[Alveolar proteinosis. Treatment with total lung lavage].
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Bronchoalveolar Lavage↗
Biomedical subjects
C Montón
Publications and source records attributed to C Montón.
Comparison of systemic cytokine levels in patients with acute respiratory distress syndrome, severe pneumonia, and controls.
BACKGROUND: The inflammatory response has been widely investigated in patients with acute respiratory distress syndrome (ARDS) and pneumonia. Studies investigating the diagnostic values of serum cytokine levels have yielded conflicting results and only little information is available for the differential diagnosis between ARDS and pneumonia. METHODS: Clinical and physiological data, serum concentrations of tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and IL-6, and quantitative cultures of lower respiratory tract specimens were obtained from 46 patients with ARDS and 20 with severe pneumonia within 24 hours of the onset of the disease and from 10 control subjects with no inflammatory lung disease. Cytokine concentrations were compared between groups and determinants in addition to the diagnosis were tested. RESULTS: Serum TNF-alpha levels were significantly higher in ARDS patients (67 (57) pg/ml) than in patients with severe pneumonia (35 (20) pg/ml; p = 0.031) or controls (17 (8) pg/ml; p = 0.007). For IL-1beta and IL-6 the observed differences were not statistically significant between patients with ARDS (IL-1beta: 34 (65) pg/ml; IL-6: 712 (1058) pg/ml), those with severe pneumonia (IL-1beta: 3 (4) pg/ml, p = 0.071; IL-6: 834 (1165) pg/ml, p = 1.0), and controls (IL-1beta: 6 (11) pg/ml, p = 0.359; IL-6: 94 (110) pg/ml, p = 0.262). TNF-alpha (standardised coefficient beta = 0.410, p<0.001) and IL-1beta (standardised coefficient beta = 0.311, p = 0.006) were most strongly associated with the degree of lung injury, even when the diagnostic group was included in the statistical model. CONCLUSIONS: Serum TNF-alpha levels were higher in patients with ARDS than in those with severe pneumonia or in control subjects. Multivariate results suggest that the levels of systemic TNF-alpha and IL-1beta reflect the severity of the lung injury rather than the diagnosis.
Biomarkers↗
Role of glucocorticoids on inflammatory response in nonimmunosuppressed patients with pneumonia: a pilot study.
The aim of the study was to assess the potential role of glucocorticoids (GC) in modulating systemic and pulmonary inflammatory responses in mechanically ventilated patients with severe pneumonia. Twenty mechanically ventilated patients with pneumonia treated at a respiratory intensive care unit (RICU) of a 1,000-bed teaching hospital were prospectively studied. All patients had received prior antimicrobial treatment. Eleven patients received GC (mean+/-SD dose of i.v. methylprednisolone 677+/-508 mg for 9+/-7 days), mainly for bronchial dilatation. Serum and bronchoalveolar lavage fluid (BALF) tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6 and C-reactive protein levels were measured in all patients. The inflammatory response was attenuated in patients receiving GC, both systemically (IL-6 1,089+/-342 versus 630+/-385 pg x mL(-1), p=0.03; C-reactive protein 34+/-5 versus 19+/-5 mg x L(-1), p=0.04) and locally in BALF (TNF-alpha 118+/-50 versus 24+/-5 pg x mL(-1), p= 0.05; neutrophil count: 2.4+/-1.1 x 10(9) cells x L(-1) (93+/-3%) versus 1.9+/-1.8 x 10(9) cells x L(-1) (57+/-16%), p=0.03). Four of the 11 (36%) patients receiving GC died compared to six (67%) who were not receiving GC (p=0.37). The present pilot study suggests that glucocorticoids decrease systemic and lung inflammatory responses in mechanically ventilated patients with severe pneumonia receiving antimicrobial treatment.
Anti-Bacterial Agents↗
Cytokine expression in severe pneumonia: a bronchoalveolar lavage study.
