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1.
Am J Forensic Med Pathol ; 42(1): 1-8, 2021 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-33416234

RESUMO

ABSTRACT: The 2019 novel coronavirus disease (COVID-19) has spread worldwide, infiltrating, infecting, and devastating communities in all locations of varying demographics. An overwhelming majority of published literature on the pathologic findings associated with COVID-19 is either from living clinical cohorts or from autopsy findings of those who died in a medical care setting, which can confound pure disease pathology. A relatively low initial infection rate paired with a high biosafety level enabled the New Mexico Office of the Medical Investigator to conduct full autopsy examinations on suspected COVID-19-related deaths. Full autopsy examination on the first 20 severe acute respiratory syndrome coronavirus 2-positive decedents revealed that some extent of diffuse alveolar damage in every death due to COVID-19 played some role. The average decedent was middle-aged, male, American Indian, and overweight with comorbidities that included diabetes, ethanolism, and atherosclerotic and/or hypertensive cardiovascular disease. Macroscopic thrombotic events were seen in 35% of cases consisting of pulmonary thromboemboli and coronary artery thrombi. In 2 cases, severe bacterial coinfections were seen in the lungs. Those determined to die with but not of severe acute respiratory syndrome coronavirus 2 infection had unremarkable lung findings.


Assuntos
/mortalidade , Pulmão/patologia , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Autopsia , Índice de Massa Corporal , Edema Encefálico/patologia , Cardiomegalia/patologia , Comorbidade , Trombose Coronária/patologia , Bases de Dados Factuais , Fígado Gorduroso/patologia , Feminino , Patologia Legal , Glomerulosclerose Segmentar e Focal/patologia , Hepatomegalia/patologia , Humanos , Pulmão/diagnóstico por imagem , Masculino , Pessoa de Meia-Idade , Nefroesclerose/patologia , New Mexico/epidemiologia , Sobrepeso/epidemiologia , Pandemias , Derrame Pleural/diagnóstico por imagem , Derrame Pleural/patologia , Edema Pulmonar/diagnóstico por imagem , Edema Pulmonar/patologia , Distribuição por Sexo , Streptococcus pneumoniae/isolamento & purificação , Tomografia Computadorizada por Raios X , Corpo Vítreo/química , Imagem Corporal Total
2.
Medicine (Baltimore) ; 99(51): e23713, 2020 Dec 18.
Artigo em Inglês | MEDLINE | ID: mdl-33371120

RESUMO

ABSTRACT: Shoulder arthroscopy requires a large of irrigation for a better surgical view, leading circulatory overload. This study was performed to prove whether pulmonary edema will be lead by a large of irrigation.General anesthesia with interscalene block was induced before operation. The primary outcome was ultrasound evaluation of B lines from the time before nerve block to the time 10 hours after operation. The secondary outcomes included oxygenation index, arterial partial pressure of carbon dioxide, visual analogue scale, muscle strength grade.A total of 93 patients were evaluated. Before surgery, B lines failed to be detected. While the highest total incidence of B lines was 49.4%, occurred at 4 hours after surgery. The highest incidences of severe and moderate pulmonary edema were 3.2% (P = .081) and 9.7% (P = .002), respectively. B lines were also found on both the affected and healthy side. During operation, the incidence of type 1 respiratory failure was 5.4% (P = .023) and that of both type 1 and 2 respiratory failure were 6.5% (P = .013). Pain was relieved in 6 hours after surgery (VAS < 3). At 12 hours after operation, the VAS of resting and motion were 4.68 ±â€Š2.27, 6.90 ±â€Š2.43, respectively. While the grade of muscle strength was 4.48 ±â€Š0.51 at 12 hours after operation.There is a high incidence of pulmonary edema in shoulder arthroscopy, and ultrasound is a convenient tool to evaluate this complication. Pain is relieved in 6 hours after surgery by nerve block. While muscle strength can also recover at 12 hours after surgery.


Assuntos
Artroscopia/efeitos adversos , Artroscopia/métodos , Edema Pulmonar/etiologia , Edema Pulmonar/patologia , Articulação do Ombro/cirurgia , Adulto , Idoso , Anestesia Geral/métodos , Bloqueio do Plexo Braquial/métodos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Força Muscular/fisiologia , Oxigênio/sangue , Medição da Dor , Dor Pós-Operatória/terapia , Edema Pulmonar/diagnóstico por imagem , Ultrassonografia
3.
Int J Mol Sci ; 21(21)2020 Oct 28.
Artigo em Inglês | MEDLINE | ID: mdl-33126657

