Acute and chronic bovine pulmonary edema and emphysema in Uruguay / Edema e enfisema pulmonar agudo e crônico em bovinos do Uruguai

An outbreak of pulmonary edema and emphysema with acute and chronic cases is reported in a farm in Uruguay. In a herd of 40 Hereford steers, 20 died. The deaths began four days after a change of paddock, from an old pasture of Avena sativa to a lush growing pasture of the same grass. Acutely affected animals showed severe dyspnea, sialorrhea, cough, and subcutaneous edema, and died within 72 hours. Chronically affected steers showed dyspnea, respiratory noises, weight loss, and intolerance to exercise. The deaths began four days after the change of paddock. Ten days after the first death, the steers were withdrawn from the pasture, but continued dying throughout the following 40 days. Twenty animals died and six were necropsied. Grossly, the lungs were diffusely armed and glistening, with reddish and crepitant cut surface, and presented alveolar septae sharply distended by edema and emphysema. There was subpleural emphysema with air blebs distributed across the pleural surface. Presence of Dictyocaulus viviparus was observed in three steers. In some animals, the trachea was diffusely reddish with presence of pink foam; in some others, there was bloody liquid in the tracheal lumen. Histologic examination showed severe diffuse alveolar and interstitial emphysema, hyaline membranes adhered to the alveolar wall, thickening of the interlobular septae with proliferation of type II pneumocytes, and moderate-to-severe multifocal histiocytic, neutrophilic and eosinophilic infiltrate. In the trachea, there was submucosal hemorrhage and moderate multifocal eosinophilic and lymphocytic infiltrate. The steers with chronic signs presented similar lung lesions, but multifocal pulmonary fibrosis and cardiac dilatation were also observed. The diagnosis of acute bovine pulmonary emphysema and edema (ABPE) was based on the occurrence of the disease after introduction of the herd in a lush green pasture, on the characteristic gross and histologic lesions, and on the absence of other toxic or infectious agents causing similar lesions. Cattle raisers should be alert to the risks of occurrence of this disease after the introduction of the herds into paddocks with green and lush pastures.(AU)

Descreve-se um surto de edema e enfisema pulmonar com casos agudos e crônicos em bovinos em uma criação semi-intensiva no Uruguai. De um lote de 40 novilhos da raça Hereford morreram 20. As mortes começaram quatro dias após uma mudança de alimentação, de uma pastagem mais velha de Avena sativa, para uma pastagem recentemente plantada de aveia que estava em brotação. Os animais afetados apresentaram sinais clínicos agudos de dispneia, sialorreia, tosse e alguns desenvolveram edema subcutâneo, morrendo em até 72 horas. Outros novilhos mais cronicamente afetados apresentaram dispneia, ruídos respiratórios, perda de peso e intolerância ao exercício. As mortes começaram quatro dias após a mudança de pastagens. Dez dias após a primeira morte, os novilhos foram retirados do pasto, mas morreram ainda durante 40 dias mais. Ao total, morreram vinte animais e seis foram necropsiados. Nas necropsias dos animais mortos na fase aguda os pulmões estavam difusamente armados e brilhosos e ao corte de coloração avermelhada e crepitante, com os septos alveolares acentuadamente distendidos por edema e enfisema. Havia enfisema subpleural caracterizado por bolhas de ar distribuídas pela superfície pleural. Em três bovinos havia ainda presença de Dictyocaulus viviparus. Alguns animais apresentaram a traqueia difusamente avermelhada com espuma de coloração rósea ou liquido sanguinolento livre na luz traqueal. Histologicamente havia edema e enfisema alveolar e intersticial difuso severo, membranas hialinas espessas aderidas à parede alveolar, espessamento dos septos interlobulares com proliferação de pneumócitos tipo II e infiltrado inflamatório histiocítico, neutrofílico e eosinofílico multifocal moderado a severo. Na traqueia havia hemorragias na submucosa e infiltrado eosinofílico e linfocítico multifocal. Os novilhos com sinais crônicos apresentaram lesões pulmonares semelhantes, entretanto, foram observadas também, fibrose pulmonar multifocal e dilatação cardíaca. O diagnóstico de EEPAB baseou-se na ocorrência da doença após a introdução do rebanho em uma pastagem viçosa em brotação, nas características macroscópicas e histológicas e na ausência de outros agentes tóxicos ou infecciosos que causam lesões semelhantes. Se alerta para os riscos da ocorrência desta enfermidade, quando houver mudanças de pastagens.(AU)

