Acute Non-cardiogenic Pulmonary Edema Research Articles

Toxic inhalation of sodium metabisulphite by-products from a shipping container.

Logistics workers who handle cargo containers are at risk of toxic inhalation injuries, although prevalence and severities of these injuries are not well characterized. We report on a previously healthy 37-year-old supervisor who was acutely exposed to sodium metabisulphite and its thermal degradation by-products during a routine inspection of a shipping container. The employee developed chemical pneumonitis with acute non-cardiogenic pulmonary oedema and subsequent severe reactive airway dysfunction syndrome.

Lentinus edodes Polysaccharides Alleviate Acute Lung Injury by Inhibiting Oxidative Stress and Inflammation.

Acute lung injury (ALI) is a kind of lung disease with acute dyspnea, pulmonary inflammation, respiratory distress, and non-cardiogenic pulmonary edema, accompanied by the mid- and end-stage characteristics of COVID-19, clinically. It is imperative to find non-toxic natural substances on preventing ALI and its complications. The animal experiments demonstrated that Lentinus edodes polysaccharides (PLE) had a potential role in alleviating ALI by inhibiting oxidative stress and inflammation, which was manifested by reducing the levels of serum lung injury indicators (C3, hs-CRP, and GGT), reducing the levels of inflammatory factors (TNF-α, IL-1β, and IL-6), and increasing the activities of antioxidant enzymes (SOD and CAT) in the lung. Furthermore, PLE had the typical characteristics of pyran-type linked by β-type glycosidic linkages. The conclusions indicated that PLE could be used as functional foods and natural drugs in preventing ALI.

Are we missing reverse TRALI? – A real world experience from a tertiary care oncology centre in India

Transfusion related acute lung injury (TRALI) is a rare but potentially fatal pulmonary complication of transfusion that presents as acute hypoxemia and non-cardiogenic pulmonary oedema, developing during or within six hours of transfusion. Majority of the cases reported are due to transfusion of plasma rich blood components containing antibodies to human leukocyte antigen (anti-HLA) or human neutrophil antigen (anti-HNA). Rarely, anti-HLA or anti-HNA in recipients against transfused donor leukocyte antigens, cause TRALI by a reverse mechanism. Herein, we report three cases of suspected TRALI following transfusions of buffy coat derived granulocytes and peripheral blood stem cells. Three patients with hematological malignancies developed pulmonary symptoms after transfusions of leukocyte rich blood components. All cases showed findings of bilateral pulmonary infiltrates at chest radiography and patients were managed accordingly; however, all three expired within seven days of transfusion due to progressive respiratory deterioration. The patients were transfusion dependent for a long time and had received multiple non-leukoreduced blood components in the past. Clinical findings in all three cases indicate the possibility of reverse TRALI. Although, patients’ anti-HLA or anti-HNA antibodies concordance with donors’ cognate antigens (HLA and HNA) was not confirmed; yet these three cases suggest that reverse pathogenesis of TRALI is not as infrequent as reported in the literature. However, reverse TRALI has not been confirmed as the presence and nature of antibodies in the transfused recipient were not investigated due to the non availability of immunodiagnostic tests in India.

Role of chest ultrasound to differentiate between acute cardiogenic pulmonary edema and non-cardiogenic pulmonary edema (acute respiratory distress syndrome)

Role of chest ultrasound to differentiate between acute cardiogenic pulmonary edema and non-cardiogenic pulmonary edema (acute respiratory distress syndrome)

Phenotypes and personalized medicine in the acute respiratory distress syndrome.

