil., [Mendes, C.] Hosp Univ Ufpb Joao Pessoa, Joao Pessoa, Paraiba, Brazil., [Grion, C.] Hosp Univ Londrina, Londrina, Brazil., [Colozza Mecatti, G.] Hosp Univ Sao Francisco, Braganca Paulista, SP, Brazil., [Ferrreira, M.] Santa Casa Caridade Diamantina, Diamantina, MG, Brazil., [Irineu, V] Santa Casa Misericordia Tatui, Tatui, Brazil., [Guerreiro, M.] Sao Francisco de Paula Hosp, Sao Francisco De Paula, RS, Brazil., [Ugarte, S.] Clin Indisa, Providencia, Chile., [Tomicic, V] Clin Las Lilas, Providencia, Chile., [Godoy, C.] Hosp Carlos Van Buren, Valparaiso, Chile., [Samaniego, W.] Hosp Trabajador Santiago, Santiago, Chile., [Escamilla, I] Hosp El Pino, San Bernardo, Chile., [Escamilla, I] Hosp Mutual De Seguridad, Santiago, Chile., [Castro Castro, L.] Ctr Med Imbanaco, Valle Del Cauca, Colombia., [Libreros Duque, G.] Clin Colombia Cali, Cali, Colombia., [Diaz-Guio, D.] Clin Del Cafe, Armenia, Colombia., [Benitez, F.] Clin La Estancia SA, Popayan, Colombia., [Guerra Urrego, A.] Clin Medellin, Medellin, Colombia., [Buitrago, R.] Fdn Clin Shaio, Bogota, Colombia., [Ortiz, G.] Hosp Santa Clara, Bogota, Colombia., [Villalba Gaviria, M.] Hosp Univ Fdn Santa Fe De Bogota, Bogota, Colombia., [Salas, D.] Calderon Guardia Hosp, San Jose, Costa Rica., [Ramirez-Arce, J.] Hosp Dr Rafael Angel Varlderon Guardia Ccss, San Jose, Costa Rica., [Salgado, E.] Clin La Merced, Quito, Ecuador., [Morocho, D.] Hosp Eugenio Espejo, Quito, Ecuador., [Vergara, J.] Hosp Luis Vernaza, Quito, Ecuador., [Chung Sang, M.] Shdug Sistema Hosp Docente De La Univ Guayaquil, Quito, Ecuador., [Orellana-Jimenez, C.] Gen Hosp, San Salvador, El Salvador., [Garrido, L.] Hosp Ctr Med, Guatemala City, Guatemala., [Diaz, O.] Inst Hondureno Seguro Social, La Ceiba, Honduras., [Resiere, D.] Ctr Hosp Univ Ft De France, Fort De France, Martinique, France., [Osorio, C.] Ctr Estatal Cuidados Crit, Salamanca, Mexico., [De La Vega, A.] Ctr Med Nacl 20 Noviembre Issste, Mexico City, DF, Mexico., [Carrillo, R.] Fdn Clin Med Sur, Mexico City, DF, Mexico., [Sanchez, V] Hosp San Jose TEC Monterrey, Monterrey, Mexico., [Villagomez, A.] Hosp 1 Octubre, Issste, Mexico., [Martinez Zubieta, R.] Hosp Espanol Mexico, Mexico City, DF, Mexico., [Sandia, M.] Hosp Gen Ajusco Medio, Mexico City, DF, Mexico., [Zalatiel, M.] Hosp Gen Guadalupe Victoria, Texcoco, Mexico., [Poblano, M.] Hosp Juarez Mexico, Mexico City, DF, Mexico., [Rodriguez Gonzalez, D.] Hosp Civil Guadalajara, Hspitaljuan I Menchaca, Guadalajara, Jalisco, Mexico., [Arrazola, F.; Juan Francisco, L.] Inst Mexicano Seguro Social, Mexico City, DF, Mexico., [Liamendys-Silva, S. A.] Inst Nacl Cancerol, Mexico City, DF, Mexico., [Hernandez, M.] ISSSTE Guerra Moya, Mexico City, DF, Mexico., [Hernandez, M.] Med Ctr ISSEMYM Toluca, Mexico City, DF, Mexico., [Rodriguez Cadena, D.] Mixta, Mexico City, DF, Mexico., [Lopez Islas, I.] Secretaria Salud Dist Fed, Mexico City, DF, Mexico., [Ballesteros Zarzavilla, C.] Hosp Santo Comas, Panama City, Panama., [Matos, A.] Social Secur Hosp, La Chorrera, Panama., [Oyanguren, I] Clin Anglo Amer, Lima, Peru., [Cerna, J.] Essalud, Lima, Peru., [Quispe Sierra, R.] Hosp Nacl Dos De Mayo, Lima, Peru., [Jimenez, R.] Hosp Rebagliati, Lince Dist, Peru., [Castillo, L.] Inst Nacl Enfermedades Neoplas, Surquillo, Peru., [Ocal, R.] Gulhane Med Fac, Istanbul, Turkey., [Sencan, A.] Izmir Ataturk Educ & Res Hosp, Izmir, Turkey., [Gianoni, S. Mareque] CAMS, Montevideo, Uruguay., [Deicas, A.] CASMU, Montevideo, Uruguay., [Hurtado, J.] Hosp Espanol Asse, Montevideo, Uruguay., [Burghi, G.] Hosp Maciel, Montevideo, Uruguay., [Martinelli, A.] Ctr Med Caracas, Caracas, Venezuela., [Von der Osten, I] Hosp Miguel Perez Carreno, Caracas, Venezuela., [Du Maine, C.] MSF Trauma Hosp Kunduz, Kunduz, Afghanistan., [Bhattacharyya, M.] Amri Hosp, Kolkata, India., [Bandyopadhyay, S.] Amri Hosp Salt Lake, Kolkata, W Bengal, India., [Yanamala, S.] Apollo Hosp, Hyderabad, India., [Gopal, P.] Apollo Hosp, Bangalore, Karnataka, India., [Sahu, S.] Apollo Hosp, Bhubaneswar, India., [Ibrahim, M.] Apollo Special Hosp, Chennai, Tamil Nadu, India., [Rathod, D.] Asian Heart Inst, Mumbai, Maharashtra, India., [Mukundan, N.] Baby Mem Hosp Ltd, Calicut, Kerala, India., [Dewan, A.] Batra Hosp & Mrc, New Delhi 110062, India., [Amin, P.] Bombay Hosp Inst Med Sci, Mumbai, Maharashtra, India., [Samavedam, S.] Care Hosp, Hyderabad, India., [Shah, B.] Cims Hosp, Ahmadabad, Gujarat, India., [Gurupal, D.] Columbiaasia Hosp, Mysore, Karnataka, India., [Lahkar, B.] Dispur Hosp, Gauhati, India., [Mandal, A.] Fortis Hosp, Bangalore, Karnataka, India., [Sircar, M.] Fortis Hosp, Noida, India., [Ghosh, S.] Fortis Escorts Hosp, Faridabad, India., [Balasubramani, V] Ganga Med Ctr & Hosp P Ltd, Coimbatore, Tamil Nadu, India., [Kapadia, F.] Hinduja Hosp, Mumbai, Maharashtra, India., [Vadi, S.] KDAH, Mumbai, Maharashtra, India., [Nair, K.] Kerala Inst Med Sci, RMCC, Thiruvananthapuram, Kerala, India., [Tripathy, S.] Kalinga Inst Med Sci, DTEM, Bhubaneswar, Odisha, India., [Nandakumar, S.] Kovai Med Ctr & Hosp, Coimbatore, Tamil Nadu, India., [Sharma, J.] Medanta Medic, Gurgaon, India., [Kar, A.] Med Superspecialty Hosp, Kolkata, W Bengal, India., [Jha, S.] Metro Heart Inst Multispecial, Faridabad, India., [Gurav, K. Zirpe] Ruby Hall Pune, Pune, Maharashtra, India., [Patel, M.] Saifee Hosp, Mumbai, Maharashtra, India., [Bhaysar, A.] Spandan Multispecial Hosp, Vadodara, India., [Samaddar, D.] Tata Main Hosp, Jamshedpur, Jharkhand, India., [Kulkarni, A.] Tata Mem Hosp, Mumbai, Maharashtra, India., [Hashmi, M.] Aga Khan Univ, Karachi, Pakistan., [Ali, W.] Hearts Int Hosp, Rawalpindi, Pakistan., [Nadeem, S.] Liaquat Natl