Transbronchial biopsies' histopathological findings leading to successful late steroid therapy in Covid-19 acute respiratory failure.

We present results from clinical, radiologic, gas exchange, lung mechanics, and fibre-optic bronchoscopy-guided transbronchial biopsies in a case of acute respiratory failure due to SARS-CoV-2 (Covid-19). This report highlights the pulmonary, immunological, and inflammatory changes found during acute diffuse alveolar damage and the later organizing phase. An early diffuse alveolar damage pattern with predominant epithelial involvement with active recruitment of T cells and monocytes was observed followed by a late organizing pattern with pneumocyte hyperplasia, inflammatory infiltration, prominent endotheliitis, and secondary germinal centers. The patient's deterioration paralleling the late immuno-pathological findings based the decision to administer intravenous corticosteroids, resulting in clinical, gasometric, and radiologic improvement. We believe that real-time clinicopathological correlation, along with the description of the immunological processes at play, will contribute to the full clinical picture of Covid-19 and might lead to a more rational approach in the precise timing of anti-inflammatory, anti-cytokine, or steroid therapies.

Diaphragm Atrophy During Pediatric Acute Respiratory Failure Is Associated With Prolonged Noninvasive Ventilation Requirement Following Extubation.

OBJECTIVES: Diaphragm atrophy is evident during invasive ventilation for pediatric acute respiratory failure, but with unknown significance. We hypothesized that diaphragm atrophy in pediatric acute respiratory failure is associated with prolonged noninvasive positive pressure ventilation following extubation. DESIGN: Prospective observational study. SETTING: Single-center academic PICU. PATIENTS: Invasively ventilated children with acute respiratory failure. INTERVENTIONS: Diaphragm ultrasound was performed within 36 hours after intubation and repeated within 48 hours preceding extubation. Rapid shallow breathing index at 15 and 30 minutes of a spontaneous breathing trial and negative inspiratory force were collected in a subset of patients concurrently with the ultrasound measurements. MEASUREMENTS AND MAIN RESULTS: Diaphragm thickness at end-expiration was measured to assess for diaphragm atrophy during mechanical ventilation. Percentage change in diaphragm thickness at end-expiration was defined as baseline diaphragm thickness at end-expiration minus final, preextubation diaphragm thickness at end-expiration divided by baseline diaphragm thickness at end-expiration. The primary outcome measure was duration of noninvasive positive pressure ventilation following extubation with prolonged use defined as noninvasive positive pressure ventilation use for greater than 24 hours postextubation. Among 56 children, 47 (median age, 15.5 mo; interquartile range, 6-53 mo) had diaphragm thickness at end-expiration measured within 48 hours prior to extubation. Fourteen (30%) had prolonged noninvasive positive pressure ventilation use with median duration 110 hours (interquartile range, 52-130 hr). The median percentage change of diaphragm thickness at end-expiration from baseline among those with and without prolonged noninvasive positive pressure ventilation use was -20% (interquartile range, -32% to -10%) versus -7% (interquartile range, -21% to 0%) (p = 0.04). CONCLUSIONS: Diaphragm atrophy is associated with prolonged postextubation noninvasive positive pressure ventilation in children with acute respiratory failure. Serial bedside diaphragm ultrasound may identify children at risk for prolonged noninvasive positive pressure ventilation use after extubation.

Neonatal Lung Disease Associated with TBX4 Mutations.

Variable lung disease was documented in 2 infants with heterozygous TBX4 mutations; their clinical presentations, pathology, and outcomes were distinct. These findings demonstrate that TBX4 gene mutations are associated with neonatal respiratory failure and highlight the wide spectrum of clinicopathological outcomes that have implications for patient diagnosis and management.

Bronquiolitis obliterante secundaria a sindrome de stevens-johnson. Presentacion de 2 casos y revision de la literatura / Obliterans bronchiolitis secondary to stevens-johnson syndrome: case reports

Stevens-Johnson syndrome corresponds to a hypersensitivity reaction produced by various etiologies, for example exposure to drugs, microbial agents, or by an idiopathic cause. It is marked by an acute vesicular-bullous eruption, which affects the skin and mucous membranes, with systemic manifestations of variable severity, and it may present a fatal evolution. Stevens-Johnson syndrome can occasionally present chronic pulmonary complications, such as bronchiolitis obliterans; however, other etiologies are more frequent in our environment, for example severe pneumonia due to adenovirus. Our objective is to present two cases of bronchiolitis obliterans post Stevens-Johnson syndrome and to make a literature review.