OBJECTIVE: To assess the cytokine expression (tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]-1beta, and IL-6) in severe pneumonia, both locally (in the lungs) and systemically (in blood). DESIGN: Prospective sequential study with bronchoalveolar lavage (BAL) and blood sampling. SETTING: Six-bed respiratory intensive care unit of a 1,000-bed teaching hospital. PATIENTS: Thirty mechanically ventilated patients (>48 hrs) were allocated to either the pneumonia group (n = 20) or a control group (n = 10). INTERVENTIONS: Protected specimen brush and BAL samples for quantitative cultures, and serum and BAL fluid TNF-alpha, IL-1beta, and IL-6 levels were measured on days 1, 3, and 7. In the control group, the procedure was done on day 1 only. MEASUREMENTS AND MAIN RESULTS: Serum TNF-alpha levels were significantly higher in patients with pneumonia compared with controls (35 +/- 4 vs. 17 +/- 3 pg/mL, respectively, p = .001). IL-6 levels in serum and BAL fluid were higher in pneumonia than in control patients (serum, 837 +/- 260 vs. 94 +/- 35 pg/mL, respectively, p = .017; BAL fluid, 1176 +/- 468 vs. 234 +/- 83 pg/mL, respectively, p = .05). On days 1, 3, and 7 in patients with pneumonia, IL-1beta levels turned out to be higher in BAL fluid than in serum (71 +/- 17 vs. 2 +/-1 pg/mL on day 1; 49 +/- 8 vs. 6 +/- 2 pg/mL on day 3; and 47 +/- 16 vs. 3 +/- 2 pg/mL on day 7 for BAL fluid and serum, respectively, p < .05). No significant correlation between BAL fluid cytokine levels and lung bacterial burden was shown in presence of antibiotic treatment. Although no clear relationship was found between BAL fluid and serum cytokines and mortality, there was a trend toward higher serum IL-6 levels in nonsurvivors (1209 +/- 433 pg/mL) with pneumonia compared with survivors (464 +/- 260 pg/mL). In addition, serum TNF-alpha and IL-6 correlated with multiple organ failure score (r2 = .36, p = .004 for both) and with lung injury score (r2 = .30, p = .01, and r2 = .22, p = .03, for TNF-alpha and IL-6, respectively). CONCLUSIONS: The present study describes the lung and systemic inflammatory response in severe pneumonia. The lung cytokine expression seems to be independent from the lung bacterial burden in the presence of antibiotic treatment. Because of the limited sample size, we did not find a clear relationship between serum and BAL fluid cytokine levels and outcome.
Aged↗
Gastric intramucosal acidosis in mechanically ventilated patients: role of mucosal blood flow.
OBJECTIVE: To investigate whether gastric intramucosal acidosis is associated with a decreased gastric mucosal blood flow in mechanically ventilated patients. DESIGN: Prospective, clinical investigation. SETTING: University hospital intensive care unit. PATIENTS: Seventeen mechanically ventilated patients with stable hemodynamic status. INTERVENTIONS: Gastric tonometry and endoscopic assessment of mucosal blood flow. MEASUREMENTS AND MAIN RESULTS: Six patients had gastric intramucosal acidosis (intramucosal pH [pHi] of 7.24 +/- 0.06), whereas the remaining 11 patients had pHi values within the normal range (7.44 +/- 0.01). No differences were found between intramucosal acidotic and nonacidotic patients with respect to their general and hemodynamic characteristics. Patients with intramucosal acidosis had a lower gastric mucosal blood flow, as assessed by laser-Doppler flowmetry, than nonacidotic patients (1.4 +/- 0.1 vs. 2.1 +/- 0.2 volts, respectively; p < .05). Reflectance spectrophotometry disclosed that patients with low gastric pHi had also a significantly (p < .05) lower hemoglobin content index (61 +/- 4 arbitrary units) than patients with normal pHi (81 +/- 3 arbitrary units), whereas oxygen saturation index was similar for both groups. CONCLUSION: Our results support the hypothesis that gastric mucosal hypoperfusion underlies the development of intramucosal acidosis in mechanically ventilated patients.
APACHE↗
Pulmonary function tests and CT scan in the management of idiopathic pulmonary fibrosis.
Relationships between pulmonary function testing and high-resolution computed tomography (HRCT) were studied in 39 untreated patients with idiopathic pulmonary fibrosis (IPF) at diagnosis, 23 of whom were followed during 7.5 +/- 0.3 mo (mean +/- SEM). At diagnosis, the extent of overall lung involvement in the HRCT scans showed a moderate but significant correlation only with FVC (r = -0.46, p = 0. 003) and DLCO (r = -0.40, p = 0.03). The extent of ground glass pattern also correlated with FVC (r = -0.58, p = 0.0001). Arterial PO2 at peak exercise (n = 13 patients) showed a significant association with the extent of both ground-glass pattern and overall lung involvement in HRCT (r = -0.60, p = 0.02; and r = -0.64, p = 0. 01, respectively). On multivariate analysis a significant independent correlation between the global disease extent in HRCT and both FVC and DLCO was observed. Changes over time in the total extent of the disease evaluated with HRCT scans were also related to those observed in DLCO and in FVC (r = -0.57, p = 0.01, and r = -0. 51, p = 0.01, respectively). The present study suggests that FVC and DLCO are the physiological variables that best reflect the global extent of disease in IPF and thus may provide significant information for the assessment of the disease's progression.
