Validation of the Predisposition Infection Response Organ (PIRO) dysfunction score for the prognostic stratification of patients with sepsis in the Emergency Department / Validación del sistema PIRO (predisposición, infección, respuesta, fallo orgánico) para la estratificación del pronóstico en pacientes con sepsis en el servicio de urgencias

Objective: There are many different methods for computing the Predisposition Infection Response Organ (PIRO) dysfunction score. We compared three PIRO methods (PIRO1 (Howell), PIRO2 (Rubulotta) and PIRO3 (Rathour)) for the stratification of mortality and high level of care admission in septic patients arriving at the Emergency Department (ED) of an Italian Hospital. Design, setting and participants We prospectively collected clinical data of 470 patients admitted due to infection in the ED to compute PIRO according to three different methods. We tested PIRO variables for the prediction of mortality in the univariate analysis. Calculation and comparison were made of the area under the receiver operating curve (AUC) for the three PIRO methods, SOFA and qSOFA. Results Most of the variables included in PIRO were related to mortality in the univariate analysis. Increased PIRO scores were related to higher mortality. In relation to mortality, PIRO 1 performed better than PIRO2 at 30 d ((AUC 0.77 (0.716–0.824) vs. AUC 0.699 (0.64–0.758) (p=0.03) and similarly at 60 d (AUC 0.767 (0.715–0.819) vs AUC 0.709 (0.656–0.763)(p=0.55)); PIRO1 performed similarly to PIRO3 (AUC 0.765 (0.71–0.82) at 30 d, AUC 0.754 (0.701–0.806) at 60 d, p=ns). Both PIRO1 and PIRO3 were as good as SOFA referred to mortality (AUC 0.758 (0.699, 0.816) at 30 d vs. AUC 0.738 (0.681, 0.795) at 60 d; p=ns). For high level of care admission, PIRO proved inferior to SOFA. Conclusions We support the use of PIRO1, which combines ease of use and the best performance referred to mortality over the short term. PIRO2 proved to be less accurate and more complex to use, suffering from missing microbiological data in the ED setting. (AU)

Objetivo: Existen muchos métodos diferentes para calcular la escala PIRO (predisposición, infección respuesta, fallo orgánico). Comparamos 3 métodos (PIRO1 [Howell], PIRO2 [Rubolotta] y PIRO3 [Rathour]) para estratificar la mortalidad y el ingreso con alto nivel de cuidados en pacientes con sepsis atendidos en el servicio de urgencias (SU) de un hospital italiano. Diseño, entorno y participantes Recopilamos datos clínicos prospectivos de 470 pacientes que llegaban con una infección al SU, con el fin de calcular la puntuación PIRO, de acuerdo con 3 métodos diferentes. Evaluamos las variables PIRO para la predicción de la mortalidad en un análisis monovariable. Calculamos y comparamos el área bajo la curva (AUC) característica de operación del receptor (ROC) de los 3 métodos PIRO, SOFA y qSOFA. Resultados La mayoría de las variables incluidas en las puntuaciones PIRO estaban relacionadas con la mortalidad en un análisis de una sola variable. El aumento de la puntuación PIRO se relacionó con una mortalidad más elevada. En cuanto a la mortalidad, PIRO1 presentó un rendimiento mejor que PIRO2 a los 30 días (AUC 0,77 [0,716-0,824] frente a AUC 0,699 [0,64-0,758]; p=0,03) y similares a los 60 días (AUC 0,767 [0,715-0,819] frente a AUC 0,709 [0,656-0,763]; p=0,55); PIRO1 presentó un rendimiento similar al de PIRO3 (AUC 0,765 [0,71-0,82] a los 30 días, AUC 0,754 [0,701-0,806] a los 60 días; p=NS). Tanto PIRO1 como PIRO3 presentaron un rendimiento similar al de SOFA para la mortalidad (AUC 0,758 [0,699-0,816) al cabo de 30 días y AUC 0,738 [0,681-0,795] al cabo de 60 días; p=NS). En cuanto al ingreso con alto nivel de cuidados, las puntuaciones PIRO resultaron ser inferiores a SOFA. Conclusiones Apoyamos el uso de la puntuación PIRO1, que resulta fácil de usar, y presenta el mejor rendimiento en cuanto a la mortalidad a largo plazo. PIRO2 resultó ser menos precisa y más compleja de usar ... (AU)

Validation of the Predisposition Infection Response Organ (PIRO) dysfunction score for the prognostic stratification of patients with sepsis in the Emergency Department.

