Pleuroscopy in exudative pleural effusion: A North Malaysia experience

Background: Pleuroscopy is one of the investigation modalities available for further evaluation of exudative pleural effusion. Aims of this study is to determine the diagnostic yield and common cause for pleural effusion that underwent pleuroscopy in Respiratory department, Hospital Sultanah Bahiyah .Methods: This is a retrospective descriptive analysis study of 106 patient who underwent pleuroscopy in Hospital Sultanah Bahiyah between July 2014 till Dec 2016. Hospital Sultanah Bahiyah is the only centre doing this procedure in North Malaysia.Result: Biopsy were done in 91% of the cases with diagnostic yield of up to 97%. Most common finding were malignancy (55%) with adenocarcinoma being the commonest subtype. Second commonest finding are granulomatous inflammation (19%) which is not surprising given our burden of tuberculosis. Majority of our patient were male (58%) with mean age of 60 years old. With regard to safety only one case develop complication where the patient develops re-expansion pulmonary oedema with no procedure related mortality.Conclusion: Pleuroscopy is a very safe procedure. Despite the high Tuberculosis burden in Malaysia the most common cause for exudative pleural effusion were due to malignancy, hence pleuroscopy should be consider in all cases of exudative pleural effusion.

Anti-Inflammatory, Antioxidant, and Antifibrotic Effects of Gingival-Derived MSCs on Bleomycin-Induced Pulmonary Fibrosis in Mice

Background: Mesenchymal stem cell (MSC) intervention has been associated with lung protection. We attempted to determine whether mouse gingival-derived mesenchymal stem cells (GMSCs) could protect against bleomycin-induced pulmonary fibrosis. Methods: Mice were divided into three groups: control (Con), bleomycin (Bl), and bleomycin + MSCs (Bl + MSCs). Mice were treated with 5 mg/kg bleomycin via transtracheal instillation to induce pulmonary fibrosis. We assessed the following parameters: histopathological severity of injury in the lung, liver, kidney, and aortic tissues; the degree of pulmonary fibrosis; pulmonary inflammation; pulmonary oedema; profibrotic factor levels in bronchoalveolar lavage fluid (BALF) and lung tissue; oxidative stress-related indicators and apoptotic index in lung tissue; and gene expression levels of IL-1β, IL-8, TNF-α, lysophosphatidic acid (LPA), lysophosphatidic acid receptor 1 (LPA1), TGF-β, matrix metalloproteinase 9 (MMP-9), neutrophil elastase (NE), MPO, and IL-10 in lung tissue. Results: GMSC intervention attenuated bleomycin-induced pulmonary fibrosis, pulmonary inflammation, pulmonary oedema, and apoptosis. Bleomycin instillation notably increased expression levels of the IL-1β, IL-8, TNF-α, LPA, LPA1, TGF-β, MMP-9, NE, and MPO genes and attenuated expression levels of the IL-10 gene in lung tissue, and these effects were reversed by GMSC intervention. Bleomycin instillation notably upregulated MDA and MPO levels and downregulated GSH and SOD levels in lung tissue, and these effects were reversed by GMSC intervention. GMSC intervention prevented upregulation of neutrophil content in the lung, liver, and kidney tissues and the apoptotic index in lung tissue. Conclusions: GMSC intervention exhibits anti-inflammatory and antioxidant capacities. Deleterious accumulation of neutrophils, which is reduced by GMSC intervention, is a key component of bleomycin-induced pulmonary fibrosis. GMSC intervention impairs bleomycin-induced NE, MMP-9, LPA, APL1, and TGF-β release.

741 A complex clinical mosaic of severe autoimmune calcific constrictive pericarditis with striking haemodynamic response to immunosuppressive therapy

