Postemetic rupture of the esophagus, also known as spontaneous rupture or Boerhaave's syndrome, was first described by Herman Boerhaave in 1724. This is a severe disease that causes high mortality rates and is difficult to diagnose not only because it is rare but also because it is frequently confused with other severe clinical conditions, such as acute myocardial infarction, perforated peptic ulcer, and acute pancreatitis. Herein, we describe three cases of patients with this syndrome. Two underwent primary repair of the rupture, and one underwent esophagectomy followed by reconstruction. There was one death due to septic shock in the immediate postoperative period. The other two patients presented favorable long-term evolution.

Keywords: Esophageal diseases; Rupture, spontaneous; Mediastinitis; Esophagectomy.

The authors describe the case of a 54 year-old female with adenoid cystic carcinoma of the trachea at the cricoid level upon whom extensive surgical resection was performed, including the larynx, part of the trachea and esophagus. Reconstruction of the digestive tract was done by means of a gastric tube and the airway with a mediastinal tracheostomy. Five years after the original procedure there was a local cutaneous recurrence which was removed. Seven years later the disease recurred in the mediastinum, which responded to irradiation. The patient is alive and well eight years and five months after the operation.

Keywords: Trachea. Neoplasm. Carcinoma, adenoid cystic. Tracheostomy.

Diaphragm rupture is generally associated with severe trauma. Spontaneous diaphragm rupture is rare, seldom reported, and does not have a clear etiology. In this report the authors show a case of spontaneous diaphragm rupture which took place during hospitalization.

Keywords: Diaphragm rupture. Spontaneous diaphragm rupture.

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: 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.

Objective: To investigate whether the presence of obstructive sleep apnea syndrome (OSAS) alters the perception of respiratory symptoms and quality of life in COPD patients, by using specific questionnaires, as well as to determine whether scales for assessing daytime sleepiness and for screening for OSAS can be used in the triad of OSAS, COPD, and obesity. Methods: We included 66 patients diagnosed with mild-to-moderate or severe COPD and presenting with a body mass index > 27 kg/m2. After polysomnography, patients completed the Epworth sleepiness scale (ESS), the Berlin questionnaire (BQ), the modified Medical Research Council (mMRC) scale, the Baseline Dyspnea Index (BDI), and the Saint George's Respiratory Questionnaire (SGRQ). Results: Patients were first divided into two groups: COPD + OSAS (n = 46); and COPD-only (n = 20). The COPD + OSAS group was subdivided into a COPD + mild-to-moderate OSAS group (n = 32) and a COPD + severe OSAS group (n = 14), all of which were compared with the COPD-only group. There was a significant difference in mean FEV1 (L) between the COPD + OSAS groups and the COPD-only group (p = 0.073). The presence of the triad did not lead to significantly higher ESS scores, and scores > 10 had a specificity of 0.58. The BQ did not identify high risk for OSAS in the presence of the triad (specificity of 0.31). There were no significant differences in domain or total scores of the SGRQ between the COPD + OSAS groups and the COPD-only group. Conclusions: The confounding factors present in the triad of OSAS, COPD, and obesity prevented the perception of increased daytime sleepiness and high risk for OSAS. We observed no worsening of dyspnea perception or quality of life.

Keywords: Sleep apnea, obstructive; Pulmonary disease, chronic obstructive; Obesity; Surveys and questionnaires.

The greatest causes of morbidity and mortality in patients infected with human immunodeficiency virus are opportunistic infections and neoplastic diseases. Most of them are lung diseases. Its correct diagnosis and proper treatment improve the quality of life as well as the survival in this group of patients.

Keywords: lung disease; acquired immunodeficiency syndrome; bronchoscopy

Objective: To analyze the available evidence regarding the effect that corticosteroids have on the prevention of fat embolism syndrome after long bone fracture of the lower limbs or pelvic fracture. Methods: In March of 2007, we performed a search of various electronic databases, including Medline, the Excerpta Medica database, the Cochrane Library, the Latin American and Caribbean Health Sciences Literature database and the Scientific Electronic Library Online. We selected randomized controlled trials that compared the effect of corticosteroids with that of placebo (or standard care) on the prevention of fat embolism syndrome after long bone fracture of the lower limbs or pelvic fracture. References from the studies included were also reviewed. Results: Six studies were included. The pooled relative risk for developing fat embolism syndrome was 0.16 (95% CI: 0.08-0.35) in the corticosteroid group as compared with the control group. The pooled relative risk for developing hypoxemia was 0.34 (95% CI: 0.19-0.59) in the corticosteroid group as compared with the control group. Conclusion: The analysis of evidence showed that corticosteroids decrease the risk of developing fat embolism syndrome and hypoxemia after long bone fracture of the lower limbs.