RESUMO

Acute respiratory distress syndrome (ARDS) is characterized by massive inflammation, increased vascular permeability and pulmonary edema. Mortality due to ARDS remains very high and even in the case of survival, acute lung injury can lead to pulmonary fibrosis. The renin-angiotensin system (RAS) plays a significant role in these processes. The activities of RAS molecules are subject to dynamic changes in response to an injury. Initially, increased levels of angiotensin (Ang) II and des-Arg9-bradykinin (DABK), are necessary for an effective defense. Later, augmented angiotensin converting enzyme (ACE) 2 activity supposedly helps to attenuate inflammation. Appropriate ACE2 activity might be decisive in preventing immune-induced damage and ensuring tissue repair. ACE2 has been identified as a common target for different pathogens. Some Coronaviruses, including SARS-CoV-2, also use ACE2 to infiltrate the cells. A number of questions remain unresolved. The importance of ACE2 shedding, associated with the release of soluble ACE2 and ADAM17-mediated activation of tumor necrosis factor-α (TNF-α)-signaling is unclear. The roles of other non-classical RAS-associated molecules, e.g., alamandine, Ang A or Ang 1-9, also deserve attention. In addition, the impact of established RAS-inhibiting drugs on the pulmonary RAS is to be elucidated. The unfavorable prognosis of ARDS and the lack of effective treatment urge the search for novel therapeutic strategies. In the context of the ongoing SARS-CoV-2 pandemic and considering the involvement of humoral disbalance in the pathogenesis of ARDS, targeting the renin-angiotensin system and reducing the pathogen's cell entry could be a promising therapeutic strategy in the struggle against COVID-19.


Assuntos
Infecções por Coronavirus/patologia , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/patologia , Sistema Renina-Angiotensina/fisiologia , Síndrome Respiratória Aguda Grave/patologia , Proteína ADAM17/metabolismo , Animais , Betacoronavirus , Permeabilidade Capilar/fisiologia , Humanos , Inflamação/patologia , Pulmão/imunologia , Pulmão/patologia , Camundongos , Pandemias , Edema Pulmonar/patologia , Ratos , Fator de Necrose Tumoral alfa/metabolismo
4.
Front Immunol ; 11: 574862, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33042157

RESUMO

It is currently believed that innate immunity is unable to prevent the spread of SARS-CoV-2 from the upper airways to the alveoli of high-risk groups of patients. SARS-CoV-2 replication in ACE-2-expressing pneumocytes can drive the diffuse alveolar injury through the cytokine storm and immunothrombosis by upregulating the transcription of chemokine/cytokines, unlike several other respiratory viruses. Here we report histopathology data obtained in post-mortem lung biopsies of COVID-19, showing the increased density of perivascular and septal mast cells (MCs) and IL-4-expressing cells (n = 6), in contrast to the numbers found in pandemic H1N1-induced pneumonia (n = 10) or Control specimens (n = 10). Noteworthy, COVID-19 lung biopsies showed a higher density of CD117+ cells, suggesting that c-kit positive MCs progenitors were recruited earlier to the alveolar septa. These findings suggest that MC proliferation/differentiation in the alveolar septa might be harnessed by the shift toward IL-4 expression in the inflamed alveolar septa. Future studies may clarify whether the fibrin-dependent generation of the hyaline membrane, processes that require the diffusion of procoagulative plasma factors into the alveolar lumen and the endothelial dysfunction, are preceded by MC-driven formation of interstitial edema in the alveolar septa.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Mastócitos/imunologia , Pneumonia Viral/imunologia , Alvéolos Pulmonares/imunologia , Edema Pulmonar/imunologia , Trombose/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Infecções por Coronavirus/patologia , Infecções por Coronavirus/virologia , Feminino , Humanos , Vírus da Influenza A Subtipo H1N1/imunologia , Influenza Humana/imunologia , Influenza Humana/patologia , Influenza Humana/virologia , Interleucina-4/imunologia , Masculino , Mastócitos/patologia , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/patologia , Pneumonia Viral/virologia , Proteínas Proto-Oncogênicas c-kit/imunologia , Alvéolos Pulmonares/patologia , Alvéolos Pulmonares/virologia , Edema Pulmonar/patologia , Edema Pulmonar/virologia , Trombose/patologia , Trombose/virologia
5.
Am J Forensic Med Pathol ; 41(4): e61-e63, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32969849

RESUMO

The autopsy findings for 3 cases of SARS-(CoV-2) pneumonia-related deaths are reported with pulmonary histology and immunohistochemistry findings. In 2 cases (cases 1 and 2), the time interval from presentation to death was approximately 1 week, whereas for case 3, the time interval from presentation to death was hours. Case 1 and case 2 presented with shortness of breath, cough, and flu-like symptoms. The decedent from case 3 died shortly after presenting to a local emergency room with high fever, chest and abdominal pain, and shortness of breath. All 3 cases had 1 or more comorbidities. The postmortem interval for cases 1 and 2 was 2 weeks as they died at sea and were stored on board within the respective cruise ships' refrigeration units, whereas case 3 was examined within 24 hours of death. The autopsies were conducted at the Miami-Dade County Medical Examiners Department under routine infectious precautions. Salient clinical history and autopsy findings are summarized. Microscopic examination revealed pneumonia with associated atypical endovascular cells.