Incidencia del edema pulmonar no cardiogénico mediante estudio histopatológico periodo 2013 ­ 2016 / Incidence of noncardiogenic pulmonary edema by histopathological study period 2013 ­ 2016

El edema pulmonar no cardiogénico es una entidad fisiopatológica caracterizada por una lesión generalizada de los capilares pulmonares que provoca un aumento de su permeabilidad a los líquidos, proteínas y otros elementos formes de la sangre, ocasionando un constante flujo de líquidos desde la circulación pulmonar hacia el espacio intersticial y los alvéolos, resultando el edema pulmonar no cardiogénico. El objetivo de este estudio es considerar la incidencia de esta entidad en los casos de muertes súbitas, por medio del estudio histopatológico y caracterizar los factores predisponentes relacionados a esta patología. Todas las muestras fueron sometidas a procedimientos técnicos para estudio histopatológico para confirmar o descartar el diagnóstico macroscópico emitido en la necropsia. Para este estudio se analizaron 518 informes de estudio histopatológico correspondientes a los años 2013, 2014, 2015 y 2016, las cuales 119 correspondieron a edema pulmonar no cardiogénico, siendo el 22,97 % de estos 119 informes de estudio histopatológico se analizaron e interpretaron de acuerdo con los factores predisponentes teniendo como hallazgo importante 39,49 % al síndrome metabólico; 21,84 % a la intoxicación alcohólica; 14,28 % a la intoxicación medicamentosa, entre otros. De esto concluimos que es importante realizar el estudio histopatológico a los casos de muerte súbita sin diagnóstico, puesto que algunas pueden ser encasilladas en un síndrome metabólico o intoxicaciones que ameritan investigación para determinar la causa de muerte.

Non-cardiogenic pulmonary edema is a pathophysiological entity characterized by a generalized lesion of the pulmonary capillaries that causes an increase of its permeability to the fluids, proteins and other form elements of the blood, causing a constant flow of liquids from the pulmonary circulation towards the interstitial space and alveoli, resulting in non-cardiogenic pulmonary edema. The aim of this study is to consider the incidence of this entity in cases of sudden deaths, through the histopathological study and to characterize the predisposing factors related to this pathology. All samples were subjected to technical procedures for histopathological study to confirm or rule out the macroscopic diagnosis emitted at necropsy. For this study, 518 histopathological reports corresponding to the years 2013, 2014, 2015 and 2016 were analyzed, of which 119 corresponded to non-cardiogenic pulmonary edema, with 22.97% of these 119 histopathological reports being analyzed and interpreted according to to the predisposing factors having as important finding 39.49% to the metabolic syndrome; 21.84% to alcoholic intoxication; 14.28% to drug intoxication among others. From this we conclude that it is important to carry out the histopathological study to cases of sudden death without diagnosis since some may be pigeonholed in a metabolic syndrome or poisonings that warrant investigation to determine the cause of death.

A case of intramural coronary amyloidosis associated with hemodialysis

Dialysis-related amyloidosis predominantly occurs in osteo-articular structures and dialysis-related amyloid (DRA) substances also deposit in extra-articular tissues. Clinical manifestations of DRA include odynophagia, gastrointestinal hemorrhage, intestinal obstruction, kidney stones, myocardial dysfunction, and subcutaneous tumors. The pathological characteristics of DRA in the heart of hemodialysis patients have rarely been reported. We report the case of a 73-year-old female with a history of cerebral palsy and end-stage renal disease status post two failed renal transplants who had been on hemodialysis for 30 years. The patient was admitted with the working diagnosis of pneumonia. An echocardiography showed markedly reduced biventricular function manifested by low blood pressure with systolic in the 70s and elevated pulmonary artery pressure of 45 mmHg, which did not respond to therapy. Following her demise, the autopsy revealed bilateral pulmonary edema and pleural effusions. There was cardiac amyloid deposition exclusively in the coronary arteries but not in the perimyocytic interstitium. Amyloids were also found in pulmonary and intrarenal arteries and the colon wall. Previous case reports showed that beta 2-microglobulin amyloid deposits in various visceral organs but less frequently in the atrial and/or the ventricular myocardium. In the present case, amyloids in the heart were present in the intramural coronary arteries causing myocardial ischemia and infarction, which was the immediate cause of death.

