scholarly journals Acute Lung Injury – From Pathophysiology to Treatment

2021 ◽  
pp. S353-S366
Author(s):  
D Mokra
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Compliance ◽  
Acute Onset ◽  
Consensus Conference ◽  
Response To Treatment ◽  
Lung Protective Ventilation ◽  
General Description ◽  
X Ray ◽  
Chest X Ray

Acute lung injury is characterized by acute respiratory insufficiency with tachypnea, cyanosis refractory to oxygen, decreased lung compliance, and diffuse alveolar infiltrates on chest X-ray. The 1994 American-European Consensus Conference defined “acute respiratory distress syndrome, ARDS” by acute onset after a known trigger, severe hypoxemia defined by PaO2/FiO2≤200 mm Hg, bilateral infiltrates on chest X-ray, and absence of cardiogenic edema. Milder form of the syndrome with PaO2/FiO2 between 200-300 mm Hg was named „acute lung injury, ALI“. Berlin Classification in 2012 defined three categories of ARDS according to hypoxemia (mild, moderate, and severe), and the term “acute lung injury” was assigned for general description or for animal models. ALI/ARDS can originate from direct lung triggers such as pneumonia or aspiration, or from extrapulmonary reasons such as sepsis or trauma. Despite growing understanding the ARDS pathophysiology, efficacy of standard treatments, such as lung protective ventilation, prone positioning, and neuromuscular blockers, is often limited. However, there is an increasing evidence that direct and indirect forms of ARDS may differ not only in the manifestations of alterations, but also in the response to treatment. Thus, individualized treatment according to ARDS subtypes may enhance the efficacy of given treatment and improve the survival of patients.

scholarly journals Transfusion-related acute lung injury (TRALI) in two thalassaemia patients caused by the same multiparous blood donor

2017 ◽  
Vol 9 (1) ◽  
pp. e2017060
Author(s):  
George J Kontoghiorghes
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Blood Donor ◽  
Intensive Therapy ◽  
Hla Antigens ◽  
Hla Class I ◽  
Intensive Therapy Unit ◽  
X Ray ◽  
Red Blood Cell Transfusions ◽  
Chest X Ray

Two separate episodes of transfusion-related acute lung injury (TRALI) in thalassaemia patients caused by red blood cell transfusions from the same multiparous blood donor are reported. Both cases had the same symptomatology and occurred 10-60 minutes of transfusion. The patients presented dyspnea, sweating, fatigue, dizziness, fever, and sense of losing consciousness. The chest x-ray showed a pulmonary oedema-like picture with both lungs filled with fluid. The patients were treated in the intensive therapy unit. They were weaned off the ventilator and discharged following hospitalization 7 and 9 days respectively. The TRALI syndrome was diagnosed to be associated with HLA-specific donor antibodies against mismatched HLA-antigens of the transfused patients. Haemovigilance improvements are essential for reducing the morbidity and mortality in transfused patients. Blood from multiparous donors should be tested for the presence of IgG HLA-Class I and –Class II antibodies before being transfused in thalassaemia and other chronically transfused patients.

scholarly journals Transfusion related acute lung injury-TRALI: a review

2019 ◽  
Vol 7 (5) ◽  
pp. 1985
Author(s):  
Javier Alcazar-Castro ◽  
Alejandro Zarate-Aspiros ◽  
Elias Andrade-Cuellar ◽  
Brenda Alvarez-Perez ◽  
Alan I. Valderrama-Treviño ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Bacterial Contamination ◽  
Biological Response ◽  
Sudden Onset ◽  
X Ray ◽  
Pulmonary Damage ◽  
Hemodynamic Overload ◽  
Chest X Ray ◽  
Complications Of Blood Transfusion

Acute pulmonary damage caused by transfusion is characterized by the sudden onset of respiratory distress in newly transfused patients within 6 hours after the transfusion, bilateral infiltrative changes in chest X-ray, PaO2/FIO2 <300 mmHg, absence of other risk factors for acute lung injury and absence of signs suggesting cardiogenic origin of pulmonary edema. Being one of the most serious complications of blood transfusion, plasma is the most involved factor, although all blood components can cause it, and is caused by antigen reactions/leukocyte antibody and lipid activity with ability to modify the biological response on primitive leukocytes. The diagnosis is based on the integration of clinical, radiological and gasometric elements, ruling out the rest of the possible causes of acute lung injury. Its differential diagnosis should include hemodynamic overload, anaphylactic reaction, bacterial contamination of transfused blood products and transfusion hemolytic reaction. The treatment is supportive measures based on the needs and does not differ from the treatment of acute lung injury secondary to other etiologies, severe cases require endotracheal intubation and mechanical ventilation while the non-severe can be managed with oxygen therapy.