Assuntos
Betacoronavirus , Infecções por Coronavirus/patologia , Pneumonia Viral/patologia , Adulto , Autopsia , Cardiomegalia/complicações , Cardiomegalia/patologia , Círculo Arterial do Cérebro/patologia , Comorbidade , Doença da Artéria Coronariana/complicações , Doença da Artéria Coronariana/patologia , Infecções por Coronavirus/complicações , Complicações do Diabetes/patologia , Evolução Fatal , Feminino , Humanos , Hiperlipidemias/complicações , Hiperlipidemias/patologia , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Nasofaringe/virologia , Obesidade/complicações , Obesidade/patologia , Pandemias , Pneumonia Viral/complicações , Edema Pulmonar/complicações , Edema Pulmonar/patologia , Uso de Tabaco/patologia
6.
PLoS One ; 15(7): e0236923, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32730329

RESUMO

Heart failure (HF) impairs diaphragm function. Animal models realistically mimicking HF should feature both the cardiac alterations and the diaphragmatic dysfunction characterizing this disease. The isoproterenol-induced HF model is widely used, but whether it presents diaphragmatic dysfunction is unknown. However, indirect data from research in other fields suggest that isoproterenol could increase diaphragm function. The aim of this study was to test the hypothesis that the widespread rodent model of isoproterenol-induced HF results in increased diaphragmatic contractility. Forty C57BL/6J male mice were randomized into 2 groups: HF and healthy controls. After 30 days of isoproterenol infusion to establish HF, in vivo diaphragmatic excursion and ex vivo isolated diaphragm contractibility were measured. As compared with healthy controls, mice with isoproterenol-induced HF showed the expected changes in structural and functional echocardiographic parameters and lung edema. isoproterenol-induced HF increased in vivo diaphragm excursion (by ≈30%, p<0.01) and increased by ≈50% both ex vivo peak specific force (p<0.05) and tetanic force (p<0.05) at almost all 10-100 Hz frequencies (p<0.05), with reduced fatigue resistance (p<0.01) when compared with healthy controls. Expression of myosin genes encoding the main muscle fiber types revealed that Myh4 was higher in isoproterenol-induced HF than in healthy controls (p<0.05), suggesting greater distribution of type IIb fibers. These results show that the conventional isoproterenol-induced HF model increases diaphragm contraction, a finding contrary to what is observed in patients with HF. Therefore, this specific model seems limited for translational an integrative HF research, especially when cardio-respiratory interactions are investigated.


Assuntos
Agonistas Adrenérgicos beta/toxicidade , Diafragma/fisiopatologia , Insuficiência Cardíaca/fisiopatologia , Isoproterenol/toxicidade , Fibras Musculares Esqueléticas/patologia , Proteínas Musculares/metabolismo , Edema Pulmonar/patologia , Animais , Diafragma/efeitos dos fármacos , Modelos Animais de Doenças , Insuficiência Cardíaca/induzido quimicamente , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Fibras Musculares Esqueléticas/efeitos dos fármacos , Edema Pulmonar/induzido quimicamente
7.
An Acad Bras Cienc ; 92(1): e20190261, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32401838

RESUMO

Cytarabine is effectively used in the treatment of adult acute leukemia, but it has a dose-limiting side effect of fatal pulmonary oedema because it increases the vascular permeability of the alveolar capillaries. The aim of the present study was to conduct a radiological, biochemical and histopathological investigation of the effect of rutin on cytarabine-associated pulmonary oedema in rats. Rats were treated with a combination of rutin+cytarabine by administering oral rutin at a dose of 50 mg/kg; other rat groups were orally administered the same volume of physiological saline. One hour after administration of rutin or saline, the rutin+cytarabine and cytarabine groups received an intraperitoneal injection of cytarabine (200 mg/kg). This administration procedure was repeated once a day for 14 days. Radiologically, 50% of the animals given cytarabine alone showed lung oedema, but the rutin+cytarabine group showed no oedema. The inclusion of rutin decreased the amounts of cytarabine-associated malondialdehyde, tumour necrosis factor-α, and nuclear factor-κB in the lung tissue. Rutin also inhibited the reduction of total glutathione by nitric oxide. These findings suggest that rutin may be a beneficial adjunct that can minimise the development of cytarabine-associated pulmonary oedema.


Assuntos
Anti-Inflamatórios/uso terapêutico , Antioxidantes/uso terapêutico , Citarabina/efeitos adversos , Edema Pulmonar/tratamento farmacológico , Rutina/uso terapêutico , Animais , Anti-Inflamatórios/farmacologia , Antioxidantes/farmacologia , Masculino , NF-kappa B/análise , Oxidantes/sangue , Estresse Oxidativo/efeitos dos fármacos , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/patologia , Ratos , Ratos Wistar , Rutina/farmacologia , Fator de Necrose Tumoral alfa/análise
9.
Am J Forensic Med Pathol ; 41(1): 48-51, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31977345

