WCIM 2014
42 32nd World Congress of Internal Medicine (October 24-28, 2014) OS-RES-08 Critical Care Medicine Ventilator Associated Pneumonia - Incidence, Antibio- gram of Pathogens Isolated and Clinical Outcome
ARJUN KHANNA1
VMMC And Safdarjang Hospital, India1
Background: Ventilator associated pneumonia (VAP) is an important cause of mor- bidity and mortality in mechanically ventilated patients globally. The aim of this study was to fi nd out the incidence of VAP at our institution, to evaluate the antibiotic sen- sitivity pattern of microorganisms isolated and to assess clinical outcome in VAP.
Methods: A total of 107 patients who were not having pneumonia at presentation and who were mechanically ventilated for more than 48 hours for various indications were included in the study. APACHE II score of fi rst day was recorded. The diagnosis of VAP was established using clinical pulmonary infection score of more than 6. Gram staining and culture sensitivity using Kirby –Bauer disc diffusion method was per- formed on all endotracheal aspirates and antibiotic therapy modifi ed accordingly. The results were analysed to determine the incidence and clinical outcome in VAP.
Results: 30 out of 107 patients (28.03%) developed VAP.25 patients developed late onset VAP while 5 developed early onset VAP. Most common isolates were Pseu- domonas aeruginosa (9 isolates) followed by MRSA (8isolates), Klebsiella pnueumo- niae(7 isolates) and Acinetobacter baumanii(6 isolates). Klebsiella pnueumoniae and Acinetobacter baumanii were found to be most lethal. Most isolates of Klebsiella were extended spectrum Beta Lactamase producing and all Acinetobacter were carbape- nem resistant. Mortality in VAP was 46.67% and correlated well with a higher mean APACHE II score of 18.3 as compared to a mortality of 28.57 in non VAP group with a low mean APACHE II score of 13.1.
Conclusion: The development of VAP was associated with increased morbidity and mortality and a higher mean APACHE II score at admission. The incidence of multidrug resistant pathogens is rising and therefore it is important to identify them as this in- formation will help in the selection of an appropriate antibiotic regimen and decrease the treatment costs and improve outcome.
OS-RES-10 Critical Care Medicine Intensive Care Unit Admission is Associated with Poor Outcome in Patients with Mitochondrial DNA M.3243a>g Mutation: A Multicenter Retrospective Study
Emily Han-Chung HSIUE1,2, Ni-Chung LEE3, Pei-Lin LEE1
Department of Interminal Medicine, National Taiwan University Hospital, Taiwan R.O.C1, Department of Oncology, National Taiwan University Hospital, Taiwan R.O.C2, Department of Pediatrics, National Taiwan University Hospital, Taiwan R.O.C3
Background: Mitochondrial DNA 3243A>G, one of the most common pathogenic mitochondrial mutations, often presents in adulthood and is associated with mito- chondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and other syndromes. Due to multi-organ involvement, patients with m.3243A>G frequently require critical care, but the diagnosis often remains unrecognized. This multicenter study aimed to evaluate the prognostic factors of m.3243A>G in Taiwan, and focused on those who had been admitted to ICU.
Methods: Patients diagnosed with m.3243A>G from January 1st 1997 to August 1st 2014 at the National Taiwan University Hospital were identified. Clinical features, laboratory study results, and outcomes were recorded. ICU admission course was reviewed. Prognostic factors for ICU admission, severe disability (defi ned by modifi ed Rankin Scale, mRS≧4), and death were analyzed.
Results: A total of 33 patients were identifi ed, with 19 patients (58%) demonstrating the MELAS phenotype. Thirteen patients (39%) had been admitted to ICU, and 7 (54%) were diagnosed with the mutation after ICU admission. Seizure was the most common cause for ICU admission (n=8), followed by lactic acidosis (n=2), diabetic ketoacidosis (n=1), stroke (n=1), and respiratory failure (n=1). In total, 6 patients (18%) died while 11 patients (33%) developed mRS≧4. Logistic regression analysis identifi ed sympto- matic CNS involvement as a signifi cant predictor of both ICU admission (OR 8.25, 95%
CI 1.43-47.58, p=0.018) and development of mRS≧4 (OR 14.44, 95% CI 1.56-133.58, p=0.019); while Kaplan Meier analysis showed that ICU admission was signifi cantly associated with mortality (log-rank test p=0.012, Fig.).
Conclusions: Patients with m.3243A>G often remained undiagnosed until severe complications requiring critical care have developed. Investigation for possible mito- chondrial disease is warranted in cases of unexplained seizure, stroke, lactic acidosis, and respiratory failure.
OS-RES-11 Respiratory Medicine Tetrahdrobiopterin(BH4): Novel Treatment for Pulmo- nary Hypertension
Bahaa FRANCIS1 Rivka Ziv Medical Centre, Israel1
Background: Pulmonary Hypertension (PH) is characterized by pulmonary vaso- constriction, vascular remodeling, right heart failure and death. The pathogenesis is multifactorial. The integrity of the pulmonary vascular endothelium, particularly its en- dothelial nitric oxide synthase (eNOS), is a key factor in maintaining normal pulmonary vascular homeostasis. While enzymatically coupled, eNOS produces nitric oxide (NO), otherwise eNOS activation may lead to increased superoxide production. The cofactor tetrahydrobiopterin (BH4) is an important regulator of eNOS function; by ‘recoupling’
eNOS and enhancing its enzymatic activity, BH4 increases NO bioavailability and de- creases superoxide production. Thus pharmacological supplementation with BH4 may be a novel treatment in PH.
Methods: Isolated perfused lung studies were used to explore the acute pharmacolog- ical effects of BH4 in regulating pulmonary vascular tone. Animal studies were used to evaluate the pharmacological effects of BH4 treatment and to clarify its molecular mechanism using biochemical and histological experiments.
Results: In acute ex-vivo studies, BH4 was found to regulate hypoxic pulmonary vasoconstriction. Its effects are mediated via enhancing NO and H2O2 secretion and its antioxidant properties, all leading to pulmonary vasodilation. Superoxide dismutase co-administration with BH4 enhanced its vasodilatory effect. In chronic studies, BH4 prevented the development of PH in monocrotaline model and ameliorated established PH when administered to recover the disease. BH4 partially reversed PH in hypoxia model. In both models, BH4 reduced pulmonary vascular muscularization and reversed right ventricular hypertrophy. BH4 effect was evidenced by enhancing the activity and protein levels of eNOS, recoupling eNOS activity to produce more NO, and its second messenger cGMP, and lowering the levels of superoxide.
Conclusions: BH4 bioavailability is essential for maintaining pulmonary vascular ho- meostasis, and plays a major role in the pathophysiology of PH. This study establishes a fi rm basis to explore the therapeutic potential of BH4 in human PH.