scholarly journals Evaluation of Recruited Lung Volume at Inspiratory Plateau Pressure With PEEP Using Bedside Digital Chest X-ray in Patients With Acute Lung Injury/ARDS

2013 ◽  
Vol 58 (3) ◽  
pp. 416-423 ◽  
Author(s):  
F. Wallet ◽  
B. Delannoy ◽  
A. Haquin ◽  
S. Debord ◽  
V. Leray ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lung Volume ◽  
Plateau Pressure ◽  
X Ray ◽  
Digital Chest ◽  
Chest X Ray

scholarly journals Pathophysiology of pulmonary hypertension in acute lung injury

2012 ◽  
Vol 302 (9) ◽  
pp. L803-L815 ◽  
Author(s):  
Laura C. Price ◽  
Danny F. McAuley ◽  
Philip S. Marino ◽  
Simon J. Finney ◽  
Mark J. Griffiths ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Current Knowledge ◽  
Lung Compliance ◽  
Lung Protective Ventilation ◽  
Ventilation Strategies ◽  
Protein Rich ◽  
Modern Era ◽  
Alveolar Edema

Acute lung injury (ALI) and acute respiratory distress syndrome are characterized by protein rich alveolar edema, reduced lung compliance, and acute severe hypoxemia. A degree of pulmonary hypertension (PH) is also characteristic, higher levels of which are associated with increased morbidity and mortality. The increase in right ventricular (RV) afterload causes RV dysfunction and failure in some patients, with associated adverse effects on oxygen delivery. Although the introduction of lung protective ventilation strategies has probably reduced the severity of PH in ALI, a recent invasive hemodynamic analysis suggests that even in the modern era, its presence remains clinically important. We therefore sought to summarize current knowledge of the pathophysiology of PH in ALI.

Interstitial Pneumonia in Patients with Idhiopatic Thrombocytopenic Purpura.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3953-3953
Author(s):  
Vincenzo Fontana ◽  
Elio Donna ◽  
Pamela Dudkiewicz ◽  
Gabriella Lander ◽  
Yeon S. Ahn
Keyword(s):  
Acute Lung Injury ◽  
Pulmonary Fibrosis ◽  
Lung Injury ◽  
Interstitial Pneumonia ◽  
Lung Diseases ◽  
Interstitial Lung Diseases ◽  
Mild Symptom ◽  
Thrombocytopenic Purpura ◽  
X Ray ◽  
Chest X Ray

