Acute respiratory distress syndrome (ARDS) is characterized by diffuse alveolar damage, and evolves progressively with three phases: exsudative, fibroproliferative, and fibrotic. In the exudative phase, there are interstitial and alveolar edemas with hyaline membrane. The fibroproliferative phase is characterized by exudate organization and fibroelastogenesis. There is proliferation of type II pneumocytes to cover the damaged epithelial surface, followed by differentiation into type I pneumocytes. The fibroproliferative phase starts early, and its severity is related to the patient's prognosis. The alterations observed in the phenotype of the pulmonary parenchyma cells steer the tissue remodeling towards either progressive fibrosis or the restoration of normal alveolar architecture. The fibrotic phase is characterized by abnormal and excessive deposition of extracellular matrix proteins, mainly collagen. The dynamic control of collagen deposition and degradation is regulated by metalloproteinases and their tissular regulators. The deposition of proteoglycans in the extracellular matrix of ARDS patients needs better study. The regulation of extracellular matrix remodeling, in normal conditions or in several pulmonary diseases, such as ARDS, results from a complex mechanism that integrate the transcription of elements that destroy the matrix protein and produce activation/inhibition of several cellular types of lung tissue. This review article will analyze the ECM organization in ARDS, the different pulmonary parenchyma remodeling mechanisms, and the role of cytokines in the regulation of the different matrix components during the remodeling process.

Keywords: Respiratory distress syndrome. Pulmonary alveoli/lesions. Extracellular matrix. Cytokines/ultrastructure.

Objective: To establish the incidence of acute lung injury and acute respiratory distress syndrome, as well as related risk factors and mortality in an intensive care unit. To compare patients developing lung injury with at-risk patients not presenting acute lung injury or acute respiratory distress syndrome. Methods: The study was conducted in the intensive care unit of the Ribeirão Preto Hospital das Clínicas Emergency Room. All patients admitted between May 2001 and April 2002 were monitored prospectively. Clinical data, Acute Physiologic and Chronic Health Evaluation II score, complications, length of stay in the intensive care unit and lung injury data were recorded. Results: Of the 524 patients admitted, 175 (33.4%) presented risk factors for acute lung injury and acute respiratory distress syndrome, 33 (6.3%) developed acute respiratory distress syndrome, and 12 (2.3%) developed acute lung injury. The main risk factors were pneumonia (37.7%), shock (32.0%), multiple trauma (24.6%) and sepsis (21.1%). Patients developing acute lung injury had higher Acute Physiologic and Chronic Health Evaluation II scores (p < 0.05), more frequently presented sepsis (p = 0.001), developed more complications (p = 0.001) and presented greater mortality (p = 0.001). The main cause of death was multiple organ failure (38.5%). Conclusion: The incidence of acute lung injury and acute respiratory distress syndrome was 2.3% and 6.3%, respectively.

Keywords: Respiratory distress syndrome, adult/epidemiology; Respiratory distress syndrome, adult/mortality;

Objective: To compare the American-European Consensus Conference (AECC) definition of acute respiratory distress syndrome (ARDS) to autopsy findings. Methods: All patients who died in the intensive care unit of the Federal University of Juiz de Fora University Hospital between 1995 and 2003 and were submitted to autopsy were included in the study. Patient clinical charts were reviewed to establish whether cases met the AECC criteria for a diagnosis of ARDS, histologically defined as the presence of diffuse alveolar damage (DAD). Results: During the study period, 592 patients died, and 22 were submitted to autopsy. Of those 22 patients, 10 (45%) met the AECC criteria, and 7 (32%) met the histopathological criteria for DAD. The AECC clinical criteria presented a sensitivity of 71% (95%CI: 36-92%) and a specificity of 67% (95%CI: 42-85%). The positive and negative predictive values were, respectively, 50 and 83%, whereas the positive and negative likelihood ratios were, respectively, 2.33 and 0.47. The histopathological findings in the 5 patients who met AECC criteria but did not present DAD were pneumonia (n = 2), pulmonary embolism (n = 1), tuberculosis (n = 1), and cryptococcosis (n = 1). Conclusion: The accuracy of the AECC definition of ARDS was godless than satisfactory. Due to the low positive predictive value and the low positive likelihood ratio, other hypotheses must be considered when ARDS is suspected.

Keywords: Respiratory distress syndrome, adult; Diagnostic Techniques and Procedures; Autopsy.