El síndrome de Stevens-Johnson corresponde a una respuesta de hipersensibilidad producida por diversas etiologías, que incluyen exposición a drogas, agentes microbianos o idiopática. Se manifiesta por una erupción vesículo-bulosa aguda, que afecta la piel y las mucosas, con manifestaciones sistémicas de severidad variable, pudiendo presentar una evolución fatal. El síndrome de Stevens-Johnson puede presentar ocasionalmente complicaciones pulmonares crónicas, como bronquiolitis obliterante, siendo en nuestro medio más frecuente otras etiologías, como la observada luego de una neumonía grave por adenovirus. El objetivo es presentar dos casos de bronquiolitis obliterante post síndrome de Stevens-Johnson y hacer una revisión de la literatura.

Pathology and causes of death in stranded humpback whales (Megaptera novaeangliae) from Brazil.

This study describes the pathologic findings of 24 humpback whales (Megaptera novaeangliae) found stranded along the Brazilian coast from 2004 to 2016. Eighteen (75%) animals evaluated were found stranded alive. From these, 13 died naturally on shore and five were euthanized. Six died at sea and were washed ashore. Of the 24, 19 (79.2%) were calves, four (16.7%) were juveniles, and one (4.2%) was an adult. The most probable cause of stranding and/or death (CSD) was determined in 23/24 (95.8%) individuals. In calves, CSD included neonatal respiratory distress (13/19; 68.4%), infectious disease (septicemia, omphaloarteritis and urachocystitis; 3/19; 15.8%), trauma of unknown origin (2/19; 10.5%), and vehicular trauma (vessel strike; 1/19; 5.3%). In juveniles and adult individuals, CSD was: emaciation (2/5; 40%), sunlight-thermal burn shock (1/5; 20%); and discospondylitis (1/5; 20%). In one juvenile, the CSD was undetermined (1/5; 20%). This study integrates novel findings and published case reports to delineate the pathology of a South-western Atlantic population of humpback whales. This foundation will aid in the assessment of the population health and establish a baseline for development of conservation policies.

Progressive Diaphragm Atrophy in Pediatric Acute Respiratory Failure.

OBJECTIVES: Diaphragm atrophy is associated with delayed weaning from mechanical ventilation and increased mortality in critically ill adults. We sought to test for the presence of diaphragm atrophy in children with acute respiratory failure. DESIGN: Prospective, observational study. SETTING: Single-center tertiary noncardiac PICU in a children's hospital. PATIENTS: Invasively ventilated children with acute respiratory failure. MEASUREMENTS AND MAIN RESULTS: Diaphragm thickness at end-expiration and end-inspiration were serially measured by ultrasound in 56 patients (median age, 17 mo; interquartile range, 5.5-52), first within 36 hours of intubation and last preceding extubation. The median duration of mechanical ventilation was 140 hours (interquartile range, 83-201). At initial measurement, thickness at end-expiration was 2.0 mm (interquartile range, 1.8-2.5) and thickness at end-inspiration was 2.5 mm (interquartile range, 2-2.8). The change in thickness at end-expiration during mechanical ventilation between first and last measurement was -13.8% (interquartile range, -27.4% to 0%), with a -3.4% daily atrophy rate (interquartile range, -5.6 to 0%). Thickening fraction = ([thickness at end-inspiration - thickness at end-expiration]/thickness at end-inspiration) throughout the course of mechanical ventilation was linearly correlated with spontaneous breathing fraction (beta coefficient, 9.4; 95% CI, 4.2-14.7; p = 0.001). For children with a period of spontaneous breathing fraction less than 0.5 during mechanical ventilation, those with exposure to a continuous neuromuscular blockade infusion (n = 15) had a significantly larger decrease in thickness at end-expiration compared with children with low spontaneous breathing fraction who were not exposed to a neuromuscular blockade infusion (n = 18) (-16.4%, [interquartile range, -28.4% to -7.0%] vs -7.3%; [interquartile range, -10.9% to -0%]; p = 0.036). CONCLUSIONS: Diaphragm atrophy is present in children on mechanical ventilation for acute respiratory failure. Diaphragm contractility, measured as thickening fraction, is strongly correlated with spontaneous breathing fraction. The combination of exposure to neuromuscular blockade infusion with low overall spontaneous breathing fraction is associated with a greater degree of atrophy.