RESUMO

Chikungunya is a mosquito-transmitted viral illness with clinical hallmarks of rash, fever, arthralgia, and myalgia. It is rarely fatal, although vulnerable populations, to include elderly, children, and those with multiple comorbid illnesses, are more susceptible to severe infection and death. There have been multiple areas of the world with periodic chikungunya epidemics. With increased immigration, foreign travel, epidemics, and global spread of the virus, it is prudent to consider chikungunya as a diagnosis both clinically and postmortem when a patient presents with rash, fevers, and arthralgia. We present a case of a patient with recent foreign travel, a rash, fever, and arthralgia with mosquito bites who succumbed to chikungunya viral infection with pneumonia. His diagnosis was established postmortem. A review of the literature is included in this report. This case stresses the delayed time to diagnose chikungunya with serologic testing and the importance of using reverse transcriptase-polymerase chain reaction to aid in rapid and accurate diagnosis and management.


Assuntos
Febre de Chikungunya/diagnóstico , Doença Relacionada a Viagens , Artralgia/virologia , Vírus Chikungunya/genética , El Salvador , Doenças Endêmicas , Exantema/patologia , Exantema/virologia , Patologia Legal , Humanos , Los Angeles , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Pneumonia Viral/etiologia , Reação em Cadeia da Polimerase , Edema Pulmonar/patologia , Edema Pulmonar/virologia
10.
J Forensic Sci ; 65(1): 112-116, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31483504

RESUMO

Given the common occurrence of both opioid and cardiovascular deaths, and the concomitant use of opioids in those with cardiac disease, the present study was undertaken to see whether the old adage of using the triad of cerebral and pulmonary edema and bladder fullness to suggest an opioid death could be used to differentiate deaths due to opioid toxicity from deaths due to cardiac disease. Brain weight, lung weight, and bladder fullness were compared among opioid-related deaths, cardiac deaths, and a control population. It was found that opioid-related deaths were more likely to have heavy lungs, a heavy brain, and a full bladder, while cardiac-related deaths had smaller volumes of urine in the bladder and heavier hearts. In conjunction with a thorough investigation, these findings may be useful to forensic pathologists when determining whether a death is opioid-related, especially in the setting of concomitant cardiac disease.


Assuntos
Analgésicos Opioides/envenenamento , Doenças Cardiovasculares/diagnóstico , Transtornos Relacionados ao Uso de Opioides/diagnóstico , Adolescente , Adulto , Distribuição por Idade , Idoso , Analgésicos Opioides/efeitos adversos , Autopsia , Encéfalo/patologia , Edema Encefálico/patologia , Estudos de Casos e Controles , Overdose de Drogas , Feminino , Patologia Legal , Humanos , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Miocárdio/patologia , Tamanho do Órgão , Edema Pulmonar/patologia , Estudos Retrospectivos , Distribuição por Sexo , Bexiga Urinária/patologia , Adulto Jovem
11.
J Ethnopharmacol ; 248: 112355, 2020 Feb 10.
Artigo em Inglês | MEDLINE | ID: mdl-31669667

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Thalictrum minus L., a Mongolian folk medicinal plant, was applied for the treatment of bacterial and fungal infection, tuberculosis and lung inflammation. AIM OF THE STUDY: The present work aims to elucidate the protective effects of Thalictrum minus L.(TML) against lipopolysaccharide (LPS)-induced acute lung injury and the underlying mechanisms. METHODS: The mice model of acute lung injury was induced by LPS via endotracheal drip, and TML (10, 20, 40 mg/kg) were administered orally 1 h prior to LPS. The efficacy and molecular mechanisms in the presence or absence of TML were investigated. RESULTS: We demonstrated that treatment with TML aqueous extract protected the mice from acute lung injury induced by LPS administration. TML significantly inhibited weight loss in mice, decreased the lung wet to dry weight (W/D) ratios and attenuated lung histopathological changes, such as infiltration of inflammatory cells and coagulation, pulmonary edema. Furthermore, we found that TML markedly reduced the LPS-induced inflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß), decreased nitric oxide (NO), and increased superoxide dismutase (SOD) in bronchoalveolar lavage fluid (BALF), and effectively ameliorated LPS-induced increased total protein, leukocyte and macrophages in BALF. In addition, TML pronouncedly suppressed the activation of the MAPKs p38-NLRP3/caspase-1 and COX2, increased the expression of p-AMPK-Nrf2, and suppressed the expression of KEAP, apoptotic-related protein as well as autophagy. CONCLUSIONS: These results suggested that TML ameliorated LPS-induced acute lung injury by inhibiting the release of inflammatory cytokines and reducing oxidative damage associated with the MAPKs p38-NLRP3/caspase-1 and COX2 signaling pathways, AMPK-Nrf2/KEAP signaling pathways, as well as apoptosis and autophagy.