Although the acute respiratory distress syndrome (ARDS) is well defined by the development of acute hypoxemia, bilateral infiltrates and non-cardiogenic pulmonary edema, ARDS is heterogeneous in terms of clinical risk factors, physiology of lung injury, microbiology, and biology, potentially explaining why pharmacologic therapies have been mostly unsuccessful in treating ARDS. Identifying phenotypes of ARDS and integrating this information into patient selection for clinical trials may increase the chance for efficacy with new treatments. In this review, we focus on classifying ARDS by the associated clinical disorders, physiological data, and radiographic imaging. We consider biologic phenotypes, including plasma protein biomarkers, gene expression, and common causative microbiologic pathogens. We will also discuss the issue of focusing clinical trials on the patient’s phase of lung injury, including prevention, administration of therapy during early acute lung injury, and treatment of established ARDS. A more in depth understanding of the interplay of these variables in ARDS should provide more success in designing and conducting clinical trials and achieving the goal of personalized medicine.

Acute non-cardiogenic pulmonary oedema: a rare side effect of olanzapine

Olanzapine is a safe and potent second generation atypical antipsychotic drug with a very good safety profile among its counterparts. Respiratory failure due to olanzapine is an extremely rare life threatening side effect. Here we report a case of respiratory failure due to non cardiogenic pulmonary oedema in a patient with schizophrenia who has been on olanzapine for 10 years.

239. Cardiogenic and non-cardiogenic acute pulmonary edema in hypertensive disorder in pregnancy

Introduction Acute pulmonary edema (APE) in hypertensive disorder in pregnancy (HDP) is one of the serious conditions and may have various origins, which roughly classified into non-cardiogenic(NCPE) and cardiogenic (CPE). Treatment strategy may be different from each other. Objective Similarity and difference of symptoms, physical or laboratory findings, and treatment between NCPE and CPE were investigated and appropriate approach may be established. Methods The HDP cases which had acute dyspnea and underwent echocardiography in our hospital between January 2014 and March 2018 were recruited to the study. The medical records were retrospectively reviewed. Results Twenty HDP cases were reviewed. Sixteen cases were confirmed as NCPE including one beta-adrenergic drug-induced, two transfusions related, which were mainly treated with diuretics. Based on the echocardiography findings, four cases were confirmed as CPE all of which were diagnosed with peripartum cardiomyopathy (PPCM). While only one NCPE case had orthopnea, all of CPE cases did. Furthermore, most of NCPE cases showed systemic edema, but none of CPE cases did not. No significant difference was observed in other clinical or laboratory findings between two groups. Discussion Orthopnea is known to be a typical symptom of heart failure. CPE is basically caused by pulmonary congestion followed by left heart dysfunction. From this study, it could be one of the characteristic symptoms of CPE. Severe hypertension may sometimes increase afterload leading to left heart dysfunction. NCPE was the most common cause of dyspnea in HDP, but it may come from various situation Hyperpermeability and hypoosmolality, are essential features of HDP. Some medical interventions such as steroid for fetal lung maturation, and beta-adrenergic drugs for tocolysis may possibly cause NCPE. Infusion overload or transfusion-related acute lung injury may sometimes accompany with serious conditions of HDP such as placental abruption, HELLP syndrome.

Fatal aspiration of iodine oral contrast

We report on a case of massive iodine oral contrast aspiration with consequential cardiorespiratory arrest. The patient was successfully resuscitated and treated with mechanical ventilatory support and an urgent bronchoscopy toilet with only modest success. Instead of esophagography, the X-ray image showed an almost classical “bronchography.” A few hours later, the chest X-ray was indicative of acute noncardiogenic pulmonary edema. Respiratory status additionally deteriorated due to bilateral pleural effusions, severe exacerbation of chronic obstructive pulmonary disease, and heart failure, and the patient died of multiorgan failure 8 days after admission to the Intensive Care Unit. The incidence of fatal complications of oral iodine contrast aspiration is very rare but can be even lower if fully cooperative, and well-instructed patients are selected. Special attention should be paid to those with any kind of swallowing difficulties.

