Search

Breath-hold diving, known also as freediving, is a form of underwater diving in which one holds their breath, making use of no breathing equipment. The complications associated with breath-hold diving have not been well studied in literature, in contrast to scuba diving. Hemoptysis risk is known to be correlated with deep diving. We present here the computed tomography findings of a breath-hold diver who presented with hemoptysis following a dive to 4 meters, which can be considered shallow in the sport. The patient’s chest computed tomography revealed multiple pneumatoceles within the areas of pulmonary hemorrhage. To the best of our knowledge, there have been only a few cases reported to date in which pneumatoceles were identified associated with free diving. [ABSTRACT FROM AUTHOR]

COPA syndrome is a recently described autosomal dominant inborn error of immunity characterized by high titer autoantibodies and interstitial lung disease, with many individuals also having arthritis and nephritis. Onset is usually in early childhood, with unique disease features including alveolar hemorrhage, which can be insidious, pulmonary cyst formation, and progressive pulmonary fibrosis in nonspecific interstitial pneumonia or lymphocytic interstitial pneumonia patterns. This review explores the clinical presentation, genetics, molecular mechanisms, organ manifestations, and treatment approaches for COPA syndrome, and presents a diagnostic framework of suggested indications for patient testing.

Diffuse alveolar hemorrhage (DAH) is characterized by a syndrome of alveolar bleeding, a fall in hemoglobin, and respiratory failure. It can occur because of various immunologic and non-immunologic conditions. The etiology of DAH is important, as treatment varies with the etiology. This retrospective observational study evaluates the diverse etiologies, time to diagnosis from symptom onset, management strategies, and outcome of DAH in a span of 12 months at our tertiary care center. A total of 8 patients were identified with 8 different etiologies. 6/8 (75%) patients had immunologic causes, and 2/8 (25%) had non-immunologic causes of DAH. 6/8 (75%) patients were females, the mean time to DAH diagnosis was 4.25 months from symptom onset, 6/8 (75%) patients improved, and 2/8 (25%) died due to complications. It is necessary to differentiate between the etiologies of DAH and establish an early diagnosis to plan management and improve outcomes.

Abstract Background Cryoglobulinemia with pulmonary involvement is rare, and its characteristics, radiological findings, and outcomes are still poorly understood. Methods Ten patients with pulmonary involvement of 491 cryoglobulinemia patients at Peking Union Medical College Hospital were enrolled in this retrospective study. We analyzed the characteristics, radiological features and management of pulmonary involvement patients, and compared with those of non-pulmonary involvement with cryoglobulinemia. Results The 10 patients with pulmonary involvement (2 males; median age, 53 years) included three patients with type I cryoglobulinemia and seven patients with mixed cryoglobulinemia. All of 10 patients were IgM isotype cryoglobulinemia. All type I patients were secondary to B-cell non-Hodgkin lymphoma. Four mixed patients were essential, and the remaining patients were secondary to infections (n = 2) and systemic lupus erythematosus (n = 1), respectively. Six patients had additional affected organs, including skin (60%), kidney (50%), peripheral nerves (30%), joints (20%), and heart (20%). The pulmonary symptoms included dyspnea (50%), dry cough (30%), chest tightness (30%), and hemoptysis (10%). Chest computed tomography (CT) showed diffuse ground-glass opacity (80%), nodules (40%), pleural effusions (30%), and reticulation (20%). Two patients experienced life-threatening diffuse alveolar hemorrhage. Five patients received corticosteroid-based regimens, and four received rituximab-based regimens. All patients on rituximab-based regimens achieved clinical remission. The estimated two-year overall survival (OS) was 40%. Patients with pulmonary involvement had significantly worse OS and progression-free survival than non-pulmonary involvement patients of cryoglobulinemia (P

Primary cardiac tumors are a rarity, and sarcomas emerge as the prevailing form of primary malignant cardiac tumors across age groups, encompassing both children and adults. Within this category, angiosarcoma stands out, constituting around 31% of all primary malignant cardiac tumors. Primary cardiac angiosarcoma displays a notably aggressive nature, characterized by early systemic metastasis, and is accompanied by a generally unfavorable prognosis.We describe a case concerning a previously healthy teenage girl who displayed persistent constitutional symptoms and hemoptysis for 15 days. Subsequent investigation uncovered alveolar hemorrhage, ultimately linked to a cardiac angiosarcoma. The difficulty in this instance arose from the vague nature of the initial symptoms, posing a challenge to promptly and accurately diagnose the condition.This case highlights the aggressive nature of primary cardiac angiosarcoma. The vague initial symptoms underscore the need for early detection and optimized treatment to improve the generally unfavorable prognosis associated with this condition. Increased awareness and a multidisciplinary approach are crucial in addressing the diagnostic and therapeutic challenges posed by primary cardiac angiosarcoma.

Systemic Lupus Erythematosus (SLE) is a multifaceted, multisystem autoimmune disorder with diverse clinical expressions. While prevalence reports vary widely, pulmonary involvement accounts for significant morbidity and mortality in SLE. This comprehensive review explores the spectrum of pulmonary disease in SLE, including upper airway manifestations (e.g., laryngeal affection), lower airway conditions (e.g., bronchitis, bronchiolitis, bronchiectasis), parenchymal diseases (e.g., interstitial lung disease, acute lupus pneumonitis, diffuse alveolar hemorrhage), pleural diseases (e.g., serositis, shrinking lung syndrome), and vascular diseases (e.g., pulmonary arterial hypertension, pulmonary embolism, acute reversible hypoxemia syndrome). We discuss diagnostic modalities, treatment strategies, and prognosis for each pulmonary manifestation. With diagnostics remaining a challenge and with the absence of standardized treatment guidelines, we emphasize the need for evidence-based guidelines to optimize patient care and improve outcomes in this complex disease. [ABSTRACT FROM AUTHOR]

Background: Cryoglobulinemia with pulmonary involvement is rare, and its characteristics, radiological findings, and outcomes are still poorly understood. Methods: Ten patients with pulmonary involvement of 491 cryoglobulinemia patients at Peking Union Medical College Hospital were enrolled in this retrospective study. We analyzed the characteristics, radiological features and management of pulmonary involvement patients, and compared with those of non-pulmonary involvement with cryoglobulinemia. Results: The 10 patients with pulmonary involvement (2 males; median age, 53 years) included three patients with type I cryoglobulinemia and seven patients with mixed cryoglobulinemia. All of 10 patients were IgM isotype cryoglobulinemia. All type I patients were secondary to B-cell non-Hodgkin lymphoma. Four mixed patients were essential, and the remaining patients were secondary to infections (n = 2) and systemic lupus erythematosus (n = 1), respectively. Six patients had additional affected organs, including skin (60%), kidney (50%), peripheral nerves (30%), joints (20%), and heart (20%). The pulmonary symptoms included dyspnea (50%), dry cough (30%), chest tightness (30%), and hemoptysis (10%). Chest computed tomography (CT) showed diffuse ground-glass opacity (80%), nodules (40%), pleural effusions (30%), and reticulation (20%). Two patients experienced life-threatening diffuse alveolar hemorrhage. Five patients received corticosteroid-based regimens, and four received rituximab-based regimens. All patients on rituximab-based regimens achieved clinical remission. The estimated two-year overall survival (OS) was 40%. Patients with pulmonary involvement had significantly worse OS and progression-free survival than non-pulmonary involvement patients of cryoglobulinemia (P < 0.0001). Conclusions: A diagnosis of pulmonary involvement should be highly suspected for patients with cryoglobulinemia and chest CT-indicated infiltrates without other explanations. Patients with pulmonary involvement had a poor prognosis. Rituximab-based treatment may improve the outcome. [ABSTRACT FROM AUTHOR]

We present here two cases who developed diffuse alveolar hemorrhage (DAH) after using inhaled anesthetic sevoflurane and warfarin as an anticoagulant. The first patient was a 32-year-old male who underwent general surgery for appendicitis, and who developed sudden hypoxemia and bleeding at the end of the operation. Bilateral diffuse alveolar infiltrates were identified on chest X-ray, and decreased serum hemoglobin in the postoperative period. The hypoxemia resolved on the fifth day, and alveolar infiltrates disappeared from the chest X-ray. The second case was prescribed Coumadin for the treatment of atrial fibrillation and was found to have an INR value of 12.6 upon presentation to the emergency department with a complaint of hemoptysis. The patient was administered intramuscular vitamin K, and the pulmonary infiltrates were noted to have regressed radiologically on the fifth day. Although DAH is rare with both drugs, early diagnosis and treatment can be lifesaving. [ABSTRACT FROM AUTHOR]

Abstract Background Dysregulated long noncoding RNA (lncRNA) expression with increased apoptosis has been demonstrated in systemic lupus erythematosus (SLE) patients with alveolar hemorrhage (AH). SNHG16, a lncRNA, can enhance pulmonary inflammation by sponging microRNAs, and upregulate toll-like receptor 4 (TLR4) expression via stabilizing its mRNAs. TRAF6, a TLR4 downstream signal transducer, can induce autophagy and NETosis formation. In this study, we investigated whether SNHG16 could regulate TLR4-mediated autophagy and NETosis formation in SLE-associated AH. Methods Expression of SNHG16, TLR4 and TRAF6 and cell death processes were examined in lung tissues and peripheral blood (PB) leukocytes from AH patients associated with SLE and other autoimmune diseases, and in the lungs and spleen from a pristane-induced C57BL/6 mouse AH model. SNHG16-overexpressed or -silenced alveolar and myelocytic cells were stimulated with lipopolysaccharide (LPS), a TLR4 agonist, for analyzing autophagy and NETosis, respectively. Pristane-injected mice received the intra-pulmonary delivery of lentivirus (LV)-SNHG16 for overexpression and prophylactic/therapeutic infusion of short hairpin RNA (shRNA) targeting SNHG16 to evaluate the effects on AH. Renal SNHG16 expression was also examined in lupus nephritis (LN) patients and a pristane-induced BALB/c mouse LN model. Results Up-regulated SNHG16, TLR4 and TRAF6 expression with increased autophagy and NETosis was demonstrated in the SLE-AH lungs. In such patients, up-regulated SNHG16, TLR4 and TRAF6 expression was found in PB mononuclear cells with increased autophagy and in PB neutrophils with increased NETosis. There were up-regulated TLR4 expression and increased LPS-induced autophagy and NETosis in SNHG16-overexpressed cells, while down-regulated TLR4 expression and decreased LPS-induced autophagy and NETosis in SNHG16-silenced cells. Pristane-injected lung tissues had up-regulated SNHG16, TLR4/TRAF6 levels and increased in situ autophagy and NETosis formation. Intra-pulmonary LV-SNHG16 delivery enhanced AH through up-regulating TLR4/TRAF6 expression with increased cell death processes, while intra-pulmonary prophylactic and early therapeutic sh-SNHG16 delivery suppressed AH by down-regulating TLR4/TRAF6 expression with reduced such processes. In addition, there was decreased renal SNHG16 expression in LN patients and mice. Conclusions Our results demonstrate that lncRNA SNHG16 regulates TLR4-mediated autophagy and NETosis formation in the human and mouse AH lungs, and provide a therapeutic potential of intra-pulmonary delivery of shRNA targeting SNHG16 in this SLE-related lethal manifestation.

Alveolar hemorrhage is a medical emergency that compromises the patient's life, which requires early and timely diagnosis and treatment. The clinical case of a patient who presented a hypertensive emergency associated with unknown renal disease with the need for chronic dialysis is presented. Subsequently, he developed a picture of diffuse alveolar hemorrhage, being a lung-kidney syndrome, for which reason immunological studies were requested, which revealed positivity for Anca P. Vasculitis associated with anticytoplasmic antibodies was suspected, for which treatment with corticosteroids and cyclophosphamide was started with Good respiratory clinical evolution, but not renal compromise, however, through complementary studies it was not possible to elucidate the definitive diagnosis. [ABSTRACT FROM AUTHOR]

Background: Dysregulated long noncoding RNA (lncRNA) expression with increased apoptosis has been demonstrated in systemic lupus erythematosus (SLE) patients with alveolar hemorrhage (AH). SNHG16, a lncRNA, can enhance pulmonary inflammation by sponging microRNAs, and upregulate toll-like receptor 4 (TLR4) expression via stabilizing its mRNAs. TRAF6, a TLR4 downstream signal transducer, can induce autophagy and NETosis formation. In this study, we investigated whether SNHG16 could regulate TLR4-mediated autophagy and NETosis formation in SLE-associated AH. Methods: Expression of SNHG16, TLR4 and TRAF6 and cell death processes were examined