OBJECTIVE: There are many different methods for computing the Predisposition Infection Response Organ (PIRO) dysfunction score. We compared three PIRO methods (PIRO1 (Howell), PIRO2 (Rubulotta) and PIRO3 (Rathour)) for the stratification of mortality and high level of care admission in septic patients arriving at the Emergency Department (ED) of an Italian Hospital. DESIGN, SETTING AND PARTICIPANTS: We prospectively collected clinical data of 470 patients admitted due to infection in the ED to compute PIRO according to three different methods. We tested PIRO variables for the prediction of mortality in the univariate analysis. Calculation and comparison were made of the area under the receiver operating curve (AUC) for the three PIRO methods, SOFA and qSOFA. RESULTS: Most of the variables included in PIRO were related to mortality in the univariate analysis. Increased PIRO scores were related to higher mortality. In relation to mortality, PIRO 1 performed better than PIRO2 at 30 d ((AUC 0.77 (0.716-0.824) vs. AUC 0.699 (0.64-0.758) (p=0.03) and similarly at 60 d (AUC 0.767 (0.715-0.819) vs AUC 0.709 (0.656-0.763)(p=0.55)); PIRO1 performed similarly to PIRO3 (AUC 0.765 (0.71-0.82) at 30 d, AUC 0.754 (0.701-0.806) at 60 d, p=ns). Both PIRO1 and PIRO3 were as good as SOFA referred to mortality (AUC 0.758 (0.699, 0.816) at 30 d vs. AUC 0.738 (0.681, 0.795) at 60 d; p=ns). For high level of care admission, PIRO proved inferior to SOFA. CONCLUSIONS: We support the use of PIRO1, which combines ease of use and the best performance referred to mortality over the short term. PIRO2 proved to be less accurate and more complex to use, suffering from missing microbiological data in the ED setting.

False-negative real-time polymerase chain reaction tests in COVID-19 patients: an epidemiological analysis of 302 patients.

OBJECTIVES: Patients who arrive at the emergency department (ED) with COVID-19, who test negative at the first real-time polymerase chain reaction (RT-PCR), represent a clinical challenge. This study aimed to evaluate if the clinical manifestation at presentation, the laboratory and imaging results, and the prognosis of COVID-19 differ in patients who tested negative at the first RT-PCR compared with those who tested positive and also to evaluate if comorbid conditions patient-related or the period of arrival are associated with negative testing. STUDY DESIGN: We retrospectively collected clinical data of patients who accessed the ED from March 1 to May 15, 2020. METHODS: We compared clinical variables, comorbid conditions, and clinical outcomes in the two groups by univariate analysis and logistic regression. RESULTS: Patients who tested negative at the first RT-PCR showed a higher prevalence of cardiopathy, immunosuppression, and diabetes, as well as a higher leukocyte and lower lymphocyte counts compared with patients who tested positive. A bilateral interstitial syndrome and a typical pattern at computed tomography scan were prevalent in the test-negative group. Test-negative patients were more likely to be admitted to the hospital but less likely to need admission in a high level of care ward. The false-negative rate increased from March to May. CONCLUSION: False-negative RT-PCR COVID-19 patients present a similar spectrum of symptoms compared with positive cohort, but more comorbidities. Imaging helps to identify them. True positives had a higher risk of serious complications.

Validation of the Predisposition Infection Response Organ (PIRO) dysfunction score for the prognostic stratification of patients with sepsis in the Emergency Department.

OBJECTIVE: There are many different methods for computing the Predisposition Infection Response Organ (PIRO) dysfunction score. We compared three PIRO methods (PIRO1 (Howell), PIRO2 (Rubulotta) and PIRO3 (Rathour)) for the stratification of mortality and high level of care admission in septic patients arriving at the Emergency Department (ED) of an Italian Hospital. DESIGN, SETTING AND PARTICIPANTS: We prospectively collected clinical data of 470 patients admitted due to infection in the ED to compute PIRO according to three different methods. We tested PIRO variables for the prediction of mortality in the univariate analysis. Calculation and comparison were made of the area under the receiver operating curve (AUC) for the three PIRO methods, SOFA and qSOFA. RESULTS: Most of the variables included in PIRO were related to mortality in the univariate analysis. Increased PIRO scores were related to higher mortality. In relation to mortality, PIRO 1 performed better than PIRO2 at 30 d ((AUC 0.77 (0.716-0.824) vs. AUC 0.699 (0.64-0.758) (p=0.03) and similarly at 60 d (AUC 0.767 (0.715-0.819) vs AUC 0.709 (0.656-0.763)(p=0.55)); PIRO1 performed similarly to PIRO3 (AUC 0.765 (0.71-0.82) at 30 d, AUC 0.754 (0.701-0.806) at 60 d, p=ns). Both PIRO1 and PIRO3 were as good as SOFA referred to mortality (AUC 0.758 (0.699, 0.816) at 30 d vs. AUC 0.738 (0.681, 0.795) at 60 d; p=ns). For high level of care admission, PIRO proved inferior to SOFA. CONCLUSIONS: We support the use of PIRO1, which combines ease of use and the best performance referred to mortality over the short term. PIRO2 proved to be less accurate and more complex to use, suffering from missing microbiological data in the ED setting.