Hosp, Karachi, Pakistan., [Indraratna, K.] Sri Jayewardenepura Gen Hosp, Sri Jayawardenepura Kott, Sri Lanka., [Margarit, A.] Hosp Nostra Senyora Meritxell, Les Escaldes, Andorra., [Urbanek, P.] Akh Wien, Vienna, Austria., [Schlieber, J.] Allgemeines & Orthopad Landeskrankenhaus Stolzalp, Stolzalpe, Austria., [Reisinger, J.] Barmherzige Schwestern Linz, Linz, Austria., [Auer, U.] Gen Hosp Braunau, Braunau, Austria., [Hartjes, A.] Krankenhaus D Barmherzigen Schwestern Ried II, Ried Im Innkreis, Austria., [Lerche, A.] Krankenhaus Floridsdorf, Vienna, Austria., [Janous, T.] LK Gmund Waidhofen Thaya Zwettl, Standort Zwettl, Austria., [Kink, E.] LKH Horgas Enzenbach, Gratwein, Austria., [Krahulec, W.] LKH West, Graz, Austria., [Smolle, K.] Univ Hosp, Graz, Austria., [Van der Schueren, M.] AZ Groeninge Kortrijk, Kortrijk, Belgium., [Thibo, P.] AZ Jan Palfijn Gent, Ghent, Belgium., [Vanhoof, M.] AZ Turnhout, Turnhout, Belgium., [Ahmet, I] Bracops Anderlecht, Anderlecht, Belgium., [Gadisseux, P.] Ctr Hosp Mouscron, Mouscron, Belgium., [Dufaye, P.] CH Peltzer La Tourelle, Verviers, Belgium., [Jacobs, O.] Chirec Edith Cavell, Auderghem, Belgium., [Fraipont, V] CHR Citadelle, Liege, Belgium., [Biston, P.] CHU Charleroi, Charleroi, Belgium., [Dive, A.] CHU Mt Godinne, Yvoir, Belgium., [Bouckaert, Y.] CHU Tivoli, La Louviere, Belgium., [Gilbert, E.] CHwapi, Tournai, Belgium., [Gressens, B.] Clin St Pierre Ottignies, Ottignies, Belgium., [Pinck, E.] Clin Maternite St Elisabeth, Namur, Belgium., [Collin, V] Clin Europe St Michel, Etterbeek, Belgium., [Vincent, J. L.] Erasme Univ Hosp, Anderlecht, Belgium., [De Waele, J.] Ghent Univ Hosp, Ghent, Belgium., [Rimachi, R.] Moliere Hosp, Forest, Belgium., [Gusu, D.] Notre Dame, Brussels, Belgium., [De Decker, K.] Onze Lieve Vrouw Hosp, Aalst, Belgium., [Mandianga, K.] Ixelles Hosp, Ixelles, Belgium., [Heytens, L.] Sint Augustinus, Antwerp, Belgium., [Wittebole, X.] St Luc Univ Hosp UCL, Brussels, Belgium., [Spapen, H.] UZ Brussel, Brussels, Belgium., [Olivier, V] Vivalia Site Libramt, Libramont, Belgium., [Vandenheede, W.] VZW Gezondheidszorg Oostkust Knokke Heist, Knokke Heist, Belgium., [Rogiers, P.] ZNA Middelheim, Antwerp, Belgium., [Kolodzeike, P.] Herning Hosp, Herning, Denmark., [Kruse, M.] Hjoerring Hosp, Hjorring, Denmark., [Andersen, T.] Vejle Hosp, Vejle, Denmark., [Harjola, V] Helsinki Univ Cent Hosp, Helsinki, Finland., [Saarinen, K.] Seinajoki Cent Hosp, Seinajoki, Finland., [Leone, M.] Aix Marseille Univ, Hop Nord, Marseille, France., [Durocher, A.] Calmette Hosp, Lille, France., [Moulront, S.] Ctr Hosp Dunkerque, Dunkerque, France., [Lepape, A.] Ctr Hosp Lyon Sud, Lyon, France., [Losser, M.] CHU Nancy Brabois, Nancy, France., [Cabaret, P.] CH St Philibert, GHICL, Lille, France., [Kalaitzis, E.] CHR Dax, Dax, France., [Zogheib, E.] CHU Amiens, Amiens, France., [Charve, P.] CHU Dijon, Dijon, France., [Francois, B.] CHU Dupuytren, Limoges, France., [Lefrant, J. Y.] CHU Nimes, Nimes, France., [Beilouny, B.] Ctr Hosp Troyes, Troyes, France., [Forceville, X.] Ctr Hosp Meaux, Grp Hosp Est Francilien, Meaux, France., [Misset, B.] Grp Hosp Paris St Joseph, Paris, France., [Jacobs, F.] Hop Antoine Beclere, Clamart, France., [Floccard, B.] Hop Edouard Herriot, Lyon, France., [Payen, D.] Hop Lariboisere, AP HP, Paris, France., [Wynckel, A.] Hop Maison Blanche, Reims, France., [Castelain, V] Hop Univ Strasbourg, Strasbourg, France., [Faure, A.] Hosp Civils Lyon, Lyon, France., [Lavagne, P.] CHU Grenoble, Grenoble, France., [Thierry, I] CHU Nantes, Nantes, France., [Moussa, M.] CHRU Lille, Reanimat Chirurg Cardiovasc, Lille, France., [Vieillard-Baron, A.] Univ Hosp Ambroise Pare, Boulogne, France., [Durand, M.] Univ Hosp Grenoble, La Tronche, France., [Gainnier, M.] Univ Hosp Marseille, Marseille, France., [Ichai, C.] Univ Nice, Nice, France., [Arens, S.] Alexianer Krefeld Gmbh, Krefeld, Germany., [Hoffmann, C.] Charite Hochschulmed Berlin, Berlin, Germany., [Kaffarnik, M.] Charite, Berlin, Germany., [Scharnofske, C.] Diakoniekrankenhaus Henriettenstiftung Gmbh, Hannover, Germany., [Voigt, I] Elisabeth Krankenhaus Essen, Essen, Germany., [Peckelsen, C.] Munich Municipal Hosp Grp, Harlaching Hosp, Munich, Germany., [Weber, M.] Helios St Johannes Klin, Duisburg, Germany., [Gille, J.] Hosp St Georg Leipzig, Leipzig, Germany., [Lange, A.] Klin Hennigsdorf Oberhavel Kliniken Gmbh, Hennigsdorf, Germany., [Schoser, G.] Klin Tettnang, Tettnang, Germany., [Sablotzki, A.] Klinikum St Georg Leipzig, Leipzig, Germany., [Jaschinski, U.; Bluethgen, A.] Klinikum Augsburg, Augsburg, Germany., [Vogel, F.] Klinikum Bremen Mitte, Bremen, Germany., [Tscheu, A.] Klinikum Bremen Ost, Bremen, Germany., [Fuchs, T.] Klinikum Heidenheim, Heidenheim, Germany., [Wattenberg, M.] Klinikum Links Weser Gmbh, Bremen, Germany., [Helmes, T.] Klinikum Luedenscheid, Luedenscheid, Germany., [Scieszka, S.] Krankenhaus Neuwerk, Monchengladbach, Germany., [Heintz, M.] Marienkrankenhaus Schwerte, Schwerte, Germany., [Sakka, S.] Med Ctr Cologne Merheim, Cologne, Germany., [Kohler, J.] Schwarzwald Baar Klinikum Villingen Schwenningen, Villingen Schwenningen, Germany., [Fiedler, F.] St Elisabeth Krankenhaus Koln Hohenlind, Cologne, Germany., [Danz, M.] St Martinus Hosp Olpe, Olpe, Germany., [Sakr, Y.] Uniklinikum Jena, Jena, Germany., [Riessen, R.] Univ Klinikum Tubingen, Tubingen, Germany., [Kerz, T.] Univ Med Mainz, Mainz, Germany., [Kersten, A.] Univ Hosp Aachen, CPACC, Aachen, Germany., [Tacke, F.] Univ Hosp Aachen, DMIII, Aachen, Germany., [Marx, G.] Univ Hosp Aachen, OIC, Aachen, Germany., [Volkert, T.] Univ Hosp Muenster, Munster, Germany., [Schmutz, A.] Univ Med Ctr Freiburg, Fr