Comprometimento pulmonar grave em paciente com associação entre diagnóstico de malária e HIV: relato de caso / Severe pulmonary involvement in a patient with associated malaria and HIV: a case report

A associação entre Vírus da Imunodeficiência Humana (HIV) e Malária é um evento de grande repercussão clínica. A grande importância de tal concomitância de diagnósticos dá-se por sua associação negativa, na qual se observa risco aumentado de infecção por malária em pacientes com HIV e o aumento de replicação viral nesses pacientes em decorrência da coinfecção pela malária. Os achados radiológicos incluem infiltrado intersticial ou alveolar, localizado preferencialmente nas regiões peri-hilares e em bases pulmonares, que pode ser associado a derrame pleural. O caso relatado é de um homem de 40 anos, branco, previamente hígido, que interna por quadro de febre, mialgia difusa e fadiga, após viagem de turismo ao continente africano. Em investigação laboratorial inicial, apresenta hemoconcentração e plaquetopenia importante. No decorrer da internação, tem diagnóstico de malária (demonstração do parasita no esfregaço sanguíneo) e inicia tratamento específico. Solicitou-se sorologia para HIV, a qual se apresentou positiva. O paciente evolui com febre ictero-hemorrágica, confusão mental, vômitos, insuficiência ventilatória e insuficiência renal aguda, sendo transferido para Unidade de Terapia Intensiva. Comprovou-se comprometimento pulmonar grave através da realização de Tomografia Computadorizada de Tórax de Alta Resolução, que evidenciou espessamento de septos interlobulares e de bainhas peribroncovasculares, com áreas esparsas de atenuação em vidro fosco e de consolidações, além de evidência de derrame pleural. Conclui-se que padrão de comprometimento radiológico do paciente foi compatível com os relatos já descritos pela literatura, o que corrobora para unificação de apresentação do quadro nos exames de imagem (AU)

The association between human immunodeficiency virus (HIV) and malaria is an event of great clinical repercussion. The great importance of such concomitance of diagnoses is due to its negative association, where there is an increased risk of malaria infection in patients with HIV and increased viral replication in these patients due to malaria co-infection. Radiological findings include interstitial or alveolar infiltrate, preferably located in the peri-hilar regions and at the lung bases, which may be associated with pleural effusion. The case reported here is of a white 40-year-old man, previously healthy, who was hospitalized for fever, diffuse myalgia and fatigue after a trip to the African continent. In initial laboratory investigation, he presented hemoconcentration and important thrombocytopenia. During the hospitalization, malaria was diagnosed (demonstration of the parasite in the blood smear) and specific treatment was initiated. HIV serology was requested and positive. As the patient progressed with icterohemorrhagic fever, mental confusion, vomiting, ventilatory failure and acute renal failure, he was transferred to the Intensive Care Unit. Severe pulmonary involvement was confirmed by high-resolution computed tomography, which showed thickening of interlobular septa and peribroncovascular sheaths, with sparse areas of ground-glass attenuation and consolidations, as well as evidence of pleural effusion. It was concluded that the patient's radiological involvement pattern was consistent with the reports already described in the literature, which corroborates the unification of the presentation of the picture in the imaging tests (AU)

Neurogenic pulmonary edema due to ventriculo-atrial shunt dysfunction: a case report / Edema pulmonar neurogênico devido à disfunção da derivação ventrículo-atrial: relato de caso

