[The 2013 Seville Consensus Document on alternatives to allogenic blood transfusion. An update on the Seville Document]. / 2013. Documento Sevilla de Consenso sobre Alternativas a la Transfusión de Sangre Alogénica. Actualización del Documento Sevilla.

Since allogeneic blood transfusion (ABT) is not harmless, multiple alternatives to ABT (AABT) have emerged, though there is great variability in their indications and appropriate use. This variability results from the interaction of a number of factors, including the specialty of the physician, knowledge and preferences, the degree of anemia, transfusion policy, and AABT availability. Since AABTs are not harmless and may not meet cost-effectiveness criteria, such variability is unacceptable. The Spanish Societies of Anesthesiology (SEDAR), Hematology and Hemotherapy (SEHH), Hospital Pharmacy (SEFH), Critical Care Medicine (SEMICYUC), Thrombosis and Hemostasis (SETH) and Blood Transfusion (SETS) have developed a Consensus Document for the proper use of AABTs. A panel of experts convened by these 6 Societies have conducted a systematic review of the medical literature and have developed the 2013 Seville Consensus Document on Alternatives to Allogeneic Blood Transfusion, which only considers those AABT aimed at decreasing the transfusion of packed red cells. AABTs are defined as any pharmacological or non-pharmacological measure aimed at decreasing the transfusion of red blood cell concentrates, while preserving patient safety. For each AABT, the main question formulated, positively or negatively, is: « Does this particular AABT reduce the transfusion rate or not?¼ All the recommendations on the use of AABTs were formulated according to the Grades of Recommendation Assessment, Development and Evaluation (GRADE) methodology.

[The 2013 Seville Consensus Document on alternatives to allogenic blood transfusion. An update on the Seville Document]. / 2013. Documento Sevilla de Consenso sobre Alternativas a la Transfusión de Sangre Alogénica. Actualización del Documento Sevilla.

Since allogeneic blood transfusion (ABT) is not harmless, multiple alternatives to ABT (AABT) have emerged, though there is great variability in their indications and appropriate use. This variability results from the interaction of a number of factors, including the specialty of the physician, knowledge and preferences, the degree of anemia, transfusion policy, and AABT availability. Since AABTs are not harmless and may not meet cost-effectiveness criteria, such variability is unacceptable. The Spanish Societies of Anesthesiology (SEDAR), Hematology and Hemotherapy (SEHH), Hospital Pharmacy (SEFH), Critical Care Medicine (SEMICYUC), Thrombosis and Hemostasis (SETH) and Blood Transfusion (SETS) have developed a Consensus Document for the proper use of AABTs. A panel of experts convened by these 6 Societies have conducted a systematic review of the medical literature and have developed the 2013 Seville Consensus Document on Alternatives to Allogeneic Blood Transfusion, which only considers those AABT aimed at decreasing the transfusion of packed red cells. AABTs are defined as any pharmacological or non-pharmacological measure aimed at decreasing the transfusion of red blood cell concentrates, while preserving patient safety. For each AABT, the main question formulated, positively or negatively, is: "Does this particular AABT reduce the transfusion rate or not?" All the recommendations on the use of AABTs were formulated according to the Grades of Recommendation Assessment, Development and Evaluation (GRADE) methodology.

Usefulness of procalcitonin clearance as a prognostic biomarker in septic shock. A prospective pilot study

Objective: To evaluate procalcitonin clearance as a prognostic biomarker in septic shock. Design: Prospective, observational pilot study. Setting: Intensive care unit. Patients: Patients admitted to the ICU due to septic shock and multiorgan dysfunction. Interventions: Serum concentrations of procalcitonin were determined within 12h of onset of septic shock and multiorgan dysfunction (coinciding with admission to the ICU), and the following extractions were obtained after 24, 48 and 72h in patients who survived. Data collected: Demographic data, Acute Physiology and Chronic Health Evaluation II score, and Sequential Organ Failure Assessment score, data on the primary focus of infection, and patient outcome (ICU mortality). Results: Procalcitonin clearance was higher in survivors than in non-survivors, with significant differences at 24h (73.9 [56.4-83.8]% vs 22.7 [-331-58.4], p<0.05) and 48h (81.6 [71.6-91.3]% vs -7.29 [-108.2-82.3], p<0.05). The area under the ROC curve was 0.74 (95%CI, 0.54-0.95, p<0.05) for procalcitonin clearance at 24h, and 0.86 (95%CI, 0.69-1.0, p<0.05) at 48h. Conclusions: ICU mortality was associated to sustained high procalcitonin levels, suggesting that procalcitonin clearance at 48h may be a valuable prognostic biomarker (AU)