Characterization and subtyping of Cronobacter spp. from imported powdered infant formulae in Argentina.

Cronobacter spp. (Enterobacter sakazakii), have been associated with severe foodborne infections in neonates and immunocompromised infants. In Argentina, we have isolated Cronobacter spp. from three different brands of imported powdered infant formulae (PIF). The objectives of this work were to characterize the recovered isolates phenotypically and to evaluate the use of a Pulsed-Field Gel Electrophoresis (PFGE) protocol for Cronobacter spp. subtyping. Out of 23 isolates studied from three brands of PIF (20 of brand A, 1 of brand B and 2 of brand C), 22 were identified as C. sakazakii and 1 as C. malonaticus. All isolates were susceptible to twelve antimicrobial agents assayed. The 19 C. sakazakii isolates of brand A showed five XbaI-PFGE patterns and the genetic clusters revealed by XbaI were confirmed with a second restriction enzyme, SpeI. The isolate from brand B showed the same XbaI and SpeI patterns as those of a group of isolates of brand A, suggesting a possible common source of contamination. The C. sakazakii isolates of brand C exhibited two unique XbaI-PFGE patterns, unrelated to the rest. Different genetic subtypes were found among isolates of a single batch of PIF from brand A and the single C. malonaticus strain also showed a distinct XbaI-PFGE pattern.

Impaired synthesis and action of antiaggregating cyclic nucleotides in platelets from obese subjects: possible role in platelet hyperactivation in obesity.

BACKGROUND: Subjects with central obesity exhibit platelet hyperactivity, which is involved in the atherosclerotic process and therefore can account for the increased risk of cardiovascular morbidity and mortality. The aim of the study was to evaluate whether alterations of platelet function in obesity involve synthesis and/or action of the two antiaggregating cyclic nucleotides adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP). MATERIALS AND METHODS: In platelets from 16 obese and 15 control subjects we investigated the influence on platelet responses to the Adenosine-5-diphosphate sodium salt (ADP) exerted by (i) prostacyclin analogue Iloprost (0.31-5 nmol L(-1)) and the cAMP analogue 8-bromo-cAMP (10-500 micro mol L(-1)); and by (ii) nitric oxide (NO) donor sodium nitroprusside (SNP) (5-100 micro mol L(-1)) and the cGMP analogue 8-bromo-cGMP (10-500 micro mol L(-1)). IC(50) (minimal concentration of each inhibitor necessary to reduce platelet response to ADP by half) was determined. Iloprost and SNP ability to increase cyclic nucleotides was also measured. RESULTS: Significantly greater IC(50) were observed in obese subjects than in healthy controls (1.59 +/- 0.16 vs. 0.80 +/- 0.08 nmol L(-1), P = 0.0001 for Iloprost, and 27.6 +/- 6.5 vs. 7.0 +/- 1.7 micro mol L(-1), P = 0.006, for SNP); when data from control and obese subjects were pooled together, IC(50) of Iloprost and SNP correlated with the homeostasis model assessment (HOMA IR), which is a parameter used to measure the insulin resistance (r = 0.588, P = 0.029 and r = 0.640, P = 0.006, respectively). Also the antiaggregating effect of 8-Br-cAMP and 8-Br-cGMP was smaller in the obese subjects. Finally, the ability of Iloprost to increase platelet cAMP and the ability of SNP to increase both cGMP and cAMP were reduced in obese subjects. CONCLUSIONS: Platelet resistance to the antiaggregating effects of prostacyclin and NO in obesity is attributable to impairment of cyclic nucleotide synthesis and action. As cyclic nucleotides are the main effectors of platelet antiaggregation, the resistance to them can account for platelet hyperactivity in obesity.