Alcohol-related traffic accidents with fatal outcomes in the city of Sao Paulo

Aims: The aims of the present study were to characterize fatal traffic accident victims in a major urban center in Brazil and their association with alcohol consumption. Methods: Cross-sectional study of 907 fatal traffic accident victims in Sao Paulo, in 2005. Results: Adult males between the ages of 25 and 54 represented the majority of cases with positive blood alcohol concentrations (BAC). Overall, males had a higher proportional BAC and mean BAC than females. Pedestrians, particularly those with no detectable BAC, were typically older than other victims. Most accidents (total and BAC-positive) happened on weekends between midnight and 6 a.m. Considering all victims, 39.4% were positive (BAC over 0.1 g/l). When only drivers (automobile, motorcycle and bicycle) were evaluated. 42.3% had BAC over the legal limit (0.6 g/l). Conclusions: Alcohol is associated with nearly half of all traffic accident deaths in the city of Sao Paulo. especially for days and times associated with parties and bars (weekends between 12 a.m. and 6 a.m.). (C) 2010 Elsevier Ltd. All rights reserved.

Fatal adenoviral necrotizing bronchiolitis case in a post-cardiac surgery intensive care unit

We report a case of a 67 year-old-male patient admitted to the intensive care unit in the post-coronary bypass surgery period who presented cardiogenic shock, acute renal failure and three episodes of sepsis, the latter with pulmonary distress at the 30th post-operative day. The patient expired within five days in spite of treatment with vancomycin, imipenem, colistimethate and amphotericin B. At autopsy severe adenovirus pneumonia was found. Viral pulmonary infections following cardiovascular surgery are uncommon. We highlight the importance of etiological diagnosis to a correct treatment approach.

Increased myoepithelial cells of bronchial submucosal glands in fatal asthma

Background: Fatal asthma is characterised by enlargement of bronchial mucous glands and tenacious plugs of mucus in the airway lumen. Myoepithelial cells, located within the mucous glands, contain contractile proteins which provide structural support to mucous cells and actively facilitate glandular secretion. Objectives: To determine if myoepithelial cells are increased in the bronchial submucosal glands of patients with fatal asthma. Methods: Autopsied lungs from 12 patients with fatal asthma (FA), 12 patients with asthma dying of non-respiratory causes (NFA) and 12 non-asthma control cases (NAC) were obtained through the Prairie Provinces Asthma Study. Transverse sections of segmental bronchi from three lobes were stained for mucus and smooth muscle actin and the area fractions of mucous plugs, mucous glands and myoepithelial cells determined by point counting. The fine structure of the myoepithelial cells was examined by electron microscopy. Results: FA was characterised by significant increases in mucous gland (p = 0.003), mucous plug (p = 0.004) and myoepithelial cell areas (p = 0.017) compared with NAC. When the ratio of myoepithelial cell area to total gland area was examined, there was a disproportionate and significant increase in FA compared with NAC (p = 0.014). Electron microscopy of FA cases revealed hypertrophy of the myoepithelial cells with increased intracellular myofilaments. The NFA group showed changes in these features that were intermediate between the FA and NAC groups but the differences were not significant. Conclusions: Bronchial mucous glands and mucous gland myoepithelial cell smooth muscle actin are increased in fatal asthma and may contribute to asphyxia due to mucous plugging.

Fatal rhabdomyolysis in systemic lupus erythematosus

The authors describe herein the sixth lupus case that evolved with rhabdomyolysis. A 36-year-old woman with systemic lupus erythematosus was admitted to our hospital with malaise, myalgia, dysphagia, fever, preserved muscle strength, leukocytosis (15,600 cells), and increased creatine kinase of 1,358 IU/L that reached 75,000 IU/L in few days. She denied the use of myotoxic drugs and alcohol. Urine 1 showed false positive for hemoglobinuria (myoglobin) without erythrocytes in the sediment, confirming the diagnosis of rhabdomyolysis. Secondary causes were excluded. She was treated with hyperhydration and alkalinization of urine. Despite treatment, the patient developed pulmonary congestion and she died. The authors also review in this article rhabdomyolysis in patients with systemic lupus erythematosus.

Fatal acute respiratory distress syndrome in a patient with paracoccidioidomycosis: first case report

Paracoccidioidomycosis is a systemic mycosis that is usually acquired early in life by inhalation of conidia which convert in the lungs into yeast forms; these in turn trigger an inflammatory process. This mycosis may appear as an acute/subacute form or a chronic, adult form. Acute/subacute presentations can be observed in children and young adults, with the reticuloendothelial system frequently involved but the lungs are usually spared or present with mild clinical or radiological alterations. Acute respiratory distress syndrome (ARDS), an extensive dysfunction of the lungs alveolar-capillary barrier has occasionally been observed in other endemic mycoses such as coccidioidomycosis, cryptococcosis, histoplasmosis and blastomycosis. We describe the first patient with acute paracoccidioidomycosis who developed fatal ARDS accompanied by multiple organ injuries. The basis of the rarity of this entity in patients with paracoccidioidomycosis, as well as the reasons that may have lead to the development of ARDS in this patient are discussed.