Aims and Objectives: Sepsis is an acute life-threatening systemic inflammatory response to infection. C-reactive protein (CRP) and albumin are positive and negative acute phase proteins respectively, following opposing patterns in sepsis. We aim to investigate whether CRP/albumin ratio is a better prognostic marker of 28-day mortality in critically ill patients with sepsis than CRP alone. Methods: In a prospective study, CRP and albumin were determined in serum of 102 critically ill patients (57 males, age 65±15 years, APACHE II 23±7, SOFA 10±3) at sepsis onset and one week after. Results: Thirty patients (29.4%) died within 28 days from enrolment. CRP and CRP/albumin ratio decreased significantly one week after sepsis onset (145±94 vs 91±71mg/L, p Conclusions: CRP/albumin ratio is a good predictor of 28-day mortality in critically ill patients with sepsis, similar to CRP but better than SOFA and APACHE II scores.

Aims and Objectives: Sepsis constitutes an acute inflammatory response to infection affecting liver function. Increased serum bilirubin as well as decreased fetuin-A, a major hepatokine, have been shown in critically ill patients with sepsis. We aim to explore the association of serum bilirubin/fetuin-A (B/F) ratio early in sepsis with severity and outcome. Methods: In a prospective study, serum total bilirubin and fetuin-A were determined in 90 critically ill patients (52 males, age 65±15 years, APACHE II 24 ±7, SOFA 10±3) at sepsis onset and one week after. B/F ratio was calculated using the formula 10.000 x Bilirubin (mg/dL) / Fetuin-A (μg/mL). Mortality rate at 28 days after enrollment was the primary outcome. Results: Twenty eight patients (31%) died within 28 days. Bilirubin and fetuin-A increased one week after sepsis onset compared to baseline (1.16±2.3 vs 1.38±2.84mg/dL, p=0.03 and 306±107 vs 372±147μg/mL, p Conclusions: B/F ratio at sepsis onset is associated with severity and outcome and may be a useful prognostic biomarker in critically ill septic patients.

Aims and Objectives: Sepsis results in severe lipid metabolic alterations. Lipids exert important immunomodulatory actions during infection. We aim to investigate whether serum lipid changes early in sepsis are associated with severity and outcome. Methods: In a prospective study, serum total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL) and triglycerides (TG) were determined in 82 critically ill patients (49 males, age 65±14 years, APACHE II 23±7, SOFA 10±3) at sepsis onset and one week after, and in 82 age and gender-matched healthy controls. Results: Upon enrollment, TC, HDL and LDL were significantly lower and TG were higher in patients compared to controls (p Conclusions: Critically ill septic patients exhibit significant alterations of serum lipids associated with sepsis severity and outcome.