Keywords: Embolism, Fat; Adrenal Cortex Hormones; Meta-Analysis.

The superior vena cava is formed by the union of the right and left brachiocephalic veins. It is located in the middle mediastinum, to the right of the aorta and anterior to the trachea. Superior vena cava syndrome consists of a group of signs (dilation of the veins in the neck, facial swelling, edema of the upper limbs, and cyanosis) and symptoms (headache, dyspnea, cough, orthopnea and dysphagia) caused by the obstruction of blood flow through the superior vena cava to the right atrium. This obstruction can be caused by extrinsic compression, tumor invasion or thrombosis. Such obstruction may also occur as a result of insufficient venous return secondary to intra-atrial or intraluminal diseases. From 73% to 93% of all cases of superior vena cava syndrome occur during the development of an intrathoracic tumor. Most patients presenting superior vena cava syndrome secondary to malignant neoplasms are treated without surgery, through radiotherapy, chemotherapy or the use of intraluminal stents. When the etiology of superior vena cava syndrome is benign, it can be treated with clinical measures (anticoagulation, raising the head, etc.) or, in refractory cases, with angioplasty, stents or surgery.

Keywords: Superior vena cava syndrome/therapy; Superior vena cava syndrome/surgery; Superior vena cava syndrome/etiology; Superior vena cava syndrome /drug therapy; Superior vena cava syndrome /radiotherapy; Superior vena cava

The physiopathology of obstructive sleep apnea syndrome is multifactorial. Gender and obesity status, as well as genetic, anatomic, and hormonal factors, together with ventilatory drive, interact in a diverse manner in the physiopathology and clinical expression of the disease. Obesity is the main risk factor, since increases in body mass index, visceral fat, and neck circumference are strong predictors of the disease. Progesterone increases the activity of the upper airway dilator muscles and therefore plays a protective role in premenopausal women. This explains the fact that the prevalence of the disease is higher in postmenopausal patients, in patients with polycystic ovary syndrome, as well as in males. Evidence supports the fact that, as individuals grow older, there is a decrease in muscle tonus, with a consequent reduction in the dimensions of the upper airway lumen. Craniofacial anomalies, such as in retrognathia or micrognathia, are accompanied by posterior positioning of the tongue and can result in narrowing of the upper airway lumen. Finally, decreased ventilatory drive has been detected in patients with obstructive sleep apnea syndrome and hypercapnia.

Keywords: Sleep apnea obstructive/physiopathology; Body mass index; Obesity

Two cases of complete bronchial rupture and one case of tracheobronchial rupture by blunt chest trauma were treated at the Thoracic Surgical and Respiratory Endoscopy Department of the Hospital Universitário Cajuru in a period of 2 years. The surgical technique used was end-to-end anastomosis with interrupt absorbable suture after either resection of the stenotic edges or debridement of the lacerated edges. All three patients have had good recovery. The mean period to remove the chest tubes was 3.6 days, and the mean period of discharge from the Thoracic Surgical Department was 5.6 days. The follow-up was made using chest X-ray (PA and lateral projections), lung function tests, and bronchoscopy.

Keywords: Tracheobronchial rupture. Blunt chest trauma. Evaluation. Treatment.

Macrophage activation syndrome is a rare and potentially life-threatening disease. It occurs due to immune dysregulation manifested as excessive macrophage proliferation, typically causing hepatosplenomegaly, pancytopenia and hepatic dysfunction. Here, we report an unusual case of macrophage activation syndrome presenting as dyspnea, as well as (reported here for the first time) high resolution computed tomography findings of an excavated nodule, diffuse ground glass opacities and consolidations (mimicking severe pneumonia or alveolar hemorrhage). The patient was successfully treated with human immunoglobulin. We recommend that macrophage activation syndrome be considered in the differential diagnosis of respiratory failure. Rapid diagnosis and treatment are essential to achieving favorable outcomes in patients with this syndrome.

Keywords: Macrophage activation; Lymphohistiocytosis, hemophagocytic; Tomography, X-ray computed; Lung diseases, interstitial.

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;

A case of a patient with Pancoast's syndrome associated with acquired immunodeficiency syndrome is reported. This association is rare and Kaposi's sarcoma and non-Hodgkin lymphoma are the most recurrent tumors in AIDS. The patient was an IV drug user and was admitted to the hospital for diagnosis of apex lung mass with signs of Pancoast's syndrome. HIV serology was positive and pathology of lung mass showed non-small cell lung cancer.

Keywords: Pancoast's syndrome. HIV. Bronchogenic carcinoma. Lung neoplasms. Acquired immunodeficiency syndrome.

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.