Objetivo: Evaluar el aclaramiento de procalcitonina como biomarcador pronóstico del shock séptico. Diseño: Estudio piloto, observacional y prospectivo. Ámbito: Servicio de Medicina Intensiva. Pacientes: Enfermos ingresados en el Servicio de Medicina Intensiva por shock séptico y disfunción multiorgánica. Intervenciones: Determinación de las concentraciones séricas de procalcitonina en las primeras 12h de evolución del shock séptico (coincidiendo con el ingreso en el Servicio de Medicina Intensiva) y posteriormente a las 24 horas, 48 horas y a las 72 horas en los pacientes supervivientes. Variables recogidas: datos demográficos, score Acute Physiology and Chronic Health Evaluation II, score Sequential Organ Failure Assessment, datos relativos al foco de sepsis y al resultado del paciente (mortalidad en el Servicio de Medicina Intensiva). Resultados: El aclaramiento de procalcitonina fue mayor en los pacientes supervivientes respecto a los no supervivientes, con diferencias significativas a las 24 horas (73,9 [56,4-83,8]% vs 22,7 [-331-58,4], p<0,05) y las 48 horas (81,6 [71,6-91,3]% vs -7,29 [-108,2-82,3], p<0,05). El área por debajo de la curva ROC fue 0,74 (IC del 95%, 0,54 a 0,95, p<0,05) para el aclaramiento de procalcitonina a las 24 horas y 0,86 (IC del 95%, 0,69 a 1,0, p<0,05) para el aclaramiento de procalcitonina a las 48 horas. Conclusiones: La persistencia de concentraciones elevadas de procalcitonina se asoció a una mayor mortalidad. El aclaramiento de procalcitonina realizado a las 48h puede ser de utilidad como biomarcador pronóstico (AU)

Usefulness of procalcitonin clearance as a prognostic biomarker in septic shock. A prospective pilot study.

OBJECTIVE: To evaluate procalcitonin clearance as a prognostic biomarker in septic shock. DESIGN: Prospective, observational pilot study. SETTING: Intensive care unit. PATIENTS: Patients admitted to the ICU due to septic shock and multiorgan dysfunction. INTERVENTIONS: Serum concentrations of procalcitonin were determined within 12h of onset of septic shock and multiorgan dysfunction (coinciding with admission to the ICU), and the following extractions were obtained after 24, 48 and 72h in patients who survived. DATA COLLECTED: Demographic data, Acute Physiology and Chronic Health Evaluation II score, and Sequential Organ Failure Assessment score, data on the primary focus of infection, and patient outcome (ICU mortality). RESULTS: Procalcitonin clearance was higher in survivors than in non-survivors, with significant differences at 24h (73.9 [56.4-83.8]% vs 22.7 [-331-58.4], p<0.05) and 48h (81.6 [71.6-91.3]% vs -7.29 [-108.2-82.3], p<0.05). The area under the ROC curve was 0.74 (95%CI, 0.54-0.95, p<0.05) for procalcitonin clearance at 24h, and 0.86 (95%CI, 0.69-1.0, p<0.05) at 48h. CONCLUSIONS: ICU mortality was associated to sustained high procalcitonin levels, suggesting that procalcitonin clearance at 48h may be a valuable prognostic biomarker.

Microvascular angina pectoris in hypertensive patients with left ventricular hypertrophy and diagnostic value of exercise thallium-201 scintigraphy.