Patient: Male, 73-year-old Final Diagnosis: Severe COVID-19 pneumonia complicated by right atrium thrombus Symptoms: Fever • dyspnea • cough Medication:— Clinical Procedure: — Specialty: Critical Care Medicine Objective: Educational purpose Background: Recent studies demonstrated evidence of coagulation dysfunction in hospitalized patients with severe coronavirus disease 2019 (COVID-19) due to excessive inflammation, hypoxia, platelet activation, endothelial dysfunction, and stasis. Effective anticoagulation therapy may play a dominant role in the management of severe COVID-19 cases. Case Report: A 73-year-old man with a 6-day history of fever up to 38.5°C, dyspnea, cough, and fatigue was diagnosed with COVID-19. He had a past medical history significant for hypertension and coronary artery bypass grafting. Two days after hospital admission, the patient developed acute respiratory failure, requiring intubation, mechanical ventilation, and transfer to the intensive care unit (ICU). He received treatment including antibiotics, hydroxychloroquine, tocilizumab, vasopressors, prone positioning, and anticoagulation with enoxaparin at a prophylactic dose. After a 15-day ICU stay, the patient was hemodynamically stable but still hypoxemic; a transthoracic echocardiogram at that time, followed by a transesophageal echocardiogram for better evaluation, revealed the presence of a right atrium thrombus without signs of acute right ventricular dilatation and impaired systolic function. Since the patient was hemodynamically stable, we decided to treat him with conventional anticoagulation under close monitoring for signs of hemodynamic deterioration; thus, the prophylactic dose of enoxaparin was replaced by therapeutic dosing, which was a key component of the patient’s successful outcome. Over the next few days he showed significant clinical improvement. The follow-up transesophageal echo-cardiogram 3 weeks after effective therapeutic anticoagulation revealed no signs of right heart thrombus. Conclusions: The presented COVID-19 case, one of the first reported cases with evidence of right heart thrombus by transesophageal echocardiography, highlights the central role of diagnostic imaging strategies and the importance of adequate anticoagulation therapy in the management of severe COVID-19 cases in the ICU.

Introduction: Antineutrophil cytoplasmic autoantibody–associated vasculitis is an immune-mediated necrotizing vasculitis, affecting small- and medium-sized vessels. Case report: A 22-year-old female patient with free medical history presented with life-threatening pulmonary hemorrhage due to antineutrophil cytoplasmic autoantibody–associated vasculitis, temporarily associated with influenza A H1N1 infection. Due to rapidly worsening respiratory failure, despite conventional management, veno-venous peripheral extracorporeal membrane oxygenation was initiated and continued for 26 days, with subsequent renal replacement therapy. Discussion: We present a case of severe antineutrophil cytoplasmic autoantibody–associated pulmonary vasculitis, managed with veno-venous extracorporeal membrane oxygenation at the initial phase. Despite the significant challenges raised with the use of extracorporeal membrane oxygenation in pulmonary hemorrhage cases, extracorporeal membrane oxygenation may have a significant impact on outcome in this setting, by providing adequate time for a successful immunosuppressive treatment.

Background De-escalation of empirical antimicrobial therapy, a key component of antibiotic stewardship, is considered difficult in ICUs with high rates of antimicrobial resistance. Objectives To assess the feasibility and the impact of antimicrobial de-escalation in ICUs with high rates of antimicrobial resistance. Methods Multicentre, prospective, observational study in septic patients with documented infections. Patients in whom de-escalation was applied were compared with patients without de-escalation by the use of a propensity score matching by SOFA score on the day of de-escalation initiation. Results A total of 262 patients (mean age 62.2 ± 15.1 years) were included. Antibiotic-resistant pathogens comprised 62.9%, classified as MDR (12.5%), extensively drug-resistant (49%) and pandrug-resistant (1.2%). In 97 (37%) patients de-escalation was judged not feasible in view of the antibiotic susceptibility results. Of the remaining 165 patients, judged as patients with de-escalation possibility, de-escalation was applied in 60 (22.9%). These were matched to an equal number of patients without de-escalation. In this subset of 120 patients, de-escalation compared with no de-escalation was associated with lower all-cause 28 day mortality (13.3% versus 36.7%, OR 0.27, 95% CI 0.11–0.66, P = 0.006); ICU and hospital mortality were also lower. De-escalation was associated with a subsequent collateral decrease in the SOFA score. Cox multivariate regression analysis revealed de-escalation as a significant factor for 28 day survival (HR 0.31, 95% CI 0.14–0.70, P = 0.005). Conclusions In ICUs with high levels of antimicrobial resistance, feasibility of antimicrobial de-escalation was limited because of the multi-resistant pathogens isolated. However, when de-escalation was feasible and applied, it was associated with lower mortality.

Background B cell function and antibody production are crucial factors in host protection during inflammation. We aimed to synthesize the available evidence on the association between the reduction of circulating B cells and plasma immunoglobulin (IgM) levels and decreased survival during sepsis. Methods We performed a systematic search in PubMed, Embase, ISI Web of Knowledge, Cochrane Central Register of Controlled Trials, BioMed Central, and Science Direct. We selected studies with data on circulating B cells and plasma IgM levels within the initial 24 h after sepsis onset. Results In total nine studies (n = 992 patients) were identified. Circulating B cells were reduced in septic patients as compared to non-septic patients (mean difference [MD] −88.2 cells/μl; 95% confidence interval [CI] −148.6–−27.9). Sepsis non-survivors showed a significant reduction of circulating B cells and IgM levels compared to sepsis survivors (MD −77.1 cells/μl; 95% CI −111.4–−42.7 and MD −20.9 mg/dl; 95% CI −33.8–−8.0, respectively). Conclusions Our results suggest that a reduction of circulating B cells and IgM levels at sepsis onset are associated with decreased sepsis survival. However, due to methodological limitations and the risk of bias, we need further prospective studies to confirm this association. Registration The protocol was registered (PROSPERO 2016:CRD42016053184).