A male farmer, 20 years old, from the countryside of the State of Piauí, developed acute respiratory infection. Despite adequate antimicrobial therapy, there was worsening respiratory manifestations demanding mechanical ventilation. Radiographs showed diffuse pulmonary infiltrates. PaO2/FiO2 was 58. Direct microscopy and culture from tracheal aspirates disclosed Coccidioides immitis. Autochthonous cases of coccidioidomycosis have only recently been described in Brazil, most of them from the State of Piauí. C. immitis has been isolated from humans, dogs and armadillos (Dasypus novemcinctus), and also from soil samples of armadillo's burrows. Therapeutic failure to antimicrobials and patient's origin from recognized endemic areas should alert for the possibility of acute pulmonary coccidioidomycosis.

Objective: To assess whether the use of ELMO, a helmet for noninvasive ventilation created in Brazil, had a positive impact on the prognosis of patients with hypoxemic respiratory failure caused by severe COVID-19. Methods: This is a retrospective study of 50 critically ill COVID-19 patients. Epidemiological, clinical, and laboratory data were collected on ICU admission, as well as before, during, and after ELMO use. Patients were divided into two groups (success and failure) according to the outcome. Results: ELMO use improved oxygenation parameters such as Pao2, Fio2, and the Pao2/Fio2 ratio, and this contributed to a gradual reduction in Fio2, without an increase in CO2, as determined by arterial blood gas analysis. Patients in the success group had significantly longer survival (p < 0.001), as determined by the Kaplan-Meier analysis, less need for intubation (p < 0.001), fewer days of hospitalization, and a lower incidence of acute kidney injury in comparison with those in the failure group. Conclusions: The significant improvement in oxygenation parameters, the longer survival, as reflected by the reduced need for intubation and by the mortality rate, and the absence of acute kidney injury suggest that the ELMO CPAP system is a promising tool for treating ARDS and similar clinical conditions.

Keywords: Respiratory distress syndrome; COVID-19; Noninvasive ventilation; Intensive care units.

Fat embolism is defined as mechanical blockage of the vascular lumen by circulating fat globules. Although it primarily affects the lungs, it can also affect the central nervous system, retina, and skin. Fat embolism syndrome is a dysfunction of these organs caused by fat emboli. The most common causes of fat embolism and fat embolism syndrome are long bone fractures, although there are reports of its occurrence after cosmetic procedures. The diagnosis is made clinically, and treatment is still restricted to support measures. We report the case of a female patient who developed adult respiratory distress syndrome due to fat embolism in the postoperative period following liposuction and fat grafting. In this case, the patient responded well to alveolar recruitment maneuvers and protective mechanical ventilation. In addition, we present an epidemiological and pathophysiological analysis of fat embolism syndrome after cosmetic procedures.

Keywords: Respiratory distress syndrome, adult; Embolism, fat; Lipectomy.

Objective: This study aimed to investigate acute and chronic effects of varenicline on lung tissue in an experimental study. Methods: A total of 34 rats were randomly allocated into study (varenicline) and control groups. The rats were divided into two groups (i) control group, (ii) varenicline group. Then, the rats in the each group were sub‑divided equally in turn as acute (C1; V1) and chronic (C2; V2) ; all rats of acute and chronic groups were sacrificed under the anesthesia on the 45th day for acute group [C1 (n=5) and V1 (n=12)] and the 90th day for chronic group [C2 (n=5) and V2 (n=12)], respectively. Thus, biochemical and histopathological analysis were carried out. Results: Thirty four rats completed the study, 24 were in varenicline group and 10 were in control group. In chronic exposure to varenicline, oxidant levels comprising of malondialdehyde (MDA), and myeloperoxidase (MPO) increased and superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx) levels, named as antioxidants, decreased significantly when compared to the control group. MDA and MPO levels were also significantly higher and SOD, CAT, GPx, GSH levels were also significantly lower in chronic varenicline group when compared to acute varenicline group. These findings were also supported by histopathological observations. Conclusion: This is the first study, which evaluated pulmonary effects of varenicline experimentally on an animal model. It was observed that chronic varenicline treatments cause inflammation and lung cell injury.

Keywords: Varenicline; Lung tissue; Oxidative stress; Pulmonary toxicity.