In a series of 120 hypertensive patients, 60 were found to have echocardiographic left ventricular (LV) hypertrophy (Devereux's method). Of these, 18 (30%) had typical stress-induced angina and underwent coronary angiography, which showed that 11 (61%) had normal coronary arteries, and 7 (39%) (p < 0.05) had coronary stenosis of the epicardial arteries. Stress-rest thallium-201 scintigraphy (Burow's quantitative method) yielded abnormal results in 21 of the 60 patients with LV hypertrophy. Five of 30 (17%) were asymptomatic, 14 of 18 (78%) had angina, and 2 of 12 (17%) had dyspnea on exertion. In 5 normal patients used as a control group, coronary flow reserve after administration of papaverine (10 coronary arteries) was 6.25 +/- 1.4 versus 3.7 +/- 0.8 in 10 thallium-negative, asymptomatic hypertensive patients with LV hypertrophy (p < 0.001). The mean coronary flow reserve of 21 patients with abnormal thallium-201 results was 2.71 +/- 0.96 (p < 0.01 compared with the group with normal thallium-201 findings) and 2.5 +/- 0.6 in the segments with lowest uptake (p < 0.05 compared with normal segments in these same patients). Thus, stress-induced angina pectoris in hypertensive patients with LV hypertrophy was due to small-vessel disease in over half of our patients (62%).

Interleukin-10 and the monocyte/macrophage-induced inflammatory response in septic shock.

Interleukin (IL)-10 is a potent immunosuppressant of monocyte/macrophage function and may help control the inflammatory response induced by bacterial infection. To analyze whether IL-10 is detectable in plasma of patients with septic shock and to evaluate its relationship with endotoxin (lipopolysaccharide [LPS])-induced and monocyte/macrophage-induced inflammatory response, plasma IL-10, tumor necrosis factor (TNF)-alpha, IL-1 beta, IL-6, IL-8, LPS, and neopterin were studied in 24 patients with septic shock and in 12 critically ill patients. Eighty-three percent of patients with septic shock and 25% of critically ill patients had detectable levels of IL-10 (P < .001). There was a significant correlation between plasma IL-10, neopterin (r = .72), TNF-alpha (r = .76), IL-6 (r = .68), and IL-8 (r = .61) levels in patients with septic shock. Monocyte/macrophage activation leads to massive secretion of IL-10, which, however, seems to be unable to control the increased production of proinflammatory mediators during septic shock.

Inflammatory mediators and their influence on haemostasis.

Sepsis is the most important cause of mortality in the Intensive Care Units. At present, sepsis is understood to be the inflammatory response of the host to infection, rather than a direct effect of microbial aggression. From the clinical standpoint, this inflammatory response is known as systemic inflammatory response syndrome (SIRS). Pathophysiologically, SIRS is characterized by the activation of several groups of cell (monocytes/macrophages, PMNs, and endothelial cells) and by the release of inflammatory mediators (cytokines and others). Tumor necrosis factor (TNF) is the first cytokine released by endotoxin action over monocyte/macrophage. TNF secretion, modulated by interferon gamma (IFN gamma) and interleukin 10 (IL-10), is followed by release of other cytokines such as interleukins (IL) (IL-1, IL-6 and IL-8). These mediators are able to act over hemostasis activating the extrinsic pathway through tissue factor expression. The action of the mediators over endothelial cells induces an increase in plasminogen activator inhibitor type 1 (PAI-1) levels with inhibition of fibrinolysis. Both coagulation activation and fibrinolysis blockade result in fibrin deposit in the microvascular system. The complexity of the mechanisms implicated in systemic inflammatory response make a general rule so difficult to establish, because patient response is highly individualized and it is not possible to know which moment of this dynamic process is being analyzed.

Functional and organic components of diastolic dysfunction in hypertensive heart disease: therapeutic implications.

The major structural and functional determinants of impaired left ventricular diastolic function in the hypertensive patient are reviewed, together with the indices normally used to detect this failure. The alteration of functional determinants can be quickly modified, while structural determinants are modified only over the long term. Drug therapy first affects the functional determinants, bringing about their attenuation and initiating the modification of the structural factors, thus accounting for the improvement in diastolic function over the long term.

Classification of hypertensive cardiomyopathy.