Fetuin-A and adiponectin, major hepatokine and adipokine respectively, have been implicated in systematic inflammation. Our aim was to jointly investigate whether kinetics of circulating fetuin-A, adiponectin and its isoform HMWA predict 28-day mortality in sepsis.In a prospective study, serum fetuin-A, adiponectin and HMWA were determined in 102 ICU patients fulfilling the diagnostic criteria of SEPSIS-3, at enrollment and one week after, and in 102 healthy controls matched on age and gender.Serum fetuin-A was significantly lower in septic patients than controls (p0.001). Among septic patients, those with septic shock and nonsurvivors presented lower fetuin-A, but higher adiponectin and HMWA compared to patients with sepsis and survivors respectively, both at baseline and day 7 (p0.001). Fetuin-A exhibited negative correlations with APACHE II, CRP, procalcitonin, adiponectin and IL-6 but a positive one with albumin. Reduced fetuin-A as well as lower serum kinetics of fetuin-A (HR: 0.55, 95% C.I. 0.34-0.91, p=0.02), adiponectin but not HMWA were independently associated with 28-day mortality adjusting for age, gender, BMI, APACHE II, septic shock and laboratory biomarkers.Circulating fetuin-A kinetics may be a prognostic biomarker in septic patients. More research is essential to elucidate fetuin-A's ontological role in sepsis pathophysiology.

OBJECTIVETo evaluate the efficacy of copper-coating in reducing environmental colonization in an intensive-care unit (ICU) with multidrug-resistant-organism (MDRO) endemicityDESIGNInterventional, comparative crossover trialSETTINGThe general ICU of Attikon University hospital in Athens, GreecePATIENTSThose admitted to ICU compartments A and B during the study periodMETHODSBefore any intervention (phase 1), the optimum sampling method using 2 nylon swabs was validated. In phase 2, 6 copper-coated beds (ie, with coated upper, lower, and side rails) and accessories (ie, coated side table, intravenous [i.v.] pole stands, side-cart handles, and manual antiseptic dispenser cover) were introduced as follows: During phase 2a (September 2011 to February 2012), coated items were placed next to noncoated ones (controls) in both compartments A and B; during phase 2b (May 2012 to January 2013), all copper-coated items were placed in compartment A, and all noncoated ones (controls) in compartment B. Patients were randomly assigned to available beds. Environmental samples were cultured quantitatively for clinically important bacteria. Clinical and demographic data were collected from medical records.RESULTSCopper coating significantly reduced the percentage of colonized surfaces (55.6% vs 72.5%; PP=.003) or by enterococci (4% vs 17%; P=.014), the total bioburden (2,858 vs 7,631 cfu/100 cm2; P=.008), and the bioburden of gram-negative isolates, specifically (261 vs 1,266 cfu/100 cm2; P=.049). This effect was more pronounced when the ratio of coated surfaces around the patient was increased (phase 2b).CONCLUSIONSCopper-coated items in an ICU setting with endemic high antimicrobial resistance reduced environmental colonization by MDROs.Infect Control Hosp Epidemiol 2017;38:765–771

Invasive fungal infections are common in intensive care units (ICUs) but there is a great variability in factors affecting costs of different antifungal treatment strategies in clinical practice. To determine factors affecting treatment cost in adult ICU patients with or without documented invasive fungal infection receiving systemic antifungal therapy (SAT) we have performed a prospective, multicentre, observational study enrolling patients receiving SAT in participating ICUs in Greece. During the study period, 155 patients received SAT at 14 participating ICUs: 37 (23.9%) for proven fungal infection before treatment began, 10 (6.5%) prophylactically, 77 (49.7%) empirically and 31 (20.0%) pre-emptively; 66 patients receiving early SAT (55.9%) were subsequently confirmed to have proven infection with Candida spp. (eight while on treatment). The most frequently used antifungal drugs were echinocandins (89/155; 57.4%), fluconazole (31/155; 20%) and itraconazole (20/155; 12.9%). Mean total cost per patient by SAT strategy was €20 458 (proven), €15 054 (prophylaxis), €23 594 (empiric) and €22 184 (pre-emptive). Factors associated with significantly increased cost were initial treatment failure, length of stay (LOS) in ICU before starting SAT (i.e. from admission until treatment start), fever and proven candidaemia (all P≤.05). Conclusion Early administration of antifungal drugs was not a substantial component of total hospital costs. However, there was a significant adverse impact on costs with increasing LOS in febrile patients in ICU for whom diagnosis of fungaemia was delayed before starting SAT, and with initial treatment failure. Awareness of potential candidaemia and initiation of pre-emptive or empirical strategy as early appropriate treatment may improve ICU patient outcomes while reducing direct medical costs.

This study was designed to identify changes in the monocytic membrane marker HLA-DR and heat shock proteins (HSPs) in relation to T-regulatory cells (T-regs) and other immunological marker changes in patients with systemic inflammatory response syndrome (SIRS) or sepsis/septic shock.Healthy volunteers, intensive care unit (ICU) patients with SIRS due to head injury and ICU patients with severe sepsis/septic shock were enrolled in the current study. Determination of CD14+/HLA-DR+ cells, intracellular heat-shock proteins and other immunological parameters were performed by flow cytometry and RT-PCR techniques as appropriate. Univariate and multivariate analysis examined associations of CD14/HLA-DR, HSPs, T-regs and suppressor of cytokine signalling (SOCS) proteins with SIRS, sepsis and outcome.Fifty patients (37 with severe sepsis and 13 with SIRS) were enrolled, together with 20 healthy volunteers used as a control group. Compared to healthy individuals, patients with SIRS and severe sepsis showed progressive decline of their CD14/HLA-DR expression (0% to 7.7% to 50% within each study subpopulation, p0.001). Mean fluorescent intensity (MFI) levels of HSP70 and HSP90 on monocytes and polymorphonuclear cells were significantly higher in SIRS patients compared to controls and fell significantly in severe sepsis/septic shock patients (p0.05 for all comparisons). There was no statistically significant difference between subgroups for levels of T-regulatory cells or relative copies of Suppressor of Cytokine Signalling 3 (SOCS3) proteins. In univariate models percent of CD14/HLA-DR was associated with mortality (OR: 1.8 95%CI 1.02-3.2, p=0.05), while in multivariate models after adjusting for CD14/HLA-DR only younger age and lower Acute Physiology and Chronic Health Evaluation II (APACHE II) scores were associated with increased chances of survival (beta -0.05, OR 0.9, 95% CI 0.9-0.99, p=0.038 for age and beta -0.11, OR 0.89, 95% CI 0.8-0.99, p=0.037 for APACHE II score).Significant associations with SIRS and sepsis were found for CD14/HLA-DR expression and monocyte and polymorphonuclear cell levels of HSP70 and 90. The role of these biomarkers in assessing the prognosis of sepsis needs to be further explored and validated in prospective studies.