Abstract INTRODUCTION: Idhiopatic thrombocytopenic purpura (ITP) is an autoimmune disease characterized by a premature destruction of platelets by macrophage, especially in the spleen. However in some cases, platelet sequestration and destruction may occur in other organs. Chromium labeled platelet sequestration study revealed that liver or precordial area are prominent sites of sequestration in some cases, suggesting that the lung might be the site in certain cases. Some cases of interstitial pneumonia are associated with immunologic injury to the lung and seen in patients with some autoimmune diseases, infections, drugs and transfusion related acute lung injury (TRALI) in which transfusions of platelets and blood products induce acute lung injury due to sequestration of platelets and neutrophils in lungs, sometimes leading to ARDS. We describe here an unusual association between ITP and interstitial pneumonia, suggesting that a lung injury similar to TRALI is involved in acute and recurrent ITP. METHODS: We have identified patients with ITP who developed interstitial pneumonia during the course of ITP. We reviewed their charts and analyzed their clinical courses of ITP and interstitial lung diseases. Laboratory tests and chest X ray or CAT scans were reviewed. The laboratory study included CBC, platelets and platelets activation was measured by PMP (platelet microparticles), expression of CD62p flowcytometrically. RESULTS: We have identified 6 patients with ITP who developed interstitial pneumonia during the course of ITP. In two of six, interstitial pneumonia was detected at the presentation of acute ITP. ITP was severe with platelet counts less than 10.000. Interstitial pneumonia was discovered incidentally by chest X ray and confirmed by CAT scans. A mild symptom of dyspnea was detected in careful examination. One underwent lung biopsy which showed findings consistent with brochiolitis obliterans organizing pneumonia. Repeated CAT scans in 1–3 months revealed marked improvement but residual interstitial infiltrates still persisted. Four others had a long standing chronic ITP with clinical courses characterized by frequent relapses in spite of surgical and medical therapy. Four of six patients had splenectomy. Interstitial lung diseases were detected at the time of a severe relapse with platelet counts of less than 20.000. One patient underwent chromium labeled platelet sequestration study which revealed rapid sequestration of platelets in the lung. Interstitial infiltrates improved following improvement of ITP but two progressed to interstitial pulmonary fibrosis. CD62P measured by flowcytometry was very high in all 3 patients tested, indicating persisting platelet activation in this clinical setting. SUMMARY: We report interstitial pneumonia developing in 6 patients with ITP. Clinically all were asymptomatic and detection of interstitial pneumonia was incidental radiology finding. A mild symptom of exertional dyspnea was present in careful investigation. Chest X ray or CT scans showed nonspecific interstitial infiltrates and showed an overall improvement within months but residual infiltrates persisted. Two progressed to pulmonary fibrosis. We suggest that platelets are sequestered and destroyed in the lung in some patients with ITP, to generate cytokines and lipid mediators that lead to a nonspecific interstitial lung disease.

Complement Activation in Transfusion Related Acute Lung Injury (TRALI).

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 954-954
Author(s):  
Daniel R. Ambruso ◽  
Christopher C. Silliman ◽  
Marguerite Kelher ◽  
Gail Thurman ◽  
Patsy Giclas
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Complement Activation ◽  
Class Ii ◽  
Hla Class Ii ◽  
X Ray ◽  
Factor Xi Deficiency ◽  
Activation Products ◽  
Chest X Ray ◽  
Priming Activity

Abstract Background: TRALI is defined as acute lung injury occurring within six hours of a transfusion of blood products. Two major etiologies have been identified and include leukocyte antibodies activating complement. We report two patients with TRALI reactions who had documented activation of complement. Case Studies. Case 1: A 59 year old male with Factor XI deficiency and hematochezia was given 3 units of fresh frozen plasma (FFP). During infusion of the third unit, the patient developed dyspnea and cyanosis requiring ventilator support. A chest x-ray showed new diffuse infiltrates; CVP and an echocardiogram were normal. The symptoms resolved in 3 days. Case 2: An 87 year old female required surgical repair of a hip fracture. Four units were infused and with the last one, the patient developed chills, fever and tachypnea. On 6 l/min of O2, she had a saturation of 58%. Chest x-ray showed bilateral infiltrates; the echocardiogram was normal. The patient sustained a cardiac arrest and could not be resuscitated. Methods: Samples from donors or FFP units were screened for HLA and granulocyte antibodies. Priming of the fMLP stimulated neutrophil oxidase activity was performed by standard assay. Plasma from products implicated in TRALI and plasma samples from patients before and during the TRALI reaction were assayed for priming of the fMLP stimulated respiratory burst in neutrophils; C3a, C4a, C5a, C5–9, and Bb were measured by standard techniques. Results: In Case 1, HLA Class II, IgG reactivity by flow cytometry was documented with plasma from the implicated donor and recipient cells. Priming of neutrophils was detected in the implicated unit as well as the recipient’s plasma during the reaction in comparison to pre-transfusion specimen. Complement activation products were increased in samples during the reaction and the product being infused at the onset of TRALI. In the second case, HLA Class II antibodies with a specificity which would interact with the recipient’s antigens were detected in the product related to the TRALI reaction. Priming activity of the neutrophil oxidase was documented in the infused product and in post vs. pre reaction patient samples. Complement activation products were increased in the implicated FFP unit and C5a was increased in the patient’s post samples. Additional cases are being assessed for complement activation. Conclusions: In these cases of TRALI, the implicated products exhibited priming activity as well as antibodies which reacted with recipient antigens by flow crossmatch or by documentation of the cognate antigen. Complement activation was documented in patient samples during the reaction as opposed to those collected before the transfusion. Most importantly, complement was activated in the product transfused during the onset of TRALI symptoms. Thus, complement activation in the product is the most likely cause of the TRALI reaction. Infusion of products containing activated complement components may provide an alternative mechanism for TRALI reactions.