Aged↗
Lung inflammatory response in pneumonia.
In normal conditions, alveolar macrophages (AMs) are the main cells that respond to bacteria that reach lower airways. However, if the microbial inoculum is too high or too virulent to be stopped by AM alone, these cells recruit polymorphonuclear neutrophils (PMN) into the alveoli from the vascular compartment. Cytokines, such as tumour necrosis factor-alpha (TNF-alpha), interleukin-1-beta (IL-beta), interleukin-6 (IL-6), and interleukin-8 (IL-8), secreted by the AM are able to attract PMN enhanced for phagocytosis, ready to destroy the invading pathogens. However, excessive cytokine production has deleterious effects, with a systemic inflammatory response (sepsis) that can lead to multiorganic failure and death. Other cytokines, such as interleukin-10 (IL-10) balance this response, attenuating several inflammatory mechanisms. The inflammatory lung response in pneumonia has been well studied in animals, and more recently in humans, using bronchoalveolar lavage to measure some inflammatory mediators (TNF-alpha, IL-1 beta, IL-6, IL-8). From these studies, it seems that: 1) the inflammatory response to pneumonia is compartmentalized for most cytokines (in contrast to adult respiratory distress syndrome (ARDS)), except for IL-6 which is a general marker of inflammation. On the other hand, C-reactive-protein is an acute-phase protein synthesized by the liver through the stimulus of IL-6 that may also be an easy-to-measure marker of inflammation that is directly related to IL-6; 2) some of these cytokines may be useful as prognostic indices; 3) there is no clear relationship between the local lung bacterial burden and the intensity of the inflammatory response; and 4) the administration of granulocyte colony-stimulating factor (G-CSF) is a promising therapeutic approach that is still under clinical investigation. In the future, it is probable that the therapeutic goal in severe pneumonia will be to find the exact point at which inflammation is beneficial but not deleterious. The measurement of the inflammatory response may serve for this purpose.
Bronchoalveolar Lavage Fluid↗
[Inflammatory response in pneumonia].
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Humans↗
[Experience in rotation in health centers of 6th year students of School of Medicine of Saragossa].
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Primary Health Care↗
Relationship between ventilator-associated pneumonia and intramucosal gastric pHi: a case-control study.
PURPOSE: Prior investigations have suggested a clear relationship between nosocomial pneumonia and intramucosal gastric pH (pHi), a probable marker of bacterial translocation. METHODS: We studied 33 patients (18 with pneumonia and 15 without) admitted to an intensive care unit and hospitalized longer than 72 hours with the aim of assessing the relationship between nosocomial pneumonia, pHi, and outcome. pHi was estimated at the time of inclusion of patients into the study. Arterial pH (pHa) and bicarbonate and stomach pH and tonometer PtCO2 were also recorded. Values of < 7.32 or delta pHa-pHi of > +0.06 were used to differentiate between normal and low pHi. Quantitative cultures of pharyngeal swabs, gastric lumen, and protected specimen brush from lower airways were also done. RESULTS: The mean pHi values were 7.397 +/- 0.105 (range, 7.14 to 7.53) and 7.452 +/- 0.059 (range, 7.37 to 7.56) for patients with and without pneumonia, respectively (P = .073). Five patients, all with pneumonia, had pHi < 7.32. No patients without pneumonia had pHi < 7.32 (P = .04). The mean delta pHa-pHi was 0.04 +/- 0.07 (range, -0.11 to 0.13) and 0.05 +/- 0.09 (range, -0.09 to 0.28; P = .72) for patients with and without pneumonia, respectively. However, there were significant differences when tonometer PtCO2 values of both groups were compared (38.9 +/- 8.3 and 30.6 +/- 4.7 mm Hg, respectively; P = .025). Patients with pneumonia had higher alkaline gastric lumen pH (5.2 +/- 1.0) than those without pneumonia (3.8 +/- 1.4; P = .006). Nonsurvivors (n = 7) had more acidic pHi (7.33 +/- 0.11) than survivors (7.44 +/- 0.06; P = .045). The mean gastric lumen bacterial concentration was 4.14 +/- 1.01 Log10 CFU/mL in patients with pneumonia and 4.28 +/- 1.22 Log10 CFU/mL in patients without pneumonia (P = NS). When patients with and without intramucosal gastric acidosis (pHi < 7.32) were compared, the gastric bacterial burden was 4.42 +/- 0.82 Log10CFU/mL and 4.32 +/- 1.03 Log10 CFU/mL (P = .08), respectively. CONCLUSIONS: Most patients with nosocomial pneumonia had no associated intramucosal gastric acidosis. However, low pHi was associated with increased mortality.