Acute pulmonary oedema

Acute pulmonary oedema is a distressing and life-threatening illness that is associated with a sudden onset of symptoms. For the best possible patient outcomes, it is essential that nurses in all clinical areas are equipped to accurately recognise, assess and manage patients with acute pulmonary oedema. This article outlines the pathophysiology of acute cardiogenic and non-cardiogenic pulmonary oedema, and suggests a systematic approach to the recognition and management of its most serious manifestations. Long-term care and symptom recognition are discussed and suggestions for ongoing patient self-management are provided.

Pulmonary Edema (Non-Cardiogenic) and Acute Respiratory Distress Syndrome Secondary to Amniotic Fluid Embolism Syndrome Following Preterm Delivery of Intrauterine Fetal Death: A Case Report

A 27 years old healthy female of twenty eight weeks pregnancy with history of low grade fever and dry cough for one day presented with intrauterine fetal death. Following spontaneous preterm delivery of the dead fetus, within three hours, patient developed irritable cough, dyspnea, tachypnea, restlessness and cyanosis. She was put on face mask with oxygen flow of ten litres/minute and was nebulized with Salbutamol in the delivery suite but gradually she developed desaturation of 76%. As the condition of patient was worsening patient was transferred to intensive care unit. In intensive care unit patient was intubated and put on ventilator immediately. X-ray chest was showing bilateral infiltrates and arterial blood gases was showing PaO2/FiO2 ratio of 55.6%. Pulmonary capillary wedge pressure was not checked as pulmonary catheterization is not practiced in our Intensive care unit. Cardiogenic component of pulmonary edema was ruled out indirectly by history, electrocardiogram, echocardiography, central venous pressure and X-ray chest (heart shadow). She was diagnosed as a case of severe acute respiratory distress syndrome (American European consensus conference guideline, 2012) and non-cardiogenic pulmonary edema due to amniotic fluid embolism syndrome. In course of management, maximum emphasis was given on lung protective ventilation and fluid, conservative strategy along with medical and other supportive management. On her eighth day on ventilator, she was extubated and on ninth day, she was shifted to maternity ward. On fourteenth day she was discharged from hospital. She came for follow up after one month of her discharge and was found to have no residual complication.

Acute cardiogenic pulmonary edema induced by severe hypoglycemia — A rare case report

Both of hypoglycemia and acute pulmonary edema (APE) are medical emergencies and need immediate treatment to decrease the possible morbidity and mortality. There were some rare case reports discussing about the association between hypoglycemia and APE [ 1 Baruh S. Sherman L. Hypoglycemia, a cause of pulmonary edema. Progressive, fatal pulmonary edema complicating hypoglycemia induced by alcohol and insulin. J Natl Med Assoc. May 1975; 67: 200-204 PubMed Google Scholar , 2 Ortega E. Wagner A. Caixàs A. Barcons M. Corcoy R. Hypoglycemia and pulmonary edema: a forgotten association. Diabetes Care. Jul 2000; 23: 1023-1024 Crossref PubMed Scopus (12) Google Scholar , 3 Mishriki Y.Y. Hypoglycemia-induced neurogenic-type pulmonary edema: an underrecognized association. Endocr Pract. Sep-Oct 2004; 10: 429-431 Abstract Full Text Full Text PDF PubMed Google Scholar , 4 Margulescu A.D. Sisu R.C. Cinteza M. Vinereanu D. Noncardiogenic acute pulmonary edema due to severe hypoglycemia--an old but ignored cause. Am J Emerg Med. Sep 2008; 26: 839.e3-6 Abstract Full Text Full Text PDF PubMed Scopus (5) Google Scholar ]; however, the mechanism of APE in these cases was related to neurogenic or metabolic but not cardiogenic cause. Herein, we reported a case of cardiogenic APE and respiratory failure after suffering from severe hypoglycemia and the mechanism of APE in the case was due toTakotsubo cardiomyopathy (TCMP) triggered by severe hypoglycemia.