Introduction: Non-traumatic coma (NTC) is a common cause of critical illness with diverse etiology and prognosis Aim: To investigate the etiology and outcome of NTC in ICU patients and to explore prognostic factors Methods: In a retrospective study we reviewed the medical records of all patients admitted to the ICU of a teaching hospital due to NTC, from January 2018 to January 2019. Demographic data, medical history, APACHE II score, etiology of coma and ICU mortality were recorded. Results: Among 250 medical records, we identified 30 cases (16 males, mean age 68±14, APACHE II 21±7) of NTC. The etiology of NTC was: intracerebral hemorrhage (8), respiratory failure (6), sepsis (5), post-anoxic (4), CNS infection (3), ischemic stroke (2), metabolic coma (2). Thirteen patients died in the ICU (43%) and 17 were discharged. Sepsis presented the highest ICU mortality (80%), followed by post-anoxic (75%), intracerebral hemorrhage (62%) and ischemic stroke (50%). All patients with respiratory failure, CNS infection and metabolic coma survived to discharge. Sex, age, APACHE II score and history of chronic kidney, respiratory, cardiovascular disease or malignancy were not correlated with ICU mortality (p>0.05). Elevated serum lactate (p:0.018), acute kidney injury (p:0.005) and hypotension (p:0.033) at admission were associated with ICU mortality. Acute kidney injury on the day of admission tripled the risk of death (HR:2.8, 95%CI: 1.2-6.6, p Conclusion: Intracerebral hemorrhage was the leading cause of NTC, followed by respiratory failure and sepsis. Acute kidney injury was the best predictor of ICU mortality.

Contains fulltext : 177598.pdf (Publisher’s version ) (Closed access) OBJECTIVES: Excessive fluid therapy in patients with sepsis may be associated with risks that outweigh any benefit. We investigated the possible influence of early fluid balance on outcome in a large international database of ICU patients with sepsis. DESIGN: Observational cohort study. SETTING: Seven hundred and thirty ICUs in 84 countries. PATIENTS: All adult patients admitted between May 8 and May 18, 2012, except admissions for routine postoperative surveillance. For this analysis, we included only the 1,808 patients with an admission diagnosis of sepsis. Patients were stratified according to quartiles of cumulative fluid balance 24 hours and 3 days after ICU admission. MEASUREMENTS AND MAIN RESULTS: ICU and hospital mortality rates were 27.6% and 37.3%, respectively. The cumulative fluid balance increased from 1,217 mL (-90 to 2,783 mL) in the first 24 hours after ICU admission to 1,794 mL (-951 to 5,108 mL) on day 3 and decreased thereafter. The cumulative fluid intake was similar in survivors and nonsurvivors, but fluid balance was less positive in survivors because of higher fluid output in these patients. Fluid balances became negative after the third ICU day in survivors but remained positive in nonsurvivors. After adjustment for possible confounders in multivariable analysis, the 24-hour cumulative fluid balance was not associated with an increased hazard of 28-day in-hospital death. However, there was a stepwise increase in the hazard of death with higher quartiles of 3-day cumulative fluid balance in the whole population and after stratification according to the presence of septic shock. CONCLUSIONS: In this large cohort of patients with sepsis, higher cumulative fluid balance at day 3 but not in the first 24 hours after ICU admission was independently associated with an increase in the hazard of death.

Sepsis is the dysregulated host response to an infection which leads to life-threatening organ dysfunction that varies by host genomic factors. We conducted a genome-wide association study (GWAS) in 740 adult septic patients and focused on 28 day mortality as outcome. Variants with suggestive evidence for an association (p ≤ 10− 5) were validated in two additional GWA studies (n = 3470) and gene coding regions related to the variants were assessed in an independent exome sequencing study (n = 74). In the discovery GWAS, we identified 243 autosomal variants which clustered in 14 loci (p ≤ 10− 5). The best association signal (rs117983287; p = 8.16 × 10− 8) was observed for a missense variant located at chromosome 9q21.2 in the VPS13A gene. VPS13A was further supported by additional GWAS (p = 0.03) and sequencing data (p = 0.04). Furthermore, CRISPLD2 (p = 5.99 × 10− 6) and a region on chromosome 13q21.33 (p = 3.34 × 10− 7) were supported by both our data and external biological evidence. We found 14 loci with suggestive evidence for an association with 28 day mortality and found supportive, converging evidence for three of them in independent data sets. Elucidating the underlying biological mechanisms of VPS13A, CRISPLD2, and the chromosome 13 locus should be a focus of future research activities., Highlights • A low frequency missense variant in VPS13A on chromosome 9q21.2 was associated with 28 day mortality after sepsis • A frequent intronic variant in CRISPLD2 was also supported and was reported to be associated with procalcitonin levels • Similarly supported was an intergenic frequent variant on chromosome13q21.33 – a region related to chronic kidney disease Sepsis is the dysregulated host response to an infection which leads to life-threatening organ dysfunction that is known to vary by host genomic factors. However, the detection of genetic variants related to sepsis outcomes has been challenging so far. We conducted a discovery genome-wide association study (GWAS) in 740 adult patients with sepsis looking for variants that vary with 28 day mortality. We followed-up our best findings by additional GWAS and exome sequencing data in 3544 adult patients and report three regions including the genes VPS13A and CRISPLD2 that were supported by our data and external biological evidence.

This paper deals with the estimation of glucose levels in ICU patients by the application of statistical filter theory to the data provided by a commercial continuous glucose monitoring system using a microdialysis sensor. Kalman and particle filtering are applied to simple models of the glucose dynamics. The particle filter enables the joint filtering and calibration of the sensor. The results show that the proposed filters lead to significant reduction in the estimation error with computational cost well within the capabilities of modern digital equipment. Additionally, the filters can be used for the automatic recognition of sensor faults. These results show that suitable filters can help in the construction of an artificial pancreas.