Assuntos
Lesão Pulmonar Aguda/prevenção & controle , Anti-Inflamatórios/farmacologia , Antioxidantes/farmacologia , Mediadores da Inflamação/metabolismo , Pulmão/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/farmacologia , Pneumonia/prevenção & controle , Thalictrum , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/patologia , Animais , Anti-Inflamatórios/isolamento & purificação , Antioxidantes/isolamento & purificação , Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Modelos Animais de Doenças , Lipopolissacarídeos , Pulmão/metabolismo , Pulmão/patologia , Masculino , Camundongos , Extratos Vegetais/isolamento & purificação , Pneumonia/induzido quimicamente , Pneumonia/metabolismo , Pneumonia/patologia , Edema Pulmonar/metabolismo , Edema Pulmonar/patologia , Edema Pulmonar/prevenção & controle , Transdução de Sinais , Thalictrum/química
12.
World Neurosurg ; 135: e505-e509, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-31863887

RESUMO

OBJECTIVE: Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by acute onset after central nervous system injury. Here, we investigated the clinical features of NPE in patients with subarachnoid hemorrhage (SAH). METHODS: We retrospectively analyzed a total of 350 patients with SAH who were treated at our hospital from April 2014 to September 2017. Patient demographics, aneurysm size and location, clinical characteristics, and patient outcomes were reviewed and compared between an NPE and a non-NPE group. RESULTS: Sixteen patients (4.6%) presented with NPE at admission. Ten of these (62.5%) recovered from NPE immediately, and ventilatory support was withdrawn within 2 days from onset. A univariate analysis showed that patients with NPE were younger (P = 0.04), had a higher rate of vertebral artery dissection (P < 0.01), more severe World Federation of Neurosurgical Societies (WFNS) grades (P = 0.01), and lower systolic blood pressure on admission (P = 0.01). A multivariate analysis revealed significant differences in the frequency of vertebral artery dissection (odds ratio 4.83, 95% confidence interval 1.50-15.56, P < 0.01) and in WFNS grades (odds ratio 3.73, 95% confidence interval 1.02-13.66, P = 0.04) between the groups. No significant group differences were found in other factors including heart rate, radiographic sign (Fisher grade), aneurysm size and location, blood sample tests on admission, and neurologic outcomes. CONCLUSIONS: Vertebral artery dissection and severe WFNS grade on admission were confirmed as significant risk factors for NPE. However, neurologic outcomes at discharge did not differ between groups, suggesting that poor outcomes due to NPE could be reduced by appropriate diagnosis and treatment.


Assuntos
Edema Pulmonar/patologia , Hemorragia Subaracnóidea/complicações , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos , Dissecação da Artéria Vertebral/etiologia , Dissecação da Artéria Vertebral/patologia
13.
S Afr Med J ; 110(12): 1195-1200, 2020 10 19.
Artigo em Inglês | MEDLINE | ID: mdl-33403965

RESUMO

BACKGROUND: An outbreak of a novel coronavirus in China in late 2019 has resulted in a global pandemic. The virus (SARS-CoV-2) causes a severe acute respiratory syndrome and had been responsible for >14 000 deaths in South Africa (SA) at the time of writing, 30 August 2020. Autopsies in our setting have not been prioritised owing to the infective risks for staff, resulting in a lack of information on the histopathology of the disease in the SA setting. Postmortem biopsies are relatively quick and easy to perform and reduce the infective risk posed by full autopsies. OBJECTIVES: To determine whether postmortem biopsies of lung tissue could be used to determine cause of death in lieu of full autopsies in patients dying from COVID-19. METHODS: We performed postmortem biopsies of lung tissue on 4 patients with SARS-CoV-2 confirmed by reverse transcriptase polymerase chain reaction who died in the Tygerberg Hospital (Cape Town, SA) intensive care unit (ICU) in June - July 2020, in order to determine their cause of death. The biopsies were performed in the ICU with the necessary personal protective equipment within 2 hours after death. Clinical information was obtained from the hospital records and the histopathology was reviewed by two consultant histopathologists. Microbiology and electron microscopy were also performed on this tissue. RESULTS: All 4 patients were aged >50 years and had multiple comorbidities. Pulmonary pathology was present in only 3 cases, and the findings were surprisingly heterogeneous. One case demonstrated several findings including diffuse alveolar damage, extensive fibrin thrombi in pulmonary arteries with pulmonary infarction, organising pneumonia and bronchopneumonia. Other findings included type 2 pneumocyte hyperplasia, intra-alveolar macrophages and squamous metaplasia. An organising pneumonia was present in 2 other cases, although these findings were not deemed to be severe enough to be the cause of death. Fibrin thrombi were present in pulmonary arteries of 3 cases. One case showed no significant acute pulmonary pathology. The cause of death could only be determined in 1 case. CONCLUSIONS: The pulmonary findings we observed are in keeping with those described in the international literature. However, the pathology was surprisingly heterogeneous between cases, and was only deemed severe enough to be the cause of death in 1 of 4 cases. While lung-targeted, standardised postmortem biopsies may be safe, easy to perform and provide useful insights into the disease, they are not suitable to replace full autopsies in determining cause of death.


