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Rodrigo F Alban

Publications and source records attributed to Rodrigo F Alban.

5 recordsLinked to original sources
PubMed2006

Readmission to surgical intensive care increases severity-adjusted patient mortality.

BACKGROUND: This study aims to determine whether severity-adjusted outcomes including mortality are adversely impacted by readmission to a surgical intensive care unit (SICU) during the same hospital stay. METHODS: The study included all patients admitted to the 20-bed tertiary care SICU in an urban teaching Level I trauma center and multiorgan transplant center from January 1, 1996 to December 31, 2001. This was a prospective observational study with secondary data analysis. Acute Physiology and Chronic Health Evaluation (APACHE II) and Simplified Acute Physiology (SAPS) severity scores were calculated by a clinical information system. Outcomes were extracted from a computerized data warehouse. RESULTS: In-hospital mortality and SICU length of stay (LOS) were measured for patients admitted and readmitted to the SICU. Of 10,840 patients admitted to the SICU, 296 (2.73%) required readmission to the SICU during the same hospital stay. The length of the original SICU stay was 4.9 +/- 6.7 days for readmitted patients compared with 3.2 +/- 6.0 days for nonreadmitted patients (p < 0.001). Readmitted patients had a higher mean APACHE II score on the day of original SICU discharge compared with nonreadmitted patients, 15.7 +/- 6.7 versus 13.8 +/- 7.1 (p < 0.001). The average APACHE II score increased from 15.7 +/- 6.7 to 18.1 +/- 8.6 between the day of SICU discharge and readmission (p < 0.001) and SAPS increased from 12.2 +/- 4.8 to 13.5 +/- 5.4 (p < 0.001). The distributions of severity-adjusted hospital mortality for both APACHE II and SAPS revealed that readmission to the SICU significantly increased mortality independent of the admission severity score. CONCLUSIONS: Readmission to the SICU significantly increases the risk of death beyond that predicted by the APACHE II or SAPS scores alone. Higher APACHE II and SAPS scores upon discharge from the SICU and longer SICU LOS are associated with an increased incidence of readmission to the SICU on the same hospital stay. These results may be used to optimize the timing of SICU discharge and reduce the chance of readmission to intensive care.

APACHE↗
PubMed2006

Obesity does not affect mortality after trauma.

Although obesity has been proposed as a risk factor for adverse outcomes after trauma, numerous studies report conflicting results. The objective of this study was to compare outcomes of obese and nonobese patients after trauma. The study population consisted of all trauma patients admitted to a surgical intensive care unit in a Level I trauma center from January 1999 to December 2002. Admission data, demographics, injury severity score (ISS), severity of illness, hospital course, complications, and outcomes were compared between obese (OB; body mass index [BMI] > or = 30), and nonobese patients (NOB; BMI < or = 29). A total of 918 patients was included in the study, 135 OB (14.7%) and 783 NOB (85.3%). There was no significant difference in demographic data, ISS, APACHE II score, and hospital stay. Intensive care unit stay was longer for OB patients (6.8 vs 4.8 days, P = 0.04). Overall mortality was 5.9 per cent for OB and 8.0 per cent for NOB patients (P = 0.48). Mortality by mechanism of injury was 3.4 per cent OB versus 7.4 per cent NOB (P = 0.26) for blunt and 10.6 per cent OB versus 10.2 per cent NOB (P = 0.9) for penetrating injury. The three most common complications associated with death were pulmonary, cardiovascular, and neurological deterioration. Using logistic regression analysis, age and ISS and APACHE II scores were associated with mortality, but BMI was not. We conclude that obesity does not appear to be a risk factor for adverse outcomes after blunt or penetrating trauma. Further research is warranted to uncover the reason for discrepant findings between centers.

APACHE↗
PubMed2003

Regulation of activin A expression in mast cells and asthma: its effect on the proliferation of human airway smooth muscle cells.

Activin A, a homodimeric protein (betaAbetaA) and a member of the TGF-beta superfamily, is involved in the inflammatory repair process. Using cDNA microarray analysis, we discovered strong induction of the activin betaA gene in human mast cells (MC) on stimulation with PMA and calcium ionophore (A23187). Activin betaA mRNA was also highly induced in primary cultured murine bone marrow MC (BMMC) after stimulation by IgE receptor cross-linking. Secretion of activin A was evident in human mast cell-1 line cells 3 h after stimulation and progressively increased over time. Activin A was present in the cytoplasm of activated but not unstimulated murine bone marrow MC as demonstrated by immunofluorescence studies, suggesting that secretion of activin A by MC was due to de novo synthesis rather than secretion of preformed protein. Activin A also colocalized with human lung MC from patients with asthma by double-immunofluorescence staining. Furthermore, secretion of activin A was significantly increased in the airway of wild-type mice after OVA sensitization followed by intranasal challenge. Secretion of activin A, however, was greatly reduced in MC-deficient WBB6F(1)-W/W(v) mice as compared with wild-type mice, indicating that MC are an important contributor of activin A in the airways of a murine asthma model. Additionally, activin A promoted the proliferation of human airway smooth muscle cells. Taken together, these data suggest that MC-derived activin A may play an important role in the process of airway remodeling by promoting the proliferation of airway smooth muscle.

Activins↗
PubMed2002

PAI-1 promotes extracellular matrix deposition in the airways of a murine asthma model.

Dysregulation of matrix metalloproteinases (MMPs) and ineffective fibrinolysis are associated with the deposition of extracellular matrix (ECM). We hypothesized that elevated plasminogen activator inhibitor (PAI)-1 promotes ECM deposition in the asthmatic airway by inhibiting MMP-9 activity and fibrinolysis. Degree of airway inflammation was similar in PAI-1(-/-) and wild type (WT) mice after ovalbumin (OVA) challenge. PAI-1 production, deposition of collagen and fibrin, and MMP-9 activity in the lung tissue or airways were greater after OVA challenge compared with saline challenge. However, in PAI-1(-/-) mice, collagen deposition was 2-fold less, fibrin deposition was 4-fold less, and MMP-9 activity was 3-fold higher. This is the first direct evidence that the plasmin system regulates ECM deposition in the airways of a murine asthma model, independently of the effect of PAI-1 on inflammatory cells. The results suggest that the PAI-1-dependent inhibition of MMP-9 activity and fibrinolysis is a major mechanism by which ECM deposition occurs.

Animals↗