Adult↗
Stomach as a source of colonization of the respiratory tract during mechanical ventilation: association with ventilator-associated pneumonia.
The aetiopathogenesis of ventilator-associated pneumonia (VAP) requires abnormal oropharyngeal and gastric colonization and the further aspiration of their contents to the lower airways. VAP develops easily if aspiration or inoculation of microorganisms occur in patients with artificial airways, in whom mechanical, cellular and/or humoral defences are altered. Well-known risk factors for gastric colonization include: alterations in gastric juice secretion; alkalinization of gastric contents; administration of enteral nutrition; and the presence of bilirubin. However, the role of the colonized gastric reservoir in the development of VAP remains debatable. Evidence in favour of the role of the stomach in the development of VAP comes mainly from randomized, controlled trials of selective gut decontamination and stress ulcer prophylaxis in the intensive care unit (ICU), in which reducing the bacterial burden of the stomach decreases the incidence of nosocomial respiratory infections. However, at least three studies of flora have found an absence of stomach origin of pneumonia occurring during mechanical ventilation. Prophylactic measures suggested to prevent VAP in relation to the gastric reservoir include: treatment for stress ulcers with sucralfate; prevention of duodenal reflux with metoclopramide; reduction of gastric burden and bacterial translocation by selective digestive decontamination; acidification of enteral feeding; and jejunal feeding. Gastro-oesophageal reflux can be prevented by using small bore nasogastric tubes and jejunal feeding. The aspiration of gastric contents can be reduced by positioning patients in a semirecumbent position, checking the patency of the tube cuff, and aspiration of subglottic secretions. The role of the stomach as a reservoir for microorganisms causing ventilator-associated pneumonia is still controversial but despite the debate, there is major evidence in the literature in favour of the gastric origin of part of these pulmonary infections.
Colony Count, Microbial↗
Markers of ventilator-associated pneumonia.
The diagnosis of ventilator-associated pneumonia (VAP) is difficult for several reasons. Firstly, clinical markers show a large percentage of false-positive and false-negative results. Secondly, microbiological diagnosis based on quantitative cultures of protected specimen brush (PSB), bronchoalveolar lavage (BAL), and endotracheal aspirates also present false-positive and false-negative results. Furthermore, definite results are delayed for 48-72 hours. For all these reasons it would be an advantage to have a biological marker of ventilator-associated pneumonia in clinical practice. Since clinical features of pneumonia in mechanically ventilated patients are neither specific nor sensitive, rapid markers of pneumonia might be of great assistance to the clinician in deciding whether to start an empiric antibiotic regimen. A marker of ventilator-associated pneumonia could be a rapid alternative diagnostic method which permits the definite diagnosis of pneumonia. Accordingly, specific markers of VAP, namely the presence of intracellular microorganisms, the detection of elastin fibres, the antibody-coated bacteria test, the level of endotoxin in bronchoalveolar lavage fluid, the local production of interleukin-8, the levels of lactate dehydrogenase, and decreased surfactant protein A, may be important as they can provide a rapid diagnosis of VAP. Among the markers alluded to above, the search for intracellular bacteria in polymorphonuclear leukocytes or macrophages is the most widely validated technique with an excellent specificity, provided that prior antibiotics are not given. However, this technique has its own limitations; it requires a considerable time effort for the microbiologist, and also compels the performance of BAL, a technique not always harmless to the patient.
Antibody-Coated Bacteria Test, Urinary↗
The role of the gastric reservoir in ventilator-associated pneumonia.
Ventilator-associated pneumonia (VAP) is a common complication of mechanical ventilation with an incidence ranging from 9-70% and averaging around 25%. The pathogenesis of VAP requires abnormal oropharyngeal and gastric colonisation and then aspiration of these contents into the lower airways. Another co-existing mechanism could be direct oropharyngeal or lower airways inoculation of microorganisms through contaminated respiratory therapy equipment. Ventilator-associated pneumonia develops easily if aspiration or inoculation of microorganisms occur in patients with artificial airways and in whom mechanical, cellular and/or humoral defences are altered. Both host factors and treatments may alter pulmonary defence mechanisms; these too may contribute to the development of VAP. An alternative mechanism to explain VAP is bacterial translocation, although this mechanism is still under investigation. Figure 1 illustrates a schema of the pathogenesis of VAP. In this paper we review the possible role of the gastric reservoir in the aetiology of VAP, emphasising the following issues: 1. Risk factors for gastric colonisation 2. Clinical evidence of gastric aspiration to the lower airways in mechanically ventilated patients 3. Clinical evidence and controversies surrounding the role of the gastric reservoir in ventilator-associated pneumonia 4. The role of bacterial translocation as a mechanism for the development of VAP 5. A summary of prophylactic measures.