Assuntos
Biópsia , Lesão Pulmonar/patologia , Pulmão/patologia , Artéria Pulmonar/patologia , Edema Pulmonar/patologia , Infarto Pulmonar/patologia , Trombose/patologia , Idoso , Células Epiteliais Alveolares/patologia , Autopsia , Proteína C-Reativa/metabolismo , /mortalidade , Causas de Morte , Comorbidade , Diabetes Mellitus Tipo 2/epidemiologia , Feminino , Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo , Células Gigantes/patologia , Humanos , Hipertensão/epidemiologia , Linfócitos/patologia , Macrófagos Alveolares/patologia , Masculino , Pessoa de Meia-Idade , Obesidade/epidemiologia , Pró-Calcitonina/sangue , África do Sul , Centros de Atenção Terciária
14.
Sci Rep ; 9(1): 18390, 2019 12 05.
Artigo em Inglês | MEDLINE | ID: mdl-31804535

RESUMO

Oxytocin (OT) has been reported to have a protective effect in lipopolysaccharide-induced experimental acute lung injury (ALI). However, its role in heat stroke-related ALI has never been investigated. Herein, we aimed to explore the therapeutic effects and potential mechanism of action of OT on heat-induced ALI. Rats were treated with OT 60 min before the start of heat stress (42 °C for 80 min). Twenty minutes after the termination of heat stress, the effects of OT on lung histopathological changes, edema, acute pleurisy and the bronchoalveolar fluid levels of inflammatory cytokines and indicators of ischemia, cellular damage, and oxidative damage were assessed. We also evaluated the influence of OT pretreatment on heat-induced hypotension, hyperthermia, ALI score, and death in a rat model of heat stroke. The results showed that OT significantly reduced heat-induced lung edema, neutrophil infiltration, hemorrhage score, myeloperoxidase activity, ischemia, and the levels of inflammatory and oxidative damage markers in bronchoalveolar lavage fluid. The survival assessment confirmed the pathophysiological and biochemical results. An OT receptor antagonist (L-368,899) was administered 10 min before the OT injection to further demonstrate the role of OT in heat-induced ALI. The results showed that OT could not protect against the aforementioned heat stroke responses in rats treated with L-368,899. Interestingly, OT treatment 80 min after the start of heat shock did not affect survival. In conclusion, our data indicate that OT pretreatment can reduce the ischemic, inflammatory and oxidative responses related to heat-induced ALI in rats.


Assuntos
Lesão Pulmonar Aguda/prevenção & controle , Febre/tratamento farmacológico , Golpe de Calor/prevenção & controle , Hipotensão/prevenção & controle , Ocitocina/farmacologia , Substâncias Protetoras/farmacologia , Edema Pulmonar/prevenção & controle , Lesão Pulmonar Aguda/metabolismo , Lesão Pulmonar Aguda/mortalidade , Lesão Pulmonar Aguda/patologia , Animais , Líquido da Lavagem Broncoalveolar/química , Canfanos/farmacologia , Citocinas/genética , Citocinas/metabolismo , Modelos Animais de Doenças , Febre/metabolismo , Febre/mortalidade , Febre/patologia , Golpe de Calor/metabolismo , Golpe de Calor/mortalidade , Golpe de Calor/patologia , Resposta ao Choque Térmico , Hipotensão/metabolismo , Hipotensão/mortalidade , Hipotensão/patologia , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Masculino , Infiltração de Neutrófilos , Peroxidase/genética , Peroxidase/metabolismo , Piperazinas/farmacologia , Edema Pulmonar/metabolismo , Edema Pulmonar/mortalidade , Edema Pulmonar/patologia , Ratos , Ratos Sprague-Dawley , Receptores de Ocitocina/antagonistas & inibidores , Receptores de Ocitocina/genética , Receptores de Ocitocina/metabolismo , Análise de Sobrevida
15.
Undersea Hyperb Med ; 46(5): 581-601, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31683356

RESUMO

Introduction: We aimed to document identified cases of immersion pulmonary edema (IPE) in divers from Oceania (the Indo-Pacific region) from January 2002 to May 2018, inclusive. Method: Cases were identified using various sources, including searches of the Divers Alert Network Asia-Pacific (DAN AP) Fatality Database, published case reports, and interviews with survivors who had reported their incident to DAN AP. Where available, investigations, pathology and autopsy results were obtained. Only incidents diagnosed as IPE by diving physicians or pathologists with experience in the investigation of diving accidents were included. Individual case histories and outcomes, together with brief individual summaries of the associations and possible contributing factors were recorded. Results: Thirty-one IPE incidents in divers from Oceania were documented. There were two surface snorkelers, 22 scuba air divers and seven nitrox divers which included three closed-circuit rebreathers (CCR). The mean (SD) age was 53 (12) years, 58% of victims were females, and the average dive profile was to a maximum depth of 19 meters of seawater for 25 minutes. Six victims (19%) had previous episodes of IPE. There were nine recorded fatalities. Cardiac anomalies dominated the associated or possible contributing factors. These included valvular disease in 29%, transient cardiomyopathies in 26% and dysrhythmias in 16%. Conclusions: Previously reported associations of IPE such as exertion, stress, cold exposure, negative inspiratory pressure, hypertension, overhydration, ascent or surfacing, tight wetsuit, aspiration and certain medications were identified. Cardiac conditions were frequent and included chronic disorders (valvular pathology, coronary artery disease) and transient disorders (dysrhythmias, transient myocardial dysfunction, takotsubo or stress cardiomyopathy). It is likely that the chronic cardiac disorders may have contributed to the IPE, whereas the transient cases could be either sequelae, contributors or coincidental to the IPE.