ABSTRACT BACKGROUND AND OBJECTIVES: Pulmonary edema is caused by the accumulation of fluid within the air spaces and the interstitium of the lung. Neurogenic pulmonary edema is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant central nervous system insult. It may be a less-recognized consequence of raised intracranial pressure due to obstructive hydrocephalus by blocked ventricular shunts. It usually appears within minutes to hours after the injury and has a high mortality rate if not recognized and treated appropriately. CASE REPORT: We report a patient with acute obstructive hydrocephalus due to ventriculo-atrial shunt dysfunction, proposed to urgent surgery for placement of external ventricular drainage, who presented with neurogenic pulmonary edema preoperatively. She was anesthetized and supportive treatment was instituted. At the end of the procedure the patient showed no clinical signs of respiratory distress, as prompt reduction in intracranial pressure facilitated the regression of the pulmonary edema. CONCLUSIONS: This report addresses the importance of recognition of neurogenic pulmonary edema as a possible perioperative complication resulting from an increase in intracranial pressure. If not recognized and treated appropriately, neurogenic pulmonary edema can lead to acute cardiopulmonary failure with global hypoperfusion and hypoxia. Therefore, awareness of and knowledge about the occurrence, clinical presentation and treatment are essential.

RESUMO JUSTIFICATIVA E OBJETIVOS: o edema pulmonar é causado pelo acúmulo de líquido nos alvéolos e no interstício pulmonar. Edema pulmonar neurogênico é uma síndrome clínica caracterizada por edema pulmonar de início agudo após um acometimento súbito do sistema nervoso central. Pode ser uma consequência menos reconhecida de pressão intracraniana aumentada por causa da hidrocefalia obstrutiva por derivações ventriculares bloqueadas. Geralmente aparece em minutos ou horas após o insulto e tem uma alta taxa de mortalidade, caso não seja identificado e tratado adequadamente. RELATO DE CASO: relatamos o caso de paciente com hidrocefalia obstrutiva aguda por causa da disfunção da derivação ventrículo-atrial, programado para cirurgia em caráter de urgência para a colocação de derivação ventricular externa, que apresentou edema pulmonar neurogênico no pré-operatório. A paciente foi anestesiada e o tratamento de manutenção instituído. No fim do procedimento, a paciente não apresentou quaisquer sinais de distúrbio respiratório, pois a redução rápida da pressão intracraniana facilitou a regressão do edema pulmonar. CONCLUSÕES: este relato aborda a importância da identificação de um edema pulmonar neurogênico como uma possível complicação no período perioperatório resultante de um aumento da pressão intracraniana. Quando não identificado e tratado adequadamente, o edema pulmonar neurogênico pode levar à insuficiência cardiorrespiratória aguda, com hipoperfusão global e hipóxia. Portanto, a conscientização e o conhecimento de sua ocorrência, apresentação clínica e seu tratamento são essenciais.

Characterization of oleic acid-induced acute respiratory distress syndrome model in rat.

Animal studies using oleic acid (OA) model to produce acute respiratory distress syndrome (ARDS) have been inconsistent. Therefore, the present study was undertaken to establish an acute model of ARDS in rats using OA and to characterize its effect on cardio-respiratory parameters and lethality. The trachea, jugular vein and femoral artery of anesthetized adult rats were cannulated. A dose of OA (30-90 µL; iv) was injected in each animal and changes in respiratory frequency (RF), heart rate (HR) and mean arterial pressure (MAP) were recorded. Minute ventilation and PaO2/FiO2 (P/F) ratio were also determined. At the end, lungs were excised for determination of pulmonary water content and histological examination. At all doses of OA, there was immediate decrease followed by increase in RF, however at 75 and 90 µL of OA, RF decreased abruptly and the animals died by 63 ± 8.2 min and 19 ± 6.3 min; respectively. In all the groups, HR and MAP changes followed the respiratory changes. The minute ventilation increased in a dose-dependent manner while the values of P/F ratio decreased correspondingly. Pulmonary edema was induced at all doses. Histological examination of the lung showed alveolar damage, microvascular congestion, microvascular injury, infiltration of inflammatory cells, pulmonary edema and necrosis in a dose-dependent manner. With these results, OA can be used to induce different grades of ARDS in rats and OA doses of 50, 60 and 75 µL resemble mild, moderate and severe forms of ARDS respectively. Hence, OA model serves as a useful tool to study the pathophysiology of ARDS.