A clinical pathophysiological classification of hypertensive cardiomyopathy has been established on the basis of the degree to which the heart is affected by chronic, systemic arterial hypertension: Degree I: Asymptomatic patients without left ventricular hypertrophy but with left ventricular diastolic dysfunction according to Doppler mitral inversion relation (E/A < 0.9) or to gamma scintigraphy (peak filling rate reduction < or = 2.7 EDC.s-1. These patients are classified as Group 1. Degree II: Asymptomatic or mildly symptomatic patients (New York Heart Association class I) with echocardiographic left ventricular hypertrophy; classified as Group IIA or IIB according to whether weight-adjusted maximal oxygen uptake is normal or below normal, respectively. Degree III: The basic characteristic is the presence of congestive heart failure with normal ejection fraction (EF > or = 50%). Two subsets can be distinguished on the basis of degree of hypertrophy: Group IIIA, with a mass/volume index > 1.8, and IIIB with a mass/volume index < 1.8. The differences between the two are as follows: patients classified as IIIA had a lower rate of regional ischaemia, a higher ejection fraction, a more frequently audible fourth sound, rarely a third sound and a cardiothoracic ratio < 0.5; IIIB patients had a higher prevalence of regional ischaemia (thallium-positive), a frequently audible third sound and a cardiothoracic ratio > 0.5. Degree IV: This category is characterized by the presence of depressed contractility, which could cause heart failure, by an ejection fraction < 50% and an increase in ventricular volumes. Echocardiography shows increased distance between mitral point E and the septum.

[Snake bites in our environment. A biannual review of 7 cases]. / Mordeduras de serpientes en nuestro medio. A propósito de una revisión bianual de siete casos.

The clinical picture, treatment and evolution of seven patients presenting snake bites are analyzed. Local symptoms were constant, with a spontaneous favorable evolution in 7 to 10 days. The most relevant systemic manifestations were coagulation anomalies which appeared in two patients. Treatment always included local wound care, antitetanicum antibiotic and anticoagulant prophylaxis with specific antiophidic serum in five patients.

[Isotopic radioangiography in hepatic cirrhosis. Changes induced by somatostatin]. / Radioangiografía isotópica en la cirrosis hepática. Modificaciones inducidas por la somatostatina.

The value of first step isotopic angiography (FSIA) with 99-TC in the study of altered liver kidney and spleen circulation in patients with liver cirrhosis and alcoholic hepatitis is analyzed. This technique is used to evaluate the effect of a 250 mcg IV bolus of somatostatin on the activity/time curve at the three circulatory levels. The ratio of basal hepatic artery/portal flow in cirrhotics was 59 + 11/41 + 11% and 39 + 6/61 + 4 in alcoholic hepatitis, significantly different from normal controls (p less than 0.001). In cirrhotics the degree of alteration in FSIA correlated with the severity of liver disease. Somatostatin significantly improved the ratio of basel hepatic artery/portal flow and diminished the pressure at the root of suprahepatic veins (18.5 +/- - v.s. 16 +/- mmHg, p greater than 0.001). Neither the slopes nor the time of maximum isotopic activity of renal and splenic activity/time curves were modified. We concluded highlighting the clinical value of FSIA as a non invasive test in the study of chronic liver diseases.

[Somatostatin and ventricular function in liver cirrhosis]. / Somatostatina y función ventricular en cirrosis hepática.

Left ventricular function is studied in cirrhotic patients and in patients with alcoholic hepatitis by means of isotopic ventriculography (Tc99m) both in basal conditions and after the i.v. injection of a somatostatin bolus (250 mcg). The results obtained are compared to those of conventional hemodynamics. Basal ventricular function is normal in both groups and somatostatin induces a significant decrease (p less than 0.001) in heart rate (74 + 12 vs 67 + 11 bpm), ejection fraction (60 + 6 vs 57 + 65) and maximal ejection rate (-3.3 + 0.4 vs -2.0 + 0.3) in patients and normal controls respectively. The hormone induces a significant increase (p less than 0.01) in telediastolic pressure of the left ventricle (8.1 + 4 vs 21 + 7 mmHg) with no change in systemic resistance. The results suggest that somatostatin has a negative inotropic effect on the heart as well as causing bradycardia.