BACKGROUND: Early diagnosis of ventilator-associated pneumonia (VAP) is necessary to reduce morbidity and improve survival of critically ill patients in the ICU. The purpose of the present study is to examine the performance of macroscopic bronchoscopic findings and cytological analysis of bronchoalveolar lavage fluid (BALF) as an early diagnostic tool for VAP, either alone or in combination with clinically oriented scores (modified Clinical Pulmonary Infection Score [CPIS] or Johanson criteria). METHODS: BAL was performed in 54 consecutive mechanically ventilated subjects. The predictive value of isolated or combined clinical characteristics, BALF, and/or other laboratory measurements in diagnosing VAP was analyzed by logistic regression analysis. A separate diagnostic score was derived from a linear combination of independent variables included in the multivariate model and compared with CPIS, Johanson criteria, and their combinations with BALF cytology (receiver operating characteristic curve analysis). RESULTS: Integrating relative neutrophil cell count in CPIS or Johanson criteria optimized their specificity (>80%) but decreased sensitivity (

Hypercoagulability and thrombosis remain a challenge in severe coronavirus disease 2019 (COVID-19) infections. Our aim is to investigate the hemostatic profile of critically ill COVID-19 patients on therapeutic anticoagulant treatment.Forty one patients were enrolled into the study. We recruited 11 consecutive, COVID-19, patients who received therapeutic anticoagulant treatment on intensive care unit (ICU) admission. Disease severity indexes, biochemical, hematological and haemostatic parameters, endogenous thrombin potential (ETP), plasminogen activator inhibitor-1 (PAI-1) activity and extrinsically activated rotational thromboelastometry assay (EXTEM) were recorded on days 1, 3, 7. We also enrolled 9 ICU non-COVID-19, 21 non-ICU COVID-19 patients and 20 healthy blood donors as control populations.Critically ill COVID-19 patients demonstrated a more hypercoagulable and hypofibrinolytic profile related to those with COVID-19 mild illness, based on EXTEM amplitude at 10 min (A10), maximum clot firmness (MCF) and lysis index at 60 min (LI60) variables (p = 0.020, 0.046 and 0.001, respectively). Similarly, a more hypercoagulable state was detected in COVID-19 ICU patients related to non-COVID-19 ICU patients based on A10 and MCF parameters (p = 0.03 and 0.04, respectively). On the contrary, ETP and EXTEM (clotting time) CT values were similar between patients with severe and mild form of the COVID-19 infection, probably due to anticoagulant treatment given.Critically ill COVID-19 patients showed a hypercoagulable profile despite the therapeutic anticoagulant doses given. Due to the small sample size and the study design, the prognostic role of the hypercoagulability in this clinical setting remains unknown and further research is required in order to be assessed.

Antimicrobial agents are currently the mainstay of treatment for bacterial infections worldwide. However, due to the increased use of antimicrobials in both human and animal medicine, pathogens have now evolved to possess high levels of multi-drug resistance, leading to the persistence and spread of difficult-to-treat infections. Several current antibacterial agents active against Gram-positive bacteria will be rendered useless in the face of increasing resistance rates. There are several emerging antibiotics under development, some of which have been shown to be more effective with an improved safety profile than current treatment regimens against Gram-positive bacteria. We will extensively discuss these antibiotics under clinical development (phase I-III clinical trials) to combat Gram-positive bacteria, such as Staphylococcus aureus, Enterococcus faecium and Streptococcus pneumoniae. We will delve into the mechanism of actions, microbiological spectrum, and, where available, the pharmacokinetics, safety profile, and efficacy of these drugs, aiming to provide a comprehensive review to the involved stakeholders.

Background: Experimental and clinical data have shown that the adipocytokines eNAMPT and resistin interact with cytokines and other inflammatory molecules in the pathogenesis of sepsis. Objective: To investigate eNAMPT and resistin’s role as biomarkers of sepsis compared to well-established inflammatory markers and cytokines. Methods: We prospectively studied 102 critically ill patients (57 males, mean age 65±15years) fulfilling the diagnostic criteria of SEPSIS-3, during the first week of sepsis. Serum eNAMPT and resistin were determined by ELISA (Phoenix Pharmaceuticals, CA, USA) at sepsis onset and one week after. We also determined C-reactive protein (CRP), procalcitonin, interleukins IL-6, IL-10, tumor necrosis factor alpha (TNF-α) and soluble urokinase-type plasminogen activator receptor (suPAR). The discriminating power of measured parameters as predictors of sepsis and septic shock was obtained by Receiver Operating Characteristic (ROC) curves. Results: Sixty patients presented with sepsis and 42 with septic shock. Mortality within 28 days was 29.4%. eNAMPT exhibited significantly positive correlations with CRP, procalcitonin and IL-10 at admission, and with procalcitonin one week after enrollment. Resistin was positively correlated with IL-6, IL-10 and TNF-α at admission and with procalcitonin one week after enrollment. Area under ROC curves showed that eNAMPT (AUROC>0.83) and CRP (AUROC>0.78) outperformed procalcitonin (AUROC>0.71), resistin (AUROC>0.69), IL-6 (AUROC>0.69), IL-10 (AUROC>0.68) and suPAR (AUROC>0.64) in discriminating sepsis from septic shock. Conclusion: eNAMPT is a better discriminator biomarker for sepsis and septic shock, while resistin’s performance is comparable to procalcitonin.

Background: Macitentan, an oral dual endothelin receptor antagonist (ERA), has demonstrated improved morbidity and mortality in patients with pulmonary arterial hypertension (PAH) in a long-term event-driven study. Aims: To provide data on clinical efficacy and safety of switching to macitentan, in adult PAH patients. Methods: PAH patients were included in this single center restrospective study, provided they were switched from another ERA to macitentan. Patients were managed following the currently held guidelines, and other PAH-specific treatment with phosphodiesterase-5 inhibitors and prostanoids were prescribed accordingly. Functional class, 6 minute walk distance, NT-proBNP levels and hemodynamic measurements were assessed. The last available measurements pre and the first available measurements post initiation of macitentan were compared. Safety end-points focused on liver enzymes and hemoglobin levels, as well as peripheral edema. Results: 10 PAH patients (3 males), aged 59±13 years, with a PAH history of 5±2years, were studied. They did not demonstrate any difference in functional class after switching to macitentan. They had an increase in 6 minute walk distance (from 407±81 m to 416±85, p=0.06), and a significant improvement in NT-proBNP levels (1044±878 ng/L to 832±901, p=0.03). A non-significant increase in cardiac output (from 4.9±0.6 L/min to 5±0.6, p=0.7) and decrease in pulmonary vascular resistance (from 5.9±2.5 Wood Units to 5.5±2.6, p=0.08) were observed. No episodes of increased liver enzymes, anemia or peripheral edema were observed. Conclusion: Switching to macitentan was well tolerated and associated with improved natriuretic peptide levels in our patient cohort.