Transfusion-Related Acute Lung Injury, an Evolving Syndrome: The Road of Discovery, With Emphasis on the Role of the Mayo Clinic

Transfusion-related acute lung injury (TRALI) is characterized by acute hypoxemia and noncardiogenic pulmonary edema. At the very least, descriptions of cases consistent with TRALI date back to the early 1950s. Early articles from the 1950s and 1960s documented transfusion-associated pulmonary edema without evidence of volume overload. Explanations for this phenomenon included hypersensitivity and transfused leukoagglutinins. Descriptions from the 1970s also implicated transfused antileukocyte antibodies and noted that blood products containing such antibodies often came from multiparous female donors. Cases implicating recipient anti-human leukocyte antigen antibody reacting with transfused donor leukocytes and donor antibodies reacting with another donor's leukocytes were also described. The 1980s marked the emergence of the Mayo Clinic as a leading contributor to the understanding of TRALI. The descriptions of the syndrome that was named "TRALI" by Mayo Clinic investigators were the most extensive and complete to date and are presented in detail. The Mayo Clinic has remained in the forefront of TRALI investigation, particularly as it pertains to the critically ill, and recent studies from this center are also presented in detail. The common thread connecting the Mayo Clinic's descriptions in the 1980s to the more contemporary studies is Dr S. Breanndan Moore. Dr Moore passed away recently, but his crucial work in the area of TRALI lives on.

A case of non-cardiogenic acute pulmonary edema in a patient with POEMS syndrome-associated pulmonary arterial hypertension

Dear Editor,POEMS syndrome is a monoclonal plasma cell disordercharacterized by polyneuropathy, organomegaly, endocrin-opathy, monoclonal protein, and skin changes [1]. It is alsoassociated with pulmonary arterial hypertension (PAH) orCastleman’s disease [1, 2]. However, there is no reportabout non-cardiogenic acute pulmonary edema (NCAPE).In this article, we describe a rare case of transient NCAPEin a patient with POEMS syndrome.A 55-year-old male with POEMS syndrome and Castle-man’s disease was referred to our institution because ofpulmonary hypertension (PH). Since no apparent causes ofPH were revealed, we reached the diagnosis of PAHconfirmed by right heart catheterization showing 49 mmHgof mean pulmonary artery pressure, 10 mmHg of meanpulmonary capillary wedge pressure, and 4.11 L/min ofcardiac output [3]. His complication included old myocar-dial infarction of distal part of left anterior descendingartery with mildly reduced left ventricular ejection fractionof 55%. Before the treatment of PAH, he acutely developeddyspnea without volume loading. Chest radiograph dem-onstrated bilateral alveolar infiltrates, and a ratio of arterialoxygen tension to fraction of inspired oxygen was89.8 mmHg. There were no changes in electrocardiographicand echocardiographic findings, and no elevations ofcardiac enzymes. Besides, no apparent causes of acuterespiratory distress syndrome such as bacteremia wereidentified [4]. We diagnosed that he developed NCAPE.He was treated with oxygen administration, nitroglycerin,and low-dose dobutamine as supportive measures. Hissymptoms diminished promptly over the next couple ofhours without ventilator support, accompanied by decreas-ing alveolar infiltrates.Since several cytokines such as vascular endothelialgrowth factor (VEGF) which act in conjunction withangiopoietin-1/2 are associated with exacerbations ofPOEMS syndrome, we evaluated these cytokines toelucidate possible mechanisms of NCAPE (Table 1)[1, 5,6]. There were acute increases in interleukin (IL)-6 andVEGF. However, no significant differences in othercytokines were revealed. Considering the Starling equation[7], we speculated that acute elevation of vascular perme-ability following VEGF elevation contributed to the onsetof NCAPE [4, 8]. It is also possible that elevated pre-capillary hydraulic pressure due to advanced PAH made thepatient susceptible to the change of vascular permeability[7]. We also speculated that acute elevation of IL-6provides essential stimulatory cues to acute VEGF eleva-tion, which may imply the risk of complication of Castle-man’s disease [8, 9].