Objective: To evaluate the pulmonary alterations of animals with Hepatopulmonary Syndrome (HPS) submitted to Biliary Duct Ligature (BDL), as well as the antioxidant effect of Melatonin (MEL). Methods: Sixteen male Wistar rats, divided into four Sham groups: BDL group, Sham + MEL group and BDL + MEL. The pulmonary and hepatic histology, lipoperoxidation and antioxidant activity of lung tissue, alveolar-arterial O2 difference and lung / body weight ratio (%) were evaluated. Results: When comparing the groups, could be observed an increase of vasodilation and pulmonary fibrosis in the BDL group and the reduction of this in relation to the BDL + MEL group. It was also observed significant changes in the activity of catalase, ApCO2, ApO2 in the LBD group when compared to the other groups. Conclusion: The use of MEL has been shown to be effective in reducing vasodilation, fibrosis levels and oxidative stress as well as gas exchange in an experimental HPS model.

Keywords: Bile duct; Hepatopulmonary Syndrome; Melatonin; Lung.

In view of the pandemic caused by a new virus, influenza A (H1N1), we report the case of a 56-year-old patient without relevant risk factors and with severe acute respiratory syndrome resulting from infection with this virus. We present the results of laboratory tests and the imaging findings (chest X-ray and CT scans). The evolution was favorable, and the patient was discharged after 14 days.

Keywords: Influenza A virus, H1N1 subtype; Severe acute respiratory syndrome; Patient care.

Background: Structural alterations to the pulmonary circulation characterize the vascular remodeling process and are likely correlated with local variations in flow and ischemia. Objective: To define the histological alterations to the pulmonary circulation seen after experimentally-induced ischemia of the pulmonary artery and to correlate those alterations with known patterns of blood redistribution and vascular remodeling. Method: Wistar rats (n = 48) were randomized into two groups with ligation of the pulmonary artery and without (controls) and were sacrificed on post-ischemia days 1, 7, 30 and 60. Lungs were removed and inspected for signs of parenchymal injury. External diameters, as well as wall thicknesses in the pulmonary, alveolar and bronchial end arterioles, were measured. Internal diameter and wall thickness percentage were calculated. Results: Infarction, necrosis and hemorrhage occurred only in ischemic lungs. In nonischemic lungs, there was a sustained increase in the internal and external arteriolar diameters, with an initial reduction in wall thickness on day 1, and day-60 values were similar to those seen in controls. In ischemic lungs, there was a transitory reduction in the internal and external diameters of the pulmonary and bronchial end arterioles, together with an initial, equally transitory, increase in their wall thickness. The alveolar arterioles presented sustained and progressive increases in external diameter and wall thickness, with concomitant reductions in internal diameter. Conclusion: This model mimics distal arterial disease in patients with chronic pulmonary thromboembolism. The vascular response in nonischemic lungs was consistent with a pattern of flow remodeling, whereas that seen in ischemic lungs was more consistent with flow and ischemia. In the pulmonary and bronchial end arterioles, the response was transitory, in contrast to the sustained and progressive response seen in the alveolar arterioles, which was probably caused by delayed local flow.

Keywords: Key-words: Pulmonary embolism. Pulmonary circulation. Vascular remodelling. Pulmonary artery.

The relationship between structure and function in asthma has been extensively studied. All the compartments of the airway have been shown to have some structural alterations contributing to functional defects. The structural alterations are thought to be a consequence of the chronic inflammation present in asthmatic airways, leading ultimately to remodeling. The decline of the ventilatory function over time in some asthmatic patients may be a consequence of airway remodeling. In this review, the authors describe the phenomena leading to airway remodeling and discuss the role of inflammatory mediators involved in this process. The structural alterations of the asthmatic airways are presented and the possible correlated functional defects are discussed.

Keywords: bronchii; pathology; asthma.

Objective: Bedside lung ultrasound (LUS) is a noninvasive, readily available imaging modality that can complement clinical evaluation. The Bedside Lung Ultrasound in Emergency (BLUE) protocol has demonstrated a high diagnostic accuracy in patients with acute respiratory failure (ARF). Recently, bedside LUS has been added to the medical training program of our ICU. The aim of this study was to investigate the accuracy of LUS based on the BLUE protocol, when performed by physicians who are not ultrasound experts, to guide the diagnosis of ARF. Methods: Over a one-year period, all spontaneously breathing adult patients consecutively admitted to the ICU for ARF were prospectively included. After training, 4 non-ultrasound experts performed LUS within 20 minutes of patient admission. They were blinded to patient medical history. LUS diagnosis was compared with the final clinical diagnosis made by the ICU team before patients were discharged from the ICU (gold standard). Results: Thirty-seven patients were included in the analysis (mean age, 73.2  14.7 years; APACHE II, 19.2  7.3). LUS diagnosis had a good agreement with the final diagnosis in 84% of patients (overall kappa, 0.81). The most common etiologies for ARF were pneumonia (n = 17) and hemodynamic lung edema (n = 15). The sensitivity and specificity of LUS as measured against the final diagnosis were, respectively, 88% and 90% for pneumonia and 86% and 87% for hemodynamic lung edema. Conclusions: LUS based on the BLUE protocol was reproducible by physicians who are not ultrasound experts and accurate for the diagnosis of pneumonia and hemodynamic lung edema.