Mac-1 deficiency induces respiratory failure by affecting type I alveolar epithelial cells.

As a ß2 integrin family member, Mac-1 plays an important role in the inflammatory response. Inflammation and lung injury are closely associated, but the involvement of Mac-1 in the occurrence and development of such pathologies remains poorly understood. We aimed to investigate the relationship between Mac-1 deficiency and respiratory failure in Mac-1 knockout {Mac-1-/-} mice, using C57BL/6J mice as a control. The newborn survival rate of Mac-1-/- mice was calculated, and mouse lung tissue was treated with hematoxylin and eosin and subjected to immunofluorescent staining. Moreover, western blotting and immunohistochemistry were used to detect the expression of molecules specific to type I and type II alveolar epithelial cells, as well as alveolar surfactant proteins secreted by the latter. Survival of Mac-1-/- pups was significantly lower than that of newborn C57BL/6J mice. In a float test, lung tissues from C57BL/6J mice were buoyant, whereas those of Mac-1-/- mice were not. Compared with C57BL/6J mice, expression of proSP-C {specific to type II alveolar epithelial cells} and alveolar surfactant proteins in Mac-1-/- mice was not significantly different, implying that type II cell function was unaltered. However, western blotting revealed expression of T1α, Aqp5, and Snx5 {type I alveolar epithelial cell markers} in Mac-1-/- mice to be significantly decreased {P < 0.05}. In conclusion, Mac-1 may play an important role in respiratory failure. Its absence leads to this condition not by influencing type II alveolar epithelial cells or their secreted surfactant proteins, but rather by reducing type I alveolar cell numbers.

Evaluación de los músculos respiratorios en la parálisis diafragmática bilateral / Assessment of respiratory muscle strength in bilateral diaphragmatic paralysis

Measurement of respiratory muscle strength is useful in order to detect respiratory muscle weakness and to quantify its severity. Apropos of a patient with bilateral diaphragmatic paralysis, we review the clinical manifestations and methods for assessing the strength of the respiratory muscles. In patients with severe respiratory muscle weakness, vital capacity and total lung capacity are reduced but are a non-specific and relatively insensitive measure. Conventionally, inspiratory and expiratory muscle strength has been assessed by maximal inspiratory and expiratory mouth pressures sustained for one second (PIMax and PEMax). The sniffmanoeuvre is natural and probably easier to perform. Sniff pressures are more reproducible and useful measure of diaphragmatic strength. However, the PIMax-PEMax and sniff manoeuvres are volition dependent, and submaximal efforts are most likely to occur in patients who are ill or breathless. Non-volitional tests include measurements of twitch esophageal, gastric and transdiaphragmatic pressure during bilateral electrical and magnetic phrenic nerve stimulation. Electrical phrenic nerve stimulation is technically difficult and is also uncomfortable and painful. Magnetic phrenic nerve stimulation is less painful and transdiaphragmatic pressure is reproducible in normal subjects. Systematic clinical evaluation and additional laboratory tests allow the diagnosis in most patients with respiratory muscle weakness.