Coexistent Wegener’s Granulomatosis and Goodpasture’s Disease

To the Editor: Wegener’s granulomatosis (WG) and Goodpasture’s disease are unique etiologies of pulmonary-renal syndromes. Given the similarity in clinical presentation, differentiating these diseases at the bedside can be challenging. A 50-year-old woman was referred to the rheumatology clinic with a presumptive diagnosis of vasculitis. She presented with a 12-month history of recurrent epistaxis, nasal crusting, migratory arthralgias, and a 20-pound weight loss. She was also diagnosed and treated for an isolated episode of scleritis in the left eye. In the week prior to presentation, she developed sores on her tongue, mild dyspnea, and new onset hemoptysis. Examination was remarkable for tongue ulcerations, nasal mucosal ulcerations, and splinter hemorrhages. Other findings included palpable purpura of the lower extremities, 3 joint effusions (both knees, left ankle), and 7 tender joints. Chest examination revealed fine crackles at bases; cardiovascular examination was normal. Laboratory investigations revealed an elevated erythrocyte sedimentation rate of 60 mm/h, and urinalysis with 3+ blood and trace protein. Creatinine at presentation was 77 μmol/l. The cytoplasmic antineutrophil antibody (c-ANCA) was positive [proteinase-3 (PR-3)-positive, myeloperoxidase-negative] as was the anti-glomerular basement membrane (anti-GBM) antibody. Chest radiograph revealed symmetric interstitial and airspace changes consistent with differential diagnosis of pulmonary hemorrhage, atypical infection, or acute noncardiogenic pulmonary edema. She underwent a computed tomography scan of the thorax, which demonstrated ground-glass opacity in keeping with pulmonary hemorrhage (Figure 1), while skin biopsy of her palpable purpura revealed a leukocytoclastic vasculitis. Figure 1. Computed … Address correspondence to Dr. S. Mulpuru, The Ottawa Hospital, University of Ottawa, Department of Medicine, 501 Smyth Road, Room 6356, Box 211, Ottawa, Ontario K1H 8L6. E-mail: sunitamulpuru{at}hotmail.com

Two Cases of Transfusion-related Acute Lung Injury Triggered by HLA and Anti-HLA Antibody Reaction

Transfusion-related acute lung injury (TRALI) is a serious adverse transfusion reaction that is presented as acute hypoxemia and non-cardiogenic pulmonary edema, which develops during or within 6 hr of transfusion. Major pathogenesis of TRALI is known to be related with anti-HLA class I, anti-HLA class II, or anti-HNA in donor's plasma. However, anti-HLA or anti-HNA in recipient against transfused donor's leukocyte antigens also cause TRALI in minor pathogenesis and which comprises about 10% of TRALI. Published reports of TRALI are relatively rare in Korea. In our cases, both patients presented with dyspnea and hypoxemia during transfusion of packed red blood cells and showed findings of bilateral pulmonary infiltrations at chest radiography. Findings of patients' anti-HLA antibodies and recipients' HLA concordance indicate that minor pathogenesis may be not as infrequent as we'd expected before. In addition, second case showed that anti-HLA class II antibodies could be responsible for immunopathogenic mechanisms, alone.

Pathologies respiratoires aiguës et subaiguës d’origine toxique

Acute or subacute chemical-induced lung injury is rarely compound specific and is most often caused by an accidental occupational, domestic or environmental exposure to an inhaled chemical agent. The industrial disaster that happened in Bhopal in 1984, accidental poisoning with chlorine and petroleum hydrocarbons and also vesicant gases used during conflicts, are specific examples. Rarely, a chemical agent can cause lung damage by being ingested and reaching the lung through the systemic circulation (for example accidental or deliberate paraquat ingestion). Household accidents should not be underestimated. An important cause of household accidents is chlorine inhalation resulting from mixing bleach with acids such as the scale removers used to clean toilets. Chemical agents can provoke direct and/or indirect damage to the respiratory tract. The acute or subacute clinical manifestations resulting from inhalation of chemical agents are very varied and include inhalation fevers, acute non-cardiogenic pulmonary oedema, adult respiratory distress syndrome, reactive airways dysfunction syndrome and acute or subacute pneumonitis. The site and the severity of chemical-induced respiratory damage caused by inhaled chemical agents depend mainly on the nature and the amount of the agent inhaled. The immediate and long-term prognosis and possible sequelae are also variable. This review excludes infectious or immunologically induced acute respiratory diseases.

