Chest Radiographic and CT Findings in Novel Swine-Origin Influenza A (H1N1) Virus (S-OIV) Infection

Agarwal, Prachi P.; Cinti, Sandro; Kazerooni, Ella A.

doi:10.2214/ajr.09.3599

Cited by 198 publications

(241 citation statements)

References 6 publications

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“…However, more severe cases may develop particularly in the patients at high risk. As in our study, it has been reported that pandemic influenza A (H1N1) is also able to cause severe cases such as pneumonia and ARDS [1,6,8,9]. Clinically, there may be fever, dry cough, headache, sore throat, cold feeling, fatigue, malaise, muscle and joint pain, vomiting, nasal drainage, and diarrhea [4].…”

supporting

confidence: 57%

H1N1 influenza A virus Related Pneumonia and Respiratory Failure

Okur

Erbey²,

Yazicioglu

et al. 2013

Indian J. Virol.

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Influenza viruses are common respiratory pathogens in humans and can cause serious infection that leads to the development of pneumonia. In this study, the clinical and laboratory features of 36 patients from Turkey who are hospitalized in intensive care unit due to pandemic influenza A (H1N1) associated pneumonia and respiratory failure were retrospectively evaluated. The most common symptoms were cough and fever. Consolidation (36.1 %) and interstitial changes (30.6 %) were the most frequently identified findings on chest radiographs at the time of admission. Six of the patients (16.7 %) died. Mortality occurred in 3 of 13 patients (23.1 %) with underlying disease, whilst it occurred in only 3 of 23 patients (13 %) who were previously healthy. Mortality was found to be significantly associated only with an elevated lactate dehydrogenase level. A significant relationship was determined only between the presence of lymphopenia and acute respiratory distress syndrome and the need for intensive care treatment. The average time elapsed from the onset of the symptoms until admission was 8.67 ± 2.87 days for the patients died, and 6.0 ± 3.8 days for the patients survived.

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supporting

confidence: 57%

H1N1 influenza A virus Related Pneumonia and Respiratory Failure

Okur

Erbey²,

Yazicioglu

et al. 2013

Indian J. Virol.

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“…Even in combination with optimal supportive care, therapy with antiviral drugs does not completely prevent mortality (8), indicating that new therapeutic approaches are needed. Given reports that microthombi are observed in the lungs of patients with severe influenza (10,19) and that platelet inhibition ameliorates certain forms of lung injury (14,15), we hypothesized that the influenza virus induces platelet adhesion to the lung endothelium and that this process contributes to the pathology of severe influenza.…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, the endothelium normally is antithrombogenic and prevents platelet adhesion. An effect of the virus to induce platelet-endothelial adhesion is plausible: numerous reports describe pulmonary thrombi as an important complication of severe infections with influenza (10,19), while endothelial activation, which would be expected to induce platelet adhesion, was highly correlated with death from influenza in a murine model (20). Furthermore, a study of patients with venous thromboembolism found that vaccination against influenza was associated with a protective effect against pulmonary clots (21).…”