The outer wall of small airways is a major site of remodeling in fatal asthma

Background: Structural and inflammatory changes in asthma involve both the large and small airways, with involvement of the distal lung being related to disease severity. We have previously shown that changes in the extracellular matrix (ECM) composition of the distal lung are associated with loss of alveolar attachments in patients with fatal asthma. However, major ECM elements, such as collagen I and fibronectin and their regulators, have not been addressed at the distal level. Objective: We sought to evaluate ECM remodeling in the distal lungs of asthmatic patients. Methods: Using immunohistochemistry and image analysis, we determined the content of collagen I and III, fibronectin, and matrix metalloproteinases; (MMPs) 1, 2, and 9 and tissue inhibitors of metalloproteinase (MMPs) 1 and 2 in the large and small airways and lung parenchyma of 24 patients with fatal asthma and compared the results with those of 11 nonasthmatic control subjects. Protein content was defined as the area of positive staining divided by basement membrane or septum length. Results: We observed increased collagen I and decreased collagen III content in the small airways of asthmatic patients compared with that seen in control subjects. Greater fibronectin and MMP-1, MMP-2, and MMP-9 content was observed at the outer area of the small airways in asthmatic patients. NIMP content was also increased in the peribronchiolar parenchyma in asthmatic patients. In contrast, TIMP expression was only increased in the large airways of asthmatic patients compared with that seen in control subjects. Conclusions: The outer area of the small airways is a major site of ECM remodeling in fatal asthma, potentially contributing to functional changes and the loss of airway-parenchyma interdependence observed in patients with fatal asthma. (J Allergy Clin Immunol 2009;123:1090-7.)

Fatal gemcitabine-induced pulmonary toxicity in metastatic gallbladder adenocarcinoma

Gemcitabine is a chemotherapy agent that may cause unpredictable side effects. In this report, we describe a fatal gemcitabine-induced pulmonary toxicity in a patient with gallbladder metastatic adenocarcinoma. A 72-year-old patient was submitted to an elective laparoscopic cholecystectomy, and a tubular adenocarcinoma in the gallbladder was incidentally diagnosed. CT scan and ultrasound before the surgery did not show any tumor. After the surgery a Pet scan was positive for a hot-spot in the left colon. The colonic lesion was conveniently removed and the histology evaluation confirmed the diagnosis of adenocarcinoma tubular. The patient was then submitted to three sections of 1,600 mg/m(2) of gemcitabine with intervals of 1 week. Three weeks later he developed severe respiratory distress. A helicoidal CT scan showed diffuse and severe interstitial pneumonitis, and lung biopsy confirmed accelerated usual interstitial pneumonia consistent with drug-induced toxicity. The patient presented unfavorable evolution with progressive worsening of respiratory function, hypotension, and renal failure. He died 1 month later in spite of methylprednisolone pulse therapy, large spectrum antimicrobial therapy, and full support of respiratory, hemodynamic and renal systems. Gemcitabine-induced pulmonary toxicity is usually a dramatic condition. Physicians should suspect pulmonary toxicity in patients with respiratory distress after gemcitabine chemotherapy, mainly in elderly patients.

Lung Pathology in Fatal Novel Human Influenza A (H1N1) Infection

Rationale: There are no reports of the systemic human pathology of the novel swine H1N1 influenza (S-OIV) infection. Objectives: The autopsy findings of 21 Brazilian patients with confirmed S-OIV infection are presented. These patients died in the winter of the southern hemisphere 2009 pandemic, with acute respiratory failure. Methods: Lung tissue was submitted to virologic and bacteriologic analysis with real-time reverse transcriptase polymerase chain reaction and electron microscopy. Expression of toll-like receptor (TLR)-3, IFN-gamma, tumor necrosis factor-alpha, CD8(+) T cells and granzyme B(+) cells in the lungs was investigated by immunohistochemistry. Measurements and Main Results: Patients were aged from 1 to 68 years (72% between 30 and 59 yr) and 12 were male. Sixteen patients had preexisting medical conditions. Diff use alveolar damage was present in 20 individuals. in six patients, diffuse alveolar damage was associated with necrotizing bronchiolitis and in five with extensive hemorrhage. There was also a cytopathic effect in the bronchial and alveolar epithelial cells, as well as necrosis, epithelial hyperplasia, and squamous metaplasia of the large airways. There was marked expression of TLR-3 and IFN-gamma and a large number of CD8(+) T cell sand granzyme B(+) cells within the lung tissue. Changes in other organs were mainly secondary to multiple organ failure. Conclusions: Autopsies have shown that the main pathological changes associated with S-OIV infection are localized to the lungs, where three distinct histological patterns can be identified. We also show evidence of ongoing pulmonary aberrant immune response. Our results reinforce the usefulness of autopsy in increasing the understanding of the novel human influenza A (H1N1) infection.