Assuntos
Mergulho/efeitos adversos , Edema Pulmonar/etiologia , Adulto , Idoso , Autopsia , Doença das Coronárias/patologia , Suscetibilidade a Doenças/etiologia , Suscetibilidade a Doenças/patologia , Evolução Fatal , Feminino , Cardiopatias/complicações , Humanos , Imersão/efeitos adversos , Masculino , Pessoa de Meia-Idade , Oceania/epidemiologia , Esforço Físico , Edema Pulmonar/diagnóstico , Edema Pulmonar/epidemiologia , Edema Pulmonar/patologia , Fatores de Risco , Água do Mar , Distribuição por Sexo , Natação , Cardiomiopatia de Takotsubo/complicações , Adulto Jovem
16.
Undersea Hyperb Med ; 46(5): 603-610, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31683357

RESUMO

Aim: To review incidents of immersion pulmonary edema (IPE) from Oceania, to determine the demographics, diving parameters, and comorbidities that may be related to this disorder. Method: Incidents of IPE, most of which were documented by Divers Alert Network Asia-Pacific (DAN AP) or reported in our medical literature, were analyzed. They included interviews with the survivors and a review of available medical records. Only incidents diagnosed as IPE by specialist diving physicians or pathologists with experience in the investigation of diving accidents were included. Results: Thirty-one IPE incidents in divers from Oceania were documented. There were two surface snorkelers, 22 scuba air divers and seven nitrox divers, which included three closed-circuit rebreathers (CCR). The mean (SD) age was 53 (12) years, 58% of victims were females, and the average dive profile was to a maximum depth of 19 msw for 25 minutes. Six victims (19%) had previous episodes of IPE. There were nine recorded fatalities in this cohort. Medical comorbidities were recorded in 68%, with 42% being cardiac. The latter included valvular disease in 29%, transient cardiomyopathies in 26% and dysrhythmias in 16%. Conclusion: IPE was more likely in middle-aged females, in experienced divers, and during ascent or after surfacing. Commonly reported associations such as exertion, stress, cold exposure, negative inspiratory pressure, hypertension, overhydration, tight wetsuit, aspiration and certain medications were identified. This series supports the hypothesis that the elderly IPE subjects are likely to have comorbidities and be susceptible to IPE recurrences and fatalities unless the contributing factors can be identified and addressed.


Assuntos
Mergulho/efeitos adversos , Edema Pulmonar/etiologia , Adulto , Fatores Etários , Idoso , Autopsia , Temperatura Baixa/efeitos adversos , Comorbidade , Mergulho/estatística & dados numéricos , Feminino , Cardiopatias/complicações , Humanos , Imersão/efeitos adversos , Masculino , Pessoa de Meia-Idade , Oceania , Edema Pulmonar/diagnóstico , Edema Pulmonar/mortalidade , Edema Pulmonar/patologia , Fatores de Risco , Água do Mar , Adulto Jovem
17.
Adv Respir Med ; 87(5): 298-300, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31680230

RESUMO

INTRODUCTION: Neurogenic pulmonary oedema (NPE) is avery rare complication of epileptic seizures, which could potentially increase mortality. MATERIAL AND METHODS: The case of a66-year-old male patient with NPE caused by repeated epileptic seizures is reported. Rapid resolution of pulmonary oedema is well documented by X-ray and computed tomography images. CONCLUSIONS: Neurogenic pulmonary oedema could potentially increase mortality, and thus, it is important to perform achest X-ray in all patients presenting with seizures and dyspnoea.


Assuntos
Doenças do Sistema Nervoso Central/fisiopatologia , Edema Pulmonar/fisiopatologia , Idoso , Sistema Nervoso Central/fisiopatologia , Doenças do Sistema Nervoso Central/patologia , Hemodinâmica/fisiologia , Humanos , Masculino , Edema Pulmonar/patologia
18.
Nat Commun ; 10(1): 4241, 2019 09 18.
Artigo em Inglês | MEDLINE | ID: mdl-31534124

RESUMO

Malaria-associated acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) are life-threatening manifestations of severe malaria infections. The pathogenic mechanisms that lead to respiratory complications, such as vascular leakage, remain unclear. Here, we confirm that depleting CD8+T cells with anti-CD8ß antibodies in C57BL/6 mice infected with P. berghei ANKA (PbA) prevent pulmonary vascular leakage. When we transfer activated parasite-specific CD8+T cells into PbA-infected TCRß-/- mice (devoid of all T-cell populations), pulmonary vascular leakage recapitulates. Additionally, we demonstrate that PbA-infected erythrocyte accumulation leads to lung endothelial cell cross-presentation of parasite antigen to CD8+T cells in an IFNγ-dependent manner. In conclusion, pulmonary vascular damage in ALI is a consequence of IFNγ-activated lung endothelial cells capturing, processing, and cross-presenting malaria parasite antigen to specific CD8+T cells induced during infection. The mechanistic understanding of the immunopathogenesis in malaria-associated ARDS and ALI provide the basis for development of adjunct treatments.