La evaluación de la fuerza de los músculos respiratorios permite diagnosticar y cuantificar la gravedad de la debilidad muscular en diferentes enfermedades. A propósito de un paciente con parálisis diafragmática bilateral, hemos revisado el cuadro clínico y los procedimientos diagnósticos para evaluar la fuerza de los músculos respiratorios. En los pacientes con debilidad muscular respiratoria severa, disminuye la capacidad vital y la capacidad pulmonar total, pero es una medida inespecífica y relativamente insensible. Tradicionalmente, la fuerza muscular respiratoria es evaluada midiendo la presión inspiratoria y espiratoria máximas en la boca sostenidas durante un segundo (PIMax y PEMax). La medición de la presión inspiratoria máxima en la nariz (SNIP) es una maniobra natural, más simple de medir y más reproducible, siendo útil en la evaluación de la fuerza diafragmática. Sin embargo, estas técnicas no invasivas son operador dependiente, por lo tanto, esfuerzos submáximos es más probable que ocurran en pacientes graves o con disnea. Las mediciones de las presiones esofágica, gástrica y transdiafragmática mediante estimulación eléctrica o magnética del nervio frénico no son dependientes de la voluntad y son más confiables. Sin embargo, la estimulación eléctrica del nervio frénico es técnicamente difícil y puede ser incómoda y dolorosa. La estimulación magnética del nervio frénico es menos dolorosa y la medición de la presión transdiafragmática es reproducible en sujetos normales. La evaluación clínica sistemática y los exámenes de laboratorio complementarios permiten establecer el diagnóstico en la mayoría de los pacientes con debilidad de los músculos respiratorios.

Presentación inusual de microcarcinoma papilar tiroideo: insuficiencia respiratoria por metástasis pulmonares / Unusual presentation of micro carcinoma of thyroid: pulmonary metastases and respiratory distress

El micro carcinoma papilar de la glándula tiroidea son lesiones de 1 cm o menos, siendo su incidencia hasta en un 35% en series de autopsias en población general, y comúnmente son de buen pronóstico. Las metástasis distantes en el carcinoma diferenciado de tiroides son bien infrecuentes y su prevalencia puede variar entre un 5% al 23% de los casos, pero son extremadamente inusuales en el micro carcinoma tiroideo. Se relata un caso clínico de una paciente de 38 años de edad; quien consultó por insuficiencia respiratoria aguda realizando el diagnóstico de micro carcinoma papilar con metástasis pulmonares y se describe su manejo, encontrándose actualmente eutiroidea, controlada su enfermedad, con tratamiento hormonal supresivo y con niveles de tiroglobulinas y anticuerpos antitiroglobulinas normales

The papillary micro carcinoma thyroid gland is injuries of 1 cm or less, with incidence until 35% in series of autopsies in general population, and is commonly considered as a good prognosis. The distant metastases in the differentiated thyroid carcinoma are infrequent and its prevalence varies from 5% to 23% of all cases, but is extremely unusual in the thyroid micro carcinoma. We describe a clinical case of a female patient of 38 years old; who consulted us by acute respiratory failure, we are making the diagnosis of a papillary micro carcinoma with lung metastases and describes its handling, and finding currently normal thyroid hormone value and controlled her disease, the suppression hormonal treatment, tyro globulin and anti- tyro globulins antibody normal levels

Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure: demographics, etiologic and pulmonary histologic analysis.

OBJECTIVES: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life. METHODS: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression. RESULTS: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema. CONCLUSIONS: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has not previously been reported.

Postmortem diagnosis of acute myocardial infarction in patients with acute respiratory failure: demographics, etiologic and pulmonary histologic analysis

OBJECTIVES: Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life. METHODS: This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression. RESULTS: In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema. CONCLUSIONS: For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has not previously been reported.

Vía aérea difícil / Difficult airway

Difficult airway is a life-threatening situation which compromises the permeability of the upper airway and thus adequate ventilation and oxygenation. Multiple factors, acute and chronic such as: infectious, neoplastic and trauma have been associated with critical airway. Morbidity and mortality related to a difficult airway management remains as a significant problem in children, so is essential for the pediatric health team to be trained to recognize and anticipate situations that in clinical practice might determine a critical airway. The aim of this review is to provide concepts and guidance to assess patients with potentially difficult airway.

Una vía aérea difícil condiciona una situación con riesgo vital, ya que pone en peligro la permeabilidad de la vía aérea superior y con esto la capacidad de mantener una adecuada ventilación y oxigenación. Múltiples factores, tanto agudos como crónicos, entre ellos factores anatómicos propios del niño/a, complicaciones infecciosas, neoplásicas y/o traumáticas se han asociado con una vía aérea crítica. La morbilidad y mortalidad asociada al manejo inadecuado de esta condición continua siendo un problema significativo en la edad pediátrica; siendo fundamental que el equipo de salud se encuentre entrenado en reconocer y anticipar situaciones que en la práctica clínica podrían asociarse con una vía aérea difícil o crítica. El objetivo de la presente revisión es otorgar conceptos y una orientación en el enfrentamiento de los pacientes con una vía aérea potencialmente difícil.