Manifestações clínicas e análise histopatológica pulmonar relacionadas a diferentes doenças em pacientes com tromboembolismo pulmonar fatal – um estudo em autópsias / Clinical manifestations and pulmonary histopathological analysis related to different diseases in patients with fatalpulmonary thromboembolism – an autopsy study

Introdução: Tromboembolismo pulmonar (TEP) é uma das mais graves complicações dentre pacientes hospitalizados e permanece subdiagnosticado. Ainda hoje, sua fisiopatologia não está completamente elucidada. Objetivos: Correlacionar comorbidades, neoplasias, cirurgias e achados histológicos às manifestações clínicas associadas ao TEP. Métodos: Entre 2001 a 2008, foram revisadas 291 autópsias de pacientes cuja causa de morte foi TEP. Os seguintes dados foram obtidos: idade, sexo, manifestações clínicas, achados histológicos e principais doenças de base/comorbidades, neoplasias e cirurgias da última internação. Os achados histológicos foram categorizados em: dano alveolar difuso (DAD), edema agudo de pulmão (EAP), hemorragia intra alveolar (HIA) e pneumonia intersticial linfo-plasmocítica (PILP). Odds ratios foram obtidas por regressão logística e foram consideradas significativas quando p < 0,05. Resultados: A mediana de idade foi 64 anos. Cerca de 64% dos pacientes apresentava doenças cardiovasculares. O achado pulmonar mais prevalente foi EAP. Apenas 13% dos casos apresentaram suspeita clínica. Insuficiência respiratória esteve associada a EAP, HIA e DAD; assim como instabilidade hemodinâmica a HIA e DAD. Conclusões: Foram encontradas importantes associações entre achados clínicos e histológicos em pacientes com TEP. A compreensão dos mecanismos fisiopatológicos envolvidos com cada doença associada a TEP pode auxiliar no diagnóstico e no tratamento da doença.

Introduction: Pulmonary thromboembolism (PTE) is one of the most fatal complications among hospitalized patients and remains undiagnosed. Its physiopathology and its epidemiology aren’t widely known in literature. Objectives: To correlate underlying diseases, different cancers and surgeries to histological findings and in-vivo manifestations associated to fatal PTE from autopsy reports. Methods: From 2,001 to 2,008, were reviewed 291 autopsies of patients whose cause of death was PTE. The following data were obtained: age, sex, clinical invivo manifestations, post-mortem pathological patterns and mainassociated underlying diseases, cancers and surgeries performed in last hospitalization. The pulmonary histopathological changes were categorized in: diffuse alveolar damage (DAD), pulmonary edema (PE), alveolar hemorrhage (AH) and lympho/plasmacytic interstitial pneumonia (LPIP). Odds ratios of positive relations were obtained by logistic regression and were considered significative when p < 0.05. Results: The median age was 64 years. 64% ofpatients presented cardiovascular illness associated to PTE. The most prevalent pulmonary finding was PE. Only 13% of cases had clinical suspect. Acute respiratory failure was positively related to PE, AH and DAD; as well hemodynamic instability to AH and DAD. Conclusions: We found important relations between clinical data and histological findings of fatal PTE patients. The understanding of pulmonary physiopathological mechanism involved with eachPTE-associated disease can improve diagnosis in order to offer prompt treatment and reduce mortality.

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.

Edema pulmonar contralateral secundario al daño por isquemia-reperfusión de un pulmón: papel de la vasoconstricción arterial pulmonar / Vasoconstriction is required for edema of contralateral lung after reperfusion injury of one lung

El daño pulmonar por isquemia-reperfusión (IR) es una importante causa de morbilidad y mortalidad en ciertas condiciones clínicas que incluyen trasplantes, tromboendarterectomía y daño pulmonar por reexpansión. El edema pulmonar contralateral posterior al daño por IR de un pulmón ha sido reportado y esta investigación tiene como objetivo esclarecer la fisiopatología de dicho fenómeno. En un modelo de pulmones aislados y perfundidos de conejo, fue ocluido el hilio pulmonar de forma unilateral induciendo isquemia/hipoxia de dicho órgano, seguido de reperfusiones con sangre o con un substituto plasmático acelular. Los efectos aislados de vasoconstricción e inflamación en el daño pulmonar contralateral fueron estudiados posterior a la reperfusión, usando papaverina e hidrocortisona como agente vasodilatador y antiinflamatorio, respectivamente. En esta investigación se observó que la IR de un pulmón induce edema en el pulmón contralateral. La ausencia de leucocitos y plaquetas en la perfusión y el uso de hidrocortisona inhibió por completo el daño por IR. La papaverina suprimió el edema en el pulmón contralateral mas no en el reperfundido. Se concluye que la IR de un pulmón produce edema en el pulmón contralateral, para lo cual se requiere la presencia de vasoconstricción.