Lesión pulmonar aguda producida por transfusión

The term Transfusion-Related Acute Lung Injury (TRALI) was coined in 1985. It is a relatively rare, life-threatening clinical syndrome characterized by acute respiratory failure and non-cardiogenic pulmonary edema during or following a blood transfusion. Although its true incidence is unknown, a rate 1 out of every 5000 transfusions has been quoted. TRALI has been the most common cause of transfusion-related fatalities during three years in the USA. Two different etiologies have been proposed. The first is a single antibody-mediated event involving the transfusion of anti-HLA or antigranulocyte antibodies into patients whose leukocytes express the cognate antigens. The second is a two-event model: the first event is related to the clinical condition of the patient (sepsis, trauma, etc.) resulting in pulmonary endothelial activation and neutrophil sequestration, and the second event is the transfusion of a biologic response modifier that activates these adherent polymorphonuclear leukocytes resulting in endothelial damage and capillary leak. The patient management is support as needed based on the severity of the clinical picture and strategies to prevent TRALI are focused on: donor-exclusion policies, product management strategies and avoidance of unnecessary transfusions.

Basiliximab induced non-cardiogenic pulmonary edema in two pediatric renal transplant recipients

We report two cases of non-cardiogenic pulmonary edema as a complication of basiliximab induction therapy in young pediatric renal transplant patients identified following a retrospective review of all pediatric renal transplant cases performed in the National Paediatric Transplant Centre, Childrens University Hospital, Temple Street, Dublin, Ireland. Twenty-eight renal transplantations, of which five were living-related (LRD) and 23 were from deceased donors (DD), were performed in 28 children between 2003 and 2006. In six cases, transplantations were pre-emptive. Immunosuppression was induced pre-operatively using a combination of basiliximab, tacrolimus and methylprednisolone in all patients. Basiliximab induction was initiated 2 h prior to surgery in all cases and, in 26 patients, basiliximab was re-administered on post-operative day 4. Two patients, one LRD and one DD, aged 6 and 11 years, respectively, developed acute non-cardiogenic pulmonary edema within 36 h of surgery. Renal dysplasia was identified as the primary etiological factor for renal failure in both cases. Both children required assisted ventilation for between 4 and 6 days. While both grafts had primary function, the DD transplant patient subsequently developed acute tubular necrosis and was eventually lost within 3 weeks due to thrombotic microangiopathy and severe acute antibody-mediated rejection despite adequate immunosuppression. Non-cardiogenic pulmonary edema is a potentially devastating post-operative complication of basiliximab induction therapy in young pediatric patients following renal transplantation. Early recognition and appropriate supportive therapy is vital for patient and, where possible, graft survival.

Negative pressure pulmonary edema complicating an electrophysiological study

We report on a case of acute non-cardiogenic negative-pressure pulmonary edema developed during an ablation procedure of an accessory pathway in a patient with no structural heart disease. That potentially serious complication has not been previously reported during an interventional cardiology procedure.

Pulmonary veno-occlusive disease presenting with recurrent pulmonary oedema and the use of nitric oxide to predict response to sildenafil

Pulmonary veno-occlusive disease (PVOD) is a disorder which causes progressive pulmonary hypertension, usually presenting with worsening dyspnoea and right heart failure. Pulmonary oedema induced by pulmonary vasodilator therapy to reduce...