Bacterial Infections↗
[A decrease in the level of CPAP required after prolonged treatment in patients with the obstructive sleep apnea syndrome].
Application of continuous positive upper airway pressure (CPAP) is the treatment of choice in obstructive sleep apnea syndrome (OSAS). CPAP keeps the upper airway open by providing a "pneumatic splint" on the pharyngeal walls. However, it has been suggested that prolonged nasal CPAP treatment may also improve the physiopathological mechanisms responsible for OSAS by a variety of mechanisms such as the reduction of edema of the pharyngeal mucosa, modification of upper airway muscle dynamics; there may even be a reduction in the intensity of phenomena responsible for brief awakening and ending of apneic episodes. The objective of this study was to determine whether prolonged nasal CPAP is associated to a reduction of CPAP pressure required for eliminating apnea in patients with OSAS. We studied 22 patients (4 women) with OSAS diagnosed by conventional polysomnography, including study of neurological variables during sleep (electroencephalogram, ocular movement, submental electromyogram), respiratory variables (nasal air flow, thoracic-abdominal movement, O2 saturation in the blood), and others (electrocardiogram, leg movement). Treatment was exclusively with nasal CPAP. All 22 patients were middle-aged (52.3 +/- 10 years), presented a mean apnea/hypoapnea index of 65.2 +/- 24 per hour. CPAP levels needed to eliminate episodes of apnea, blood O2 desaturation and snoring at the time of diagnosis and after long-term treatment (8.5 +/- 4.6 months) were applied. Weight was recorder at both measurement times. Eighteen of the 22 patients (1 woman, mean age 53.1 +/- 11.4 years and apnea/hypopnea index 64.8 +/- 23.4 per hour) experienced no weight change during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Severe community-acquired pneumonia "a new clinical concept".
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Community-Acquired Infections↗
[Anxiety scales and Goldberg's depression: an efficient interview guide for the detection of psychologic distress].
OBJECTIVES: Validation of Goldberg's Anxiety and Depression scales in our settings. DESIGN: Transverse study. Two phases screening at population previously stratified and randomly allocated. SITE. National Health Institute's Primary Care Centres at the city of Zaragoza. PATIENTS AND OTHER PARTICIPANTS: 444 patients, aged 19 and older, who attend their general practitioner for a new episode of illness. The sample has been previously stratified by sex and age. MEASUREMENTS AND MAIN RESULTS: At the first stage the sample has been studied with a Health Survey consisting of a variety of sound validity (General Health Questionnaire-28 items version, spanish version of Folstein's mini Mental Status Examination, CAGE and another drug and over the counter products screening questionnaire) and the new scales, that we attempt to validate. At the second stage "the possible cases" chosen at the first phase and 10% of possible non cases are assessed with a comprehensive Psychiatric Interview: EPEP (Standardized Polyvalent Psychiatric Interview). CONCLUSIONS: The new scales E.A.D.G. have supported their validity for the screening of the most prevalent psychiatric disturbances in primary care settings. Their validity for the screening of the most prevalent psychiatric disturbances in primary care settings. They have outstanding and promising advantages when compared to traditional methods: brevity, simplicity, discriminatory ability between anxiety and depression and usefulness as an interview guideline.
Adult↗
[Epidemic Kaposi's sarcoma in women: presentation of 4 cases].
Epidemic Kaposi's sarcoma is the neoplasm most frequently manifested in infection by the human immunodeficiency virus. Its prevalence is considerably higher among homosexual males than among intravenous drug users with practically exclusive infection in this sex. Four cases of Kaposi's sarcoma in women with the human immunodeficiency virus are described. Two of these subjects were intravenous drug users and the other two were heterosexually promiscuous as the only conduct of risk for acquiring infection by the human immunodeficiency virus. Kaposi's sarcoma was the form of presentation of the syndrome of acquired immunodeficiency syndrome in these four patients.
Acquired Immunodeficiency Syndrome↗