Ischemia-reperfusion (IR) lung injury is a significant cause of morbidity and mortality in certain clinical scenarios that include transplantation, thromboendarterectomy and reexpansion injury of the lung. Edema of the contralateral lung after IR injury of one lung has been reported and this study was aimed to clarify the pathophysiology of this phenomenon. One-lung ischemia/hypoxia followed by reperfusion with either blood or an acellular plasma substitute was achieved in an isolated rabbit lung model by hilum clamping. After reperfusion, we studied the isolated effects of vasoconstriction and inflammation on contralateral lung injury by using papaverine or hydrocortisone as vasodilator and anti-inflammatory, respectively. We observed that IR of one lung induces edema of the contralateral lung. Absence of leukocytes and platelets in the perfusate or use of hydrocortisone completely inhibits IR injury. Moreover, papaverine suppresses edema of the contralateral, but not that of the reperfused lung. We concluded that IR of one lung produces edema in the contralateral lung that requires vasoconstriction of the latter.

Cuando sospechar de edema fugaz pulmonar / When suspect pulmonary oedema flash

Edema pulmonar relámpago o edema pulmonar fugaz es una condición clínica caracterizada por episodios recurrentes y súdbitos de disnea en reposo, resultado en congestión pulmonar venosa aguda pero en la presencia de función sistólica del ventrículo izquierdo normal o preservada. Está usualmente asociada a estenosis bilateral o unilateral de la arteria renal en riñón único. Relatamos un caso de una paciente femenina de 60 años de edad, con enfermedad arterial coronaria, que desarrolló estenosis de arteria renal unilateral derecha y presentó un episodio de edema fugaz pulmonar. El tratamiento consistió en intervención percutánea en la arteria renal derecha con la colocación de prótesis metálica o stent.

Flash pulmonary edema is a condition characterizaed by sudden and recurrent episodes of dyspnea at rest resulting from acute pulmonary venous congestion in the presence of normal or well-preserved LV systolic function. This is usually associated with bilateral renal artery stenosis of a single surviving kidney. We report a case of a 60-year-old woman, with coronary artery disease who later developed unilateral renal artery atenosis and presented with one episode of flash pulmonary edema. She was successfully treated with stenting of the compromised renal artery.

Efecto de la hipocapnia/alcalosis sobre la tasa de filtración de líquidos en pulmones aislados y perfundidos de conejos / Effect of hypocapnia/alkalosis on the fluid filtration rate in isolated and perfused rabbit lungs

La hipocapnia/alcalosis es una situación que se presenta como consecuencia de diversas patologías pulmonares o metabólicas. El objetivo de este estudio fue determinar si el aumento de la tasa de filtración de liquido (TFL) que ocurre bajo estas circunstancias, está determinado por la hipocapnia, la alcalosis o la suma de ambas. Se realizaron 7 grupos (n=36), utilizando pulmones aislados de conejos. Grupo 1: Control (PCO2 6 por ciento, pH: 7,35-7,45); Grupo 2 (n=6): Hipocapnia/Alcalosis (CO2 1 por ciento, pH: 7,9); Grupo 3 (n=6): Hipocapnia/Normo-pH (CO2 1 por ciento pH 7,35-7,45), Grupo 4 (n=6) Normocapnia/Alcalosis (CO2 6 por ciento, pH: 7,9). En los grupos 5, 6 y 7 (n=4), todos bajo condición de Normocapnia/Alcalosis se añadió fenoterol, papaverina, e hidrocortisona respectivamente. La TFL y la presión de arteria pulmonar (Pap) fueron considerablemente mayores en el grupo 2 que en el control (TFL:1,92g/min ± 0,6 vs 0,0g/min ± 0,006), observándose una marcada influencia del pH, al comparar el grupo 3 y el grupo 4 (TFL: 0,02g/min ± 0,009 vs 2,3g/min ± 0,9) y (Pap: 13,5 cmH2O ± 1,4 vs 90 cmH2O ± 15). Se observó una disminución del efecto en los grupos 5 y 6 (papaverina e hidrocortisona) y su abolición total con fenoterol (grupo 7) (TFL: 0,001 ± 0,0003 g/min y Pap: 14 ± 0,8 cmH2O). El edema pulmonar inducido por Hipocapnia/Alcalosis es consecuencia principalmente de la alcalosis y no de la hipocapnia. Dicho efecto podría ser debido a un daño inflamatorio a nivel del parénquima y a la vasoconstricción causada por la alcalosis.