Autoimmune constrictive pericarditis constitutes a conundrum to modern cardiology with much uncertainty surrounding both pathophysiology and optimal treatment strategies. We hereby describe the case of a 35-year-old woman of Nigerian origin with severe right heart failure secondary to calcific constrictive pericarditis. Her past medical history included coagulation factor XI deficiency, leukopenia, 2nd trimester miscarriage and premature labour due to placenta previa with fibrin deposition. Further investigations revealed atrial fibrillation, severe biatrial enlargement, moderate tricuspid and mitral regurgitation, pericardial thickening, post-capillary pulmonary hypertension and right ventricular dip-and-plateau pattern, compatible with severe constrictive pericarditis. Extensive screening for infectious and autoimmune causes only revealed borderline positive ANA (1:80). Thereafter, the patient underwent complete surgical pericardiectomy with pericardial biopsies revealing fibrous thickening, diffuse calcification and lymphocyte/macrophage infiltrates, in the absence of giant multinucleated cells or granulomas. The patient was later discharged but soon experienced relapse of exertional dyspnoea presenting with right-sided haemo-pneumothorax (requiring pleural drainage), diffuse alveolar haemorrhage, large right-sided basal and infrascissural pleural effusion, and ascites. She was treated with high dose iv furosemide, oral ibuprofen and colchicine, suspension of rate control medications, achieving initial reduction in pulmonary oedema and ascites, relapsing however after attempts to switch to oral diuretic therapy. Due to the finding of persistent lymphopenia, further immunological tests were conducted, revealing raised IgG1 levels as well as altered peripheral lymphocyte populations (raised CD4+/CD8+ ratio and CD8+ central memory, reduced CD8 effector memory). This finding in conjunction with the history of factor XI deficiency, 2nd trimester miscarriage and placental fibrin deposition as well as the observation of painful cutaneous nodules at sites of venepuncture, suggestive of Koebner’s phenomenon, veered the diagnostic focus to a potential autoimmune aetiology and in particular to systemic lupus erythematosus (>10 ACR-EULAR score points with case reports describing all the above as potential disease manifestations). Furthermore, revision of thoracic CT scans, demonstrated bilateral migratory peribronchovascular nodules with ground-glass halo. CT- guided biopsies thereof were performed revealing focal alveolar damage with capillaritis and alveolar haemorrhage, further corroborating the clinical suspicion of autoimmune disease and justifying the introduction of high-dose oral corticosteroid therapy. In liaison with our tertiary rheumatology centre, the patient was later switched to mycophenolate with gradual weaning from corticosteroid. Concurrent cardiological follow-up revealed persistence of good haemodynamic status (NYHA class II, absence of pulmonary oedema and ascites) with oral diuretic therapy, regression of cutaneous symptoms and echocardiography demonstrating consistent reduction in both mitral and tricuspid regurgitation. This constitutes to our knowledge the first report of autoimmune calcific constrictive pericarditis with significant haemodynamic response to immunosuppressive therapy. Despite the relative rarity of this disease entity, early recognition and instatement of immunosuppressive treatment may prove fundamental to halt and potentially reverse the haemodynamic progression of this highly morbid condition.

455 Haemodynamic prediction of primary graft dysfunction in lung transplant recipients

Aims Primary graft dysfunction (PGD) is a form of acute lung injury, that occurs after lung transplantation (LTx), characterized by pulmonary oedema and diffuse alveolar damage. Pulmonary hypertension is a well-known risk factor for PGD and some invasive and non-invasive studies showed an association between PGD and altered left heart filling pressure. Despite the cardiopulmonary haemodynamic seems to be mainly involved in the pathogenesis of PGD, no reliable predictive parameter has been demonstrated. The aim of our study is to test whether pulmonary arterial pressure and left diastolic function may be considered in the risk PGD stratification. Methods and results we retrospectively analyzed the results of right heart catheterization (RHC) performed in occasion of the assessment for the LTx eligibility. All patients have been assessed at the Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico of Milan (Italy) from 2006 to 2018. We included all form of respiratory diseases except for cystic fibrosis. PGD was defined as PaO2/FIO2 < 300, with infiltrates at 72 h after reperfusion. We grouped patients in two groups according to the PGD development or absence (PGD+ and PGD−). Ninety patients were analyzed (mean age 55 ± 10; 53 male). Bilateral LTx was performed in 57 cases (63%). The most frequent indications for LTx were Interstitial Lung Disease (38%), Idiopathic Pulmonary Fibrosis (32%) an COPD (16%). Mean pulmonary arterial pressure (mPAP 29.4 ± 11.5 mmHg vs. 24.2 ± 9.7 mmHg, P = 0.016) and PAWP (12.9 ± 4.3 mmHg vs. 10.4 ±.,8 mmHg, P = 0.012) values were significantly higher in the PGD+ than in the PGD− group as well as PAWP values. At the multivariate analysis, both mPAP and PAWP were independent risk factors for PGD development even adjusted for BMI, age, or indication for LTx (mPAP non-adjusted OR: 1.05, 95% CI: 1.01–1.10, P = 0.027; mPAP adjusted OR: 1.06, 95% CI: 1.00–1.12, P = 0.046; PAWP non-adjusted OR: 1.13, 95% CI: 1.02–1.25, P = 0.016; PAWP adjusted OR: 1.14, 95% CI: 1.01–1.29, P = 0.036). No difference was observed between pulmonary vascular resistance (PVR) values. After a sub analysis of the patients with PAWP ≥15 mmHg, we observed that the ratio between PVR and PAWP was significantly higher in the PGD + group (0.18 ± 0.11 vs. 0.09 ± 0.05, P = 0.036). Conclusion s our data confirmed that pulmonary circulation plays a crucial role in the prediction of PGD and elevated mPAP is the one of the main risk factors. Of note, despite in both group PAWP in was within normal values (<15 mmHg), it was determinant in the risk stratification for PGD development. We suppose that the increased PVR due to pulmonary parenchymal diseases may “mask” and “underestimate” the role of the left ventricular diastolic dysfunction creating a sort of vascular barrage witch is overcome after lung transplantation hesitating in pulmonary oedema. This hypothesis is corroborated by the significative difference of PVR/PAWP ratio that can select patients at risk for PGD.