scholarly journals A simple classification model for hospital mortality in patients with acute lung injury managed with lung protective ventilation*

2011 ◽  
Vol 39 (12) ◽  
pp. 2645-2651 ◽  
Author(s):  
Lisa M. Brown ◽  
Carolyn S. Calfee ◽  
Michael A. Matthay ◽  
Roy G. Brower ◽  
B. Taylor Thompson ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Hospital Mortality ◽  
Protective Ventilation ◽  
Classification Model ◽  
Lung Protective Ventilation ◽  
Simple Classification

scholarly journals Alternative and Natural Therapies for Acute Lung Injury and Acute Respiratory Distress Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Vipul J. Patel ◽  
Sreeja Biswas Roy ◽  
Hiren J. Mehta ◽  
Myungsoo Joo ◽  
Ruxana T. Sadikot
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Experimental Models ◽  
Lung Protective Ventilation ◽  
Related Factor ◽  
Made In

Introduction. Acute respiratory distress syndrome (ARDS) is a complex clinical syndrome characterized by acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure and death. Current best practice for ARDS involves “lung-protective ventilation,” which entails low tidal volumes and limiting the plateau pressures in mechanically ventilated patients. Although considerable progress has been made in understanding the pathogenesis of ARDS, little progress has been made in the development of specific therapies to combat injury and inflammation. Areas Covered. In recent years, several natural products have been studied in experimental models and have been shown to inhibit multiple inflammatory pathways associated with acute lung injury and ARDS at a molecular level. Because of the pleiotropic effects of these agents, many of them also activate antioxidant pathways through nuclear factor erythroid-related factor 2, thereby targeting multiple pathways. Several of these agents are prescribed for treatment of inflammatory conditions in the Asian subcontinent and have shown to be relatively safe. Expert Commentary. Here we review natural remedies shown to attenuate lung injury and inflammation in experimental models. Translational human studies in patients with ARDS may facilitate treatment of this devastating disease.

Keratinocyte growth factor therapy in murine oleic acid-induced acute lung injury

2005 ◽  
Vol 288 (6) ◽  
pp. L1179-L1192 ◽  
Author(s):  
K. Ulrich ◽  
M. Stern ◽  
M. E. Goddard ◽  
J. Williams ◽  
J. Zhu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Acute Lung Injury ◽  
Gene Delivery ◽  
Lung Injury ◽  
Time Course ◽  
Lung Compliance ◽  
Alveolar Type ◽  
Protein Therapy ◽  
Cell Numbers ◽  
Atii Cell

Alveolar type II (ATII) cell proliferation and differentiation are important mechanisms in repair following injury to the alveolar epithelium. KGF is a potent ATII cell mitogen, which has been demonstrated to be protective in a number of animal models of lung injury. We have assessed the effect of recombinant human KGF (rhKGF) and liposome-mediated KGF gene delivery in vivo and evaluated the potential of KGF as a therapy for acute lung injury in mice. rhKGF was administered intratracheally in male BALB/c mice to assess dose response and time course of proliferation. SP-B immunohistochemistry demonstrated significant increases in ATII cell numbers at all rhKGF doses compared with control animals and peaked 2 days following administration of 10 mg/kg rhKGF. Protein therapy in general is very expensive, and gene therapy has been suggested as a cheaper alternative for many protein replacement therapies. We evaluated the effect of topical and systemic liposome-mediated KGF-gene delivery on ATII cell proliferation. SP-B immunohistochemistry showed only modest increases in ATII cell numbers following gene delivery, and these approaches were therefore not believed to be capable of reaching therapeutic levels. The effect of rhKGF was evaluated in a murine model of OA-induced lung injury. This model was found to be associated with significant alveolar damage leading to severe impairment of gas exchange and lung compliance. Pretreatment with rhKGF 2 days before intravenous OA challenge resulted in significant improvements in Po2, Pco2, and lung compliance. This study suggests the feasibility of KGF as a therapy for acute lung injury.

Sign in / Sign up

Export Citation Format

Share Document