Pulmonary histopathological alterations in patients with acute respiratory failure: an autopsy study / Alterações histopatológicas pulmonares em pacientes com insuficiência respiratória aguda: um estudo em autopsias

OBJETIVOS: Apresentar alterações histopatológicas pulmonares encontradas em autopsias de pacientes falecidos por insuficiência respiratória aguda (IRA) e verificar se doenças de base e específicos fatores de risco associados aumentam a incidência dessas alterações. MÉTODOS: Foram revisados laudos finais de autopsias e selecionadas 3.030 autopsias de pacientes > 1 ano de idade, com infiltrado pulmonar radiológico, portadores de doença de base e fatores de risco associados, que morreram por alterações pulmonares decorrentes de IRA. RESULTADOS: As principais alterações histopatológicas pulmonares causadoras de morte imediata foram: dano alveolar difuso (DAD); edema pulmonar; pneumonia intersticial linfocítica (PIL) e hemorragia alveolar. As principais doenças de base encontradas foram: AIDS; broncopneumonia; sepse; cirrose hepática; tromboembolismo pulmonar; infarto agudo do miocárdio (IAM); acidente vascular cerebral; tuberculose; câncer; insuficiência renal crônica e leucemia. Os principais fatores de risco associados foram: idade > 50 anos; hipertensão arterial; insuficiência cardíaca congestiva; doença pulmonar obstrutiva crônica e diabetes mellitus. Pacientes com esses fatores de risco e AIDS apresentaram alta probabilidade de desenvolver PIL; pacientes com esses mesmos fatores, de desenvolver DAD, se portadores de sepse ou cirrose hepática; pacientes com tromboembolismo e os mesmos fatores de risco, de desenvolver hemorragia alveolar; pacientes com esses fatores de risco e IAM, de desenvolver edema pulmonar. CONCLUSÕES: Os achados pulmonares em pacientes com óbito por IRA apresentaram quatro padrões histopatológicos: DAD, edema pulmonar, PIL e hemorragia alveolar. Doenças de base e específicos fatores de risco associados correlacionaram-se positivamente com determinados padrões histopatológicos detectados à autópsia.

OBJECTIVE: To present the pulmonary histopathological alterations found in the autopsies of patients with acute respiratory failure (ARF) and determine whether underlying diseases and certain associated risk factors increase the incidence of these histopathological patterns. METHODS: Final autopsy reports were reviewed, and 3030 autopsies of patients > 1 year of age with an underlying disease and associated risk factors were selected. All had developed diffuse infiltrates and died of ARF-related pulmonary alterations. RESULTS: The principal pulmonary histopathological alterations resulting in immediate death were diffuse alveolar damage (DAD), pulmonary edema, lymphocytic interstitial pneumonia (LIP) and alveolar hemorrhage. The principal underlying diseases were AIDS, bronchopneumonia, sepsis, liver cirrhosis, pulmonary thromboembolism, acute myocardial infarction (AMI), cerebrovascular accident, tuberculosis, cancer, chronic kidney failure and leukemia. The principal associated risk factors were as follows: age > 50 years; arterial hypertension; congestive heart failure; chronic obstructive pulmonary disease; and diabetes mellitus. These risk factors and AIDS correlated with a high risk of developing LIP; these same risk factors, if concomitant with sepsis or liver cirrhosis, correlated with a risk of developing DAD; thromboembolism and these risk factors correlated with a risk of developing alveolar hemorrhage; these risk factors and AMI correlated with a risk of developing pulmonary edema. CONCLUSION: Pulmonary findings in patients who died of ARF presented four histopathological patterns: DAD, pulmonary edema, LIP and alveolar hemorrhage. Underlying diseases and certain associated risk factors correlated positively with specific histopathological findings on autopsy.