Hantavirus pulmonary syndrome.

Hantavirus pulmonary syndrome (HPS) is a severe disease characterized by a rapid onset of pulmonary edema followed by respiratory failure and cardiogenic shock. The HPS associated viruses are members of the genus Hantavirus, family Bunyaviridae. Hantaviruses have a worldwide distribution and are broadly split into the New World hantaviruses, which includes those causing HPS, and the Old World hantaviruses [including the prototype Hantaan virus (HTNV)], which are associated with a different disease, hemorrhagic fever with renal syndrome (HFRS). Sin Nombre virus (SNV) and Andes virus (ANDV) are the most common causes of HPS in North and South America, respectively. Case fatality of HPS is approximately 40%. Pathogenic New World hantaviruses infect the lung microvascular endothelium without causing any virus induced cytopathic effect. However, virus infection results in microvascular leakage, which is the hallmark of HPS. This article briefly reviews the knowledge on HPS-associated hantaviruses accumulated since their discovery, less than 20 years ago.

Demographic, etiological, and histological pulmonary analysis of patients with acute respiratory failure: a study of 19 years of autopsies.

INTRODUCTION: Acute respiratory failure has been one of the most important causes of death in intensive care units, and certain aspects of its pulmonary pathology are currently unknown. OBJECTIVES: The objective was to describe the demographic data, etiology, and pulmonary histopathological findings of different diseases in the autopsies of patients with acute respiratory failure. METHOD: Autopsies of 4,710 patients with acute respiratory failure from 1990 to 2008 were reviewed, and the following data were obtained: age, sex, and major associated diseases. The pulmonary histopathology was categorized as diffuse alveolar damage, pulmonary edema, alveolar hemorrhage, and lymphoplasmacytic interstitial pneumonia. The odds ratio of the concordance between the major associated diseases and specific autopsy findings was calculated using logistic regression. RESULTS: Bacterial bronchopneumonia was present in 33.9% of the cases and cancer in 28.1%. The pulmonary histopathology showed diffuse alveolar damage in 40.7% (1,917) of the cases. A multivariate analysis showed a significant and powerful association between diffuse alveolar damage and bronchopneumonia, HIV/AIDS, sepsis, and septic shock, between liver cirrhosis and pulmonary embolism, between pulmonary edema and acute myocardial infarction, between dilated cardiomyopathy and cancer, between alveolar hemorrhage and bronchopneumonia and pulmonary embolism, and between lymphoplasmacytic interstitial pneumonia and HIV/ AIDS and liver cirrhosis. CONCLUSIONS: Bronchopneumonia was the most common diagnosis in these cases. The most prevalent pulmonary histopathological pattern was diffuse alveolar damage, which was associated with different inflammatory conditions. Further studies are necessary to elucidate the complete pathophysiological mechanisms involved with each disease and the development of acute respiratory failure.

Pronóstico de pacientes ingresados a Unidad de Cuidados Intensivos por falla respiratoria asociada a presencia de infiltrados pulmonares / Prognosis of patients with acute respiratory failure and pulmonary infiltrates admitted to intensive care unit

En la unidad de cuidados intensivos (UCI), la insuficiencia respiratoria aguda (IRA) asociada a infiltrados pulmonares de causa desconocida se relaciona con alta morbilidad y mortalidad. El objetivo principal de este trabajo fue conocer el pronóstico de pacientes con IRA, infiltrados pulmonares y necesidad de ventilación mecánica (VM) ingresados a UCI. Como objetivo secundario se planteó evaluar la utilidad de medios diagnósticos de uso habitual en este grupo de pacientes en relación al pronóstico y la conducta terapéutica. Se realizó un estudio observacional retrospectivo que incluyó todos los pacientes ingresados a la UCI del Hospital Naval Almirante Nef por IRA de causa desconocida asociada a infiltrados pulmonares en radiografía de tórax y que tengan necesidad de VM entre los años 2006 y 2010. Se incluyeron 90 pacientes de los cuales 45,6 por ciento fueron de sexo masculino. La edad promedio fue 66 años (DS 17,1). El puntaje promedio de score APACHE II fue 20,6 (DS 7,7). La mortalidad fue 52,2 por ciento y el tiempo promedio de estadía en UCI fueron 14 días (DS 14,4). La principal causa de IRA fue síndrome de distress respiratorio agudo (32 por ciento).Otras causas fueron neumonía adquirida en la comunidad (28,2 por ciento), neumonía aspirativa (12,2 por ciento), neumonía nosocomial (7,8 por ciento) y neumonía criptogénica organizada (6,7 por ciento). La realización de tomografía computarizada de tórax, lavado broncoalveolar y biopsia pulmonar determinó cambio de conducta terapéutica en 31 por ciento, 58 por ciento y 88 por ciento de los casos, respectivamente. En conclusión, los pacientes con IRA tienen alta mortalidad. La causa más frecuente fue el síndrome de distress respiratorio agudo. El uso de procedimientos diagnósticos pueden cambiar las medidas terapéuticas empleadas, en especial la biopsia pulmonar.