Pulmonary periarterial inflammation in fatal asthma

P>Background To date, little information has been available about pulmonary artery pathology in asthma. The pulmonary artery supplies the distal parts of the lungs and likely represents a site of immunological reaction in allergic inflammation. The objective of this study was to describe the inflammatory cell phenotype of pulmonary artery adventitial inflammation in lung tissue from patients who died of asthma. Methods We quantified the different inflammatory cell types in the periarterial region of small pulmonary arteries in lung tissue from 22 patients who died of asthma [fatal asthma (FA)] and 10 control subjects. Using immunohistochemistry and image analysis, we quantified the cell density for T lymphocytes (CD3, CD4, CD8), B lymphocytes (CD20), eosinophils, mast cells (chymase and tryptase), and neutrophils in the adventitial layer of pulmonary arteries with a diameter smaller than 500 mu m. Results Our data (median/interquartile range) demonstrated increased cell density of mast cells [FA=271.8 (148.7) cells/mm

Characterization of autopsy-proven fatal asthma patients in Sao Paulo, Brazil

Few data are available on autopsy-proven fatal asthma patients in Sao Paulo, Brazil. We characterized 73 asthma patients who were autopsied at the Servico de Verificacao de Obitos do Universidade de Sao Paulo between 1996 and 2004. An interview with the next of kin assessed socioeconomic status, history, and treatment of asthma. There were 42 women and 31 men. Fifty-six (76.7%) of them were older than 34 years. Sixty-three percent were Caucasians, 77.3% had < 8 years of schooling, and the median income was 1.6 times the minimum wage. Twenty-two patients (30.1%) were smokers and 14 (19.2%) were ex-smokers. Only 25 (34.2%) patients were regularly followed by a doctor. Only 12.3% received inhaled steroids. Thirty-five patients (47.9%) had moderate-to-severe asthma. Fifty-five (75.3%) deaths took place outside a hospital, We conclude that this population shares characteristics of severe or poorly controlled asthma, low educational and socioeconomic levels, and lack of medical care and of inhaled steroid use.

Evidence of Renal Infection in Fatal Cases of 2009 Pandemic Influenza A (HI NI)

The 2009 pandemic influenza A (H1N1) caused significant morbidity and mortality. Acute lung injury is the hallmark of the disease, but multiple organ system dysfunction can develop and lead to death. Therefore, we sought to investigate whether there was postmortem evidence of H1N1 presence and virus-induced organ injury in autopsy specimens. Five cases in which patients died of influenza A (H1N1) virus infection were studied. The lungs of all patients showed macroscopic and microscopic findings already described for H1N1 (consolidation, edema, hemorrhage, alveolar damage, hyaline membrane, and inflammation), and H1N1 viruses were present in alveolar cells in immunochemical studies. Acute tubular necrosis was present in all cases, but there was no evidence of direct virus-induced kidney injury. Nevertheless, H1N1 viruses were found in the cytoplasm of glomerular macrophages in the kidneys of 4 patients. Therefore, our data provide strong evidence that H1N1 presence is not restricted to the lungs.

Comparison of GPX with or without solvent and hand files in removing filling materials from root canals-An ex vivo study

Objective. The aim of this study was to compare GPX instruments and hand files for gutta-percha removal. Study design. Fifty maxillary central incisors with a single straight canal were instrumented and filled. The teeth were divided into 5 groups of 10 specimens each, according to the gutta-percha removal techniques: group 1: GPX (21-mm-long teeth); group 2: GPX and xylol as solvent (21-mm-long teeth); group 3: GPX (25-mm-long teeth); group 4: GPX and xylol as solvent (25-mm-long teeth); and group 5: hand files and xylol as solvent. The amount of time for gutta-percha removal and the number of fractured instruments were evaluated. Radiographs were taken, and the teeth were grooved longitudinally and split. The area of residual debris was measured using Sigma Scan software. Results. The time for filling material removal was significantly shorter when GPX was used (P < .05). Overall, hand files and solvent produced fewer remnants of filling materials (P < .05). In the GPX 25 mm-long teeth group, the filling material was not removed in the apical third. Conclusions. Under the experimental conditions, the GPX instruments proved to be faster than hand instruments in removing root filling materials; however, hand instruments left a smaller amount of residual filling materials on the canal walls. The GPX instruments did not pull the gutta-percha beyond its tip. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010; 110: 675-680)