Background: eNAMPT, an adipokine with pro-inflammatory properties, has been implicated in acute and chronic inflammation. However, its kinetics has not been studied in sepsis. Objective: To investigate whether eNAMPT and its kinetics early in sepsis predict severity and outcome. Methods: In a prospective case-control study, serum eNAMPT concentrations were determined by ELISA in 102 critically ill patients (57 males, mean age 65±15 years) fulfilling the diagnostic criteria of SEPSIS-3, at sepsis onset and one week after, and in 102 age and gender-matched healthy controls. Results: Sixty patients presented with sepsis and 42 with septic shock. Mean APACHE II was 23±7. Thirty patients died within 28 days (mortality 29.4%). At admission, serum eNAMPT was significantly higher in patients compared to controls (79.1±19.5 vs 44.9±27.5ng/mL, p Conclusion: eNAMPT in early sepsis may be a novel diagnostic and prognostic biomarker in critically ill septic patients.

Quality standards have been widely adopted in healthcare, while the Hospital Information Systems (HIS) support quality management in modern hospitals. However, staff compliance lags behind. In this study, we investigated the effect of a novel application, implemented in the HIS, on staff compliance in the Intensive Care Unit of a tertiary teaching hospital. This application integrates quality protocols to the HIS, which is routinely used by the nursing staff. Demographic data and self-reported compliance were recorded before and after the intervention. We found that the compliance rate was significantly increased and the application was well accepted by the majority of the staff. We also showed that previous ICU working experience is independently and positively associated with compliance (p=0.02, OR=2.86; 95% CI: 1.16 - 7.06), after adjustment for age and total nursing experience In conclusion, we developed an effective application for quality improvement aiming at facilitating educational processes and enhancing staff compliance.

There is a complex and not fully elucidated association between pulmonary arterial hypertension (PAH) and coagulation disorders. The goal of this study was to evaluate platelet function, coagulation and fibrinolysis in PAH patients at diagnosis, before PAH-specific treatment initiation. We enrolled 20 healthy controls and 30 PAH patients (20 with connective tissue disease (CTD-PAH) and 10 idiopathic (iPAH)). None of the participants was on any antiplatelet or anticoagulation therapy. Blood samples from PAH patients were collected during the initial right heart catheterization. All subjects were assessed with platelet function analyzer-100 (PFA-100), epinephrine (Epi) and ADP-induced light transmission aggregometry (LTA), thromboelastometry (ROTEM) and endogenous thrombin potential (ETP). Our results showed that Epi and ADP-LTA values were significantly lower in newly diagnosed PAH patients compared to controls. Disaggregation was present in 73% of patients, a characteristic not seen in healthy individuals. In ROTEM assay, CT and CFT measurements were significantly higher and a angle lower compared to controls. ETP testing revealed significantly reduced outcomes in AUC, Cmax and Tmax. When CTD-PAH and iPAH patient groups were compared, iPAH ADP-LTA values were significantly decreased compared to CTD-PAH. In conclusion, newly diagnosed PAH patients presented with decreased platelet aggregation, clot propagation and thrombin generation, along with delayed initiation of the coagulation process. These hemostatic deficits could indicate an "exhaustion" of the coagulation process that could be caused by endothelial dysfunction and chronic activation of the procoagulant pathways. Further studies are warranted to confirm these laboratory findings and assess their potential clinical significance.

Background Based on previous animal studies showing promising immunomodulatory efficacy esmolol, a selective β1-blocker, it was assumed that administration of esmolol in experimental pyelonephritis by multidrug-resistant Pseudomonas aeruginosa would prolong survival and modulate immune response. Methods Acute pyelonephritis was induced in 80 rabbits and assigned to eight groups receiving normal saline (controls), esmolol, amikacin, or both agents as pretreatment and as treatment. Blood was sampled for measurement of malondialdehyde and tumor necrosis factor alpha. Animals were followed up for survival, and after death quantitative tissue cultures were performed. The in vitro effect of esmolol on bacterial growth and on the oxidative burst of neutrophils of healthy controls and of sepsis patients was studied. Results Survival of pretreatment groups administered single esmolol or esmolol and amikacin was prolonged compared with that of controls ( P = 0.018 and P = 0.014, respectively); likewise, survival of treatment groups administered single esmolol or both agents was prolonged compared with that of controls ( P = 0.007 and P = 0.014, respectively). Circulating malondialdehyde was significantly lower in pretreated animals administered esmolol or esmolol and amikacin compared with that in controls and in treated animals administered both agents compared with in controls ( P = 0.020). In these groups, the bacterial load of the lung was significantly lower compared with controls. Serum tumor necrosis factor alpha did not change. Amikacin was increased in serum of esmolol-treated animals at levels which inhibited the in vitro growth of the studied isolate. Esmolol did not modify the in vitro growth of P aeruginosa and the oxidative burst of neutrophils. Conclusions It is concluded that esmolol prolonged survival after experimental infection by multidrug-resistant P aeruginosa . Survival benefit may be related with pleiotropic actions connected with modulation of pharmacokinetics and attenuation of inflammation.

Background : To compare the differences between elderly and non-elderly patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) due to viral infections. Methods : Patients with chronic obstructive pulmonary disease (COPD) exacerbation were recruited and classified as elderly (>65 years) and non-elderly (≤ 65 years). Sputum and oropharyngeal samples were assessed, PCR for respiratory viruses and cultures for common pathogens were performed. Results : 247 patients (median age: 69.3±9.5 years) were recruited and categorized into group A: non-elderly patients [n=81 (32.8%), median age 58±5.99] and group B: elderly patients [n=166 (67.2%), median age 74.8±4.8] years. In 133 (53.8%) patients a viral infection was identified and in 34 (13.8%) a bacterial pathogen was isolated from cultures. In 18 (7.3%) patients a double infection (bacterial+viral) was identified. In group B, the presence of cardiac failure (46.6% vs 28.3%, p

Background: Although CTEPH is a thromboembolic disorder, the effect of the coagulation process in the pathogenesis and progression of the disease has not been fully elucidated. Aims: To assess coagulation in CTEPH and to evaluate differences after the initiation of PH-specific treatment. Methods: We studied 20 CTEPH patients (not on anticoagulation therapy at the time of tests) and 20 controls. CTEPH patients were reevaluated 1 year after therapy initiation. We performed Platelet- Function Analyzer/PFA-100 testing, ADP and epinephrine/EPI induced Light Transmission Aggregometry/LTA, Thrombelastometry/ROTEM (na-TEM) and Endogenous Thrombin Potential/ETP essay. Results: Before treatment and when compared to controls, CTEPH patients presented prolonged PFA-100 closure times (174.8sec±27.3, p=0.003), lower EPI and ADP-LTA (43.9%±11.2, p Conclusions: Our data suggest that the observed coagulation defects in CTEPH persist even after PH treatment initiation. EPI-LTA was the only index displaying significant increase after treatment.