Keywords: Ultrasonography, interventional; Respiratory insufficiency; Intensive care units.

Among all causes of preventable deaths, smoking is responsible for the greatest number of deaths worldwide and predisposes to fatal, noncommunicable diseases, especially cardiovascular diseases. Lifestyle changes are effective in the treatment of patients with smoking-related diseases and assist in the prevention of premature mortality. Our objective was to investigate the available scientific evidence regarding the psychological distress related to smoking cessation in patients who have had acute myocardial infarction. To that end, we conducted an integrative review of the literature in order to summarize relevant studies on this topic. The selected databases were Scopus, PubMed Central, Institute for Scientific Information Web of Science (Core Collection), ScienceDirect, EMBASE, SciELO, LILACS e PsycINFO. On the basis of the inclusion and exclusion criteria adopted for this study, 14 articles were selected for analysis. Those studies showed that the prevalence of psychological distress is higher among smokers than among nonsmokers, and distress-related symptoms are much more common in smokers with acute myocardial infarction than in those without. Smoking cessation depends on the active participation of the smoker, whose major motivation is the underlying disease. Most studies have shown that there is a need to create treatment subgroups as a means of improving the treatment provided. This review article expands the knowledge regarding smoking cessation and shows the need to invest in future research that investigates subgroups of smokers diagnosed with the major smoking-related comorbidities, such as acute myocardial infarction, in order to develop specific interventions and psychological support strategies.

Keywords: Smoking; Stress, psychological; Myocardial infarction; Tobacco use cessation.

Acute chest syndrome is an affection, specially in young adults, of sickle cell disease and is responsible for 25% of the deaths. The authors report the case of an alcoholic 45-year-old mulatto man, without any previous manifestation of sickle cell disease, who presented with a pneumonia-like clinical picture with seven days of duration. The chest X-ray revealed bilateral lung infiltrates and spots of consolidation with air bronchograms, and left pleural effusion. The patient also had anemia and leukocytosis with neutrophilia. Treated with cefoxitin and amicacin, the patient developed acute respiratory insufficiency and died 14 hours after hospitalization. The necropsy showed lungs with intense congestion, intra-alveolar hemorrhage, diffuse alveolar damage, and sickle red blood cells. The progressive, fast, and severe character of the acute chest syndrome, which is frequently mimicked by other illnesses, makes the disease a dramatic and severe event of difficult earlier diagnosis. Therefore, in countries like Brazil, with a large black population, the physicians must always be aware of this possibility.

Objective: Various studies of emphysema involve long-term exposure of animals to cigarette smoke, focusing on the cell type involved in the protease/antiprotease imbalance and on extracellular matrix degradation. In emphysema, increased expression of metalloproteinases is associated with cytokines, and evidence suggests that the matrix metalloproteinase-12 (MMP-12) plays an important role. Our objective was to investigate tissue inhibitor of metalloproteinase-2 (TIMP-2), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) detection by immunohistochemical methods in mouse lung. Methods: Male C57BL/6 mice were exposed 3 times a day to the smoke of 3 cigarettes over a period of 10, 20, 30 or 60 days in an inhalation chamber (groups CS10, CS20, CS30 and CS60, respectively). Controls were exposed to the same conditions in room air. Results: A progressive increase in the number of alveolar macrophages was observed in the bronchoalveolar lavage fluid of the exposed mice. The mean linear intercept, an indicator of alveolar destruction, was greater in all exposed groups when compared to control group. In the CS10, CS20 and CS30 mice, the immunohistochemical index (II) for MMP-12 increased in parallel with a decrease in II for TIMP-2 in the CS10, CS20 and CS30 mice. The II for the cytokines TNF-α and IL-6 was greater in all exposed groups than in the control group. Emphysema, with changes in volume density of collagen and elastic fibers, was observed in the CS60 group. Conclusions: These findings suggest that cigarette smoke induces emphysema with major participation of TNF-α and IL-6 without participation of neutrophils.

Keywords: Macrophages, alveolar; Emphysema; Tissue inhibitor of metalloproteinase-2; Interleukin-6.