In the intensive care unit (ICU), acute respiratory failure (ARF) associated with unexplained pulmonary infiltrates is associated with high morbidity and mortality. The main objective of this study was to determine the prognosis of patients with ARF and pulmonary infiltrates admitted to ICU. The secondary objective was proposed to evaluate the usefulness of diagnostic methods frequently used in this patient group and correlated them with prognosis and therapeutic management. We performed a retrospective observational study that included all patients admitted to ICU of Almirante Nef Naval Hospital with ARF of unknown cause associated with pulmonary infiltrates on chest radiography during the years 2006-2010. We included 90 patients of which 45 percent were male. The average age was 66 years. The average APACHE II score was 20.6. Mortality was 52.2 percent and the average length of stay in the ICU was 14 days (SD 14.4). The main cause of ARF was acute respiratory distress syndrome (32 percent). Other causes were community-acquired pneumonia (28.2 percent), aspiration pneumonia (12.2 percent), nosocomial pneumonia (7.8 percent) and cryptogenic organized pneumonia (6.7 percent. The performance of chest computed tomography, bronchoalveolar lavage and lung biopsy determined therapeutic behavior change in 31 percent 58 percent and 88 percent of cases, respectively. In conclusion, patients with ARF have high mortality. The most common cause was acute respiratory distress syndrome. The use of diagnostic procedures may change the therapeutic measures used, particularly lung biopsy.

Demographic, etiological, and histological pulmonary analysis of patients with acute respiratory failure: a study of 19 years of autopsies

INTRODUCTION: Acute respiratory failure has been one of the most important causes of death in intensive care units, and certain aspects of its pulmonary pathology are currently unknown. OBJECTIVES: The objective was to describe the demographic data, etiology, and pulmonary histopathological findings of different diseases in the autopsies of patients with acute respiratory failure. METHOD: Autopsies of 4,710 patients with acute respiratory failure from 1990 to 2008 were reviewed, and the following data were obtained: age, sex, and major associated diseases. The pulmonary histopathology was categorized as diffuse alveolar damage, pulmonary edema, alveolar hemorrhage, and lymphoplasmacytic interstitial pneumonia. The odds ratio of the concordance between the major associated diseases and specific autopsy findings was calculated using logistic regression. RESULTS: Bacterial bronchopneumonia was present in 33.9 percent of the cases and cancer in 28.1 percent. The pulmonary histopathology showed diffuse alveolar damage in 40.7 percent (1,917) of the cases. A multivariate analysis showed a significant and powerful association between diffuse alveolar damage and bronchopneumonia, HIV/AIDS, sepsis, and septic shock, between liver cirrhosis and pulmonary embolism, between pulmonary edema and acute myocardial infarction, between dilated cardiomyopathy and cancer, between alveolar hemorrhage and bronchopneumonia and pulmonary embolism, and between lymphoplasmacytic interstitial pneumonia and HIV/ AIDS and liver cirrhosis. CONCLUSIONS: Bronchopneumonia was the most common diagnosis in these cases. The most prevalent pulmonary histopathological pattern was diffuse alveolar damage, which was associated with different inflammatory conditions. Further studies are necessary to elucidate the complete pathophysiological mechanisms involved with each disease and the development of acute respiratory failure.