mentioning

confidence: 99%

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

Sugiyama

Gamage

Zyla

et al. 2016

J Virol

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Lung injury after influenza infection is characterized by increased permeability of the lung microvasculature, culminating in acute respiratory failure. Platelets interact with activated endothelial cells and have been implicated in the pathogenesis of some forms of acute lung injury. Autopsy studies have revealed pulmonary microthrombi after influenza infection, and epidemiological studies suggest that influenza vaccination is protective against pulmonary thromboembolism; however, the effect of influenza infection on platelet-endothelial interactions is unclear. We demonstrate that endothelial infection with both laboratory and clinical strains of influenza virus increased the adhesion of human platelets to primary human lung microvascular endothelial cells. Platelets adhered to infected cells as well as to neighboring cells, suggesting a paracrine effect. Influenza infection caused the upregulation of von Willebrand factor and ICAM-1, but blocking these receptors did not prevent platelet-endothelial adhesion. Instead, platelet adhesion was inhibited by both RGDS peptide and a blocking antibody to platelet integrin ␣ 5 ␤ 1 , implicating endothelial fibronectin. Concordantly, lung histology from infected mice revealed viral dose-dependent colocalization of viral nucleoprotein and the endothelial marker PECAM-1, while platelet adhesion and fibronectin deposition also were observed in the lungs of influenza-infected mice. Inhibition of platelets using acetylsalicylic acid significantly improved survival, a finding confirmed using a second antiplatelet agent. Thus, influenza infection induces platelet-lung endothelial adhesion via fibronectin, contributing to mortality from acute lung injury. The inhibition of platelets may constitute a practical adjunctive strategy to the treatment of severe infections with influenza. Here, we show that this infection causes platelets to adhere to the lung endothelium. Importantly, blocking platelets using two distinct antiplatelet drugs improved survival in a mouse model of severe influenza infection. Thus, platelet inhibition may constitute a novel therapeutic strategy to improve the host response to severe infections with influenza.

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“…Lung consolidation and infiltrates with or without pleural effusion were the two plain film patterns found in chest radiographies in our patients. The possibility of an under‐diagnosis of pulmonary embolism and pneumo‐mediastinum that had previously been observed in patients with pandemic influenza A (H1N1) could not be excluded, 36 as our patients were evaluated by plain chest radiographs which were less sensitive in the detection of such abnormalities than a computed tomography 37 …”

Section: Discussionmentioning

confidence: 99%

2009 pandemic Influenza A (H1N1): clinical and laboratory characteristics in pediatric and adult patients and in patients with pulmonary involvement

Lee

Liu

Wang

et al. 2012

Influenza Resp Viruses

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Please cite this paper as: Lee and Liu et al. (2012) 2009 pandemic Influenza A (H1N1): clinical and laboratory characteristics in pediatric and adult patients and in patients with pulmonary involvement. Influenza and Other Respiratory Viruses 6(601), e152–e161. Background To better understand clinical and laboratory characteristics in children, adults, and patients with lung involvement suffering 2009 pandemic influenza A (H1N1). Methods A total of 442 patients with 2009 pandemic influenza A (H1N1) were retrospectively analyzed. Results Comparing to their adult counterpart (n = 55), pediatric patients (n = 387) had significantly higher frequencies of fever, rhinorrhea, cough, sore throat, nausea/vomiting, and longer length of fever; lower frequencies of chest pain and dyspnea; higher incidence of lymphopenia; and lower incidence of elevated serum C‐reactive protein. Among the 227 patients with radiographs available, lung involvement was found in 19 (8·4%) (52·6% consolidation and 47·4% interstitial infiltrations), including 18 children and one adult. One child with lung consolidation died of multiorgan failure. Significant findings in patients with lung involvement included predominant young age (≤10 years), prolonged fever, and delayed oseltamivir therapy (≥48 hours after onset of illness); higher frequencies of dyspnea, nausea/vomiting, and altered consciousness; and higher incidences of leukopenia, elevated serum creative kinase, and lactic dehydrogenase. Conclusions Among patients with 2009 pandemic influenza A (H1N1), we found significant difference in clinical manifestations between children and adults, and significant differences in clinical and laboratory manifestations between patients with lung involvement and those without. On the basis of data from this study and the existing literature, early treatment with oseltamivir is recommended for patients with 2009 pandemic influenza A (H1N1), regardless of age.

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Chest Radiographic and CT Findings in Novel Swine-Origin Influenza A (H1N1) Virus (S-OIV) Infection

Abstract: Chest radiographs are normal in more than half of patients with S-OIV (H1N1) and progress to bilateral extensive air-space disease in severely ill patients, who are at a high risk for PE.

Cited by 198 publications

References 6 publications

H1N1 influenza A virus Related Pneumonia and Respiratory Failure

H1N1 influenza A virus Related Pneumonia and Respiratory Failure

Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

2009 pandemic Influenza A (H1N1): clinical and laboratory characteristics in pediatric and adult patients and in patients with pulmonary involvement

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