Assuntos
Lesão Pulmonar Aguda/patologia , Linfócitos T CD8-Positivos/imunologia , Apresentação Cruzada/imunologia , Interferon gama/imunologia , Malária/imunologia , /patologia , Lesão Pulmonar Aguda/imunologia , Lesão Pulmonar Aguda/parasitologia , Animais , Modelos Animais de Doenças , Células Endoteliais/imunologia , Feminino , Pulmão/parasitologia , Pulmão/patologia , Malária/tratamento farmacológico , Malária/parasitologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Plasmodium berghei/imunologia , Edema Pulmonar/parasitologia , Edema Pulmonar/patologia , /parasitologia
19.
In Vivo ; 33(5): 1477-1484, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31471395

RESUMO

BACKGROUND/AIM: Leukocyte activation is thought to be a major step in sepsis-induced pulmonary edema. We attempted to confirm whether pulmonary edema can be reproduced under intravital microscopy in a model of transfusion-related acute lung injury (TRALI) using MHC class I-specific antibody. MATERIALS AND METHODS: The surface pulmonary microcirculation was observed using an epi-fluorescence microscope through a thoracic window in 50 male mice. Monoclonal MHC class I-specific antibody (Ab) was administered to the animals, while the control group received saline. The leukocytes and macro-molecular leakage in the pulmonary circulation were analyzed. RESULTS: Leukocytes accumulated in the capillaries (52.5±12.7 leukocytes per designated area in Ab group vs. 20.8±3.1 in control). The air-containing alveolus area significantly shrank from 2,224.9±934.9 µm2 to 509.7±380.8 µm2 in the Ab group. CONCLUSION: Pulmonary edema develops rapidly following leukocyte accumulation in the lung. We confirmed that leukocyte accumulation without an underlining condition is sufficient to induce pulmonary edema.


Assuntos
Anticorpos Monoclonais/efeitos adversos , Antígenos H-2/imunologia , Edema Pulmonar/etiologia , Edema Pulmonar/patologia , Lesão Pulmonar Aguda/etiologia , Lesão Pulmonar Aguda/patologia , Animais , Anticorpos Monoclonais/administração & dosagem , Anticorpos Monoclonais/imunologia , Anticorpos Monoclonais/farmacologia , Biomarcadores , Biópsia , Contagem de Células Sanguíneas , Gasometria , Modelos Animais de Doenças , Injeções Intravenosas , Masculino , Camundongos , Imagem Óptica , Edema Pulmonar/diagnóstico por imagem
20.
PLoS One ; 14(8): e0221029, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31415618

RESUMO

Interleukin-11 (IL-11) is an interleukin-6 (IL-6) family cytokine shown to play a protective role in acute inflammatory settings including systemic infection. In this study we addressed the role of IL-11 in acute bacterial pneumonia using a mouse model of E. coli pneumonia. Compared with other related cytokines, IL-11 protein was maintained at high levels in the lung at baseline, with only mild alterations in whole lung and BALF levels during acute infection. The primary source of IL-11 in the lung was the epithelium, but steady state production was not dependent on the inflammatory transcription factor nuclear factor kappa B in cells of either myeloid or epithelial lineage. Blockade of IL-11 with neutralizing antibodies resulted in a mild but significant decrease in neutrophil recruitment and increase in pulmonary edema during pneumonia, without detectable alterations in bacterial clearance. Exogenous IL-11 administration, however, had no effect at baseline or during infection. Overall, we conclude that maintenance of lung IL-11 concentrations may influence acute pulmonary inflammation during infection, albeit modestly.


Assuntos
Interleucina-11/imunologia , Infiltração de Neutrófilos/imunologia , Neutrófilos/imunologia , Pneumonia Bacteriana/imunologia , Edema Pulmonar/imunologia , Doença Aguda , Animais , Anticorpos Neutralizantes/farmacologia , Interleucina-11/antagonistas & inibidores , Interleucina-11/genética , Camundongos , Camundongos Knockout , Infiltração de Neutrófilos/efeitos dos fármacos , Neutrófilos/patologia , Pneumonia Bacteriana/tratamento farmacológico , Pneumonia Bacteriana/genética , Pneumonia Bacteriana/patologia , Edema Pulmonar/tratamento farmacológico , Edema Pulmonar/genética , Edema Pulmonar/patologia
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