Imaging characteristics and mechanism of negative pressure pulmonary edema in children: three case reports

This article reports three children who presented with negative pressure pulmonary oedema before or after removal of the airway foreign bodies. Of them, two cases were type I negative pressure pulmonary oedema and one case was type II negative pressure pulmonary oedema following foreign body removal from the airways. Pathogenesis and location differences between type I and type II negative pressure pulmonary oedema caused by airway foreign body obstruction, as well as diagnosis and treatment modalities of the negative pressure pulmonary oedema were discussed.

Anaesthetic emergencies

This chapter discusses anaesthetic emergencies. It begins with a description of adult basic life support (BLS) and advanced life support (ALS). It goes on to describe post resuscitation care; severe bradycardia; tachycardia; severe hypo- or hypertension; severe hypoxia; laryngospasm; air/ gas embolism; gastric aspiration; severe bronchospasm; pulmonary oedema; anaphylaxis; latex allergy; intra-arterial injection; incomplete reversal of neuromuscular blockade; local anaesthetic toxicity; failed intubation; the can’t-intubate-can’t-oxygenate (CICO) scenario and malignant hyperthermia (MH).

Safety and efficacy of a prehospital initiated protocol of nitrates plus non-invasive ventilation on prehospital and Emergency Department outcomes for acute cardiogenic pulmonary oedema

Background Acute heart failure is a common presentation to Emergency Departments (ED) the world over. Amongst the most common presenting signs and symptoms is dyspnoea due to acute pulmonary oedema, a life threatening emergency that if left untreated or poorly managed. There is increasing evidence demonstrating improved outcomes following the use of vasodilators or non invasive ventilation for these patients in the emergency setting. Consequently, the potential exists that initiating these therapies in the prehospital setting will similarly improve outcomes. Methods A historical cohort study was conducted to assess the effect of a prehospital initiated treatment protocol of nitrates plus non invasive ventilation (NIV) versus regular therapy for severe cardiogenic APO on all-cause in-hospital mortality at 7 days, 30 days, and in total. Secondary outcomes included changes in EMS respiratory and haemodynamic parameters; admission status; length of stay; and emergency endotracheal intubation. Results The intervention led to an approximate 85% reduction in adjusted odds of mortality at 7 days compared to the regular therapy (AOR 0.15, 95% CI: 0.05 to 0.46, p = 0.001); approximate 80% reduction in odds of mortality at 30 days (AOR 0.19, 95% CI: 0.07 to 48, p < 0.0001); and Approximate 60% reduction in odds of total mortality (AOR 0.25, 95% CI: 0.12 to 0.56, p = 0.001). Conclusion The results of this analysis provide strong evidence of the potential synergistic benefits that can be achieved with the early implementation of a simple treatment protocol of prehospital administered nitrates and initiation of NIV for cardiogenic APO.

Haemoptysis in breath-hold divers; where does it come from?

Introduction: The aim of reporting these two cases is to present visual evidence by bronchoscopy of the origin of haemoptysis in two elite breath-hold divers. Case reports: Two male elite breath-hold divers of similar physical characteristics presented to our clinic after performing dives of up to 75 and 59 meters of seawater depth for 2:30 and 2:35 (minutes:seconds) respectively. Both patients presented with haemoptysis. Lung ultrasound was performed. The first patient had crackles on chest auscultation, overt pulmonary oedema clinically and 90 ultrasound lung comets. The second patient had no oedema or crackles, but presented with 20 ultrasound lung comets. Video bronchoscopy was performed which showed traces of blood coming from all three segments of the right upper lobe in both patients. The rest of the airways and lungs were intact. Conclusions: These finding suggest that the apical parts of the lungs are the most prone to deep-dive induced damage. The precise mechanism of lung barotrauma and haemoptysis in breath-hold divers remains to be elucidated. These findings may be of importance for a better understanding of the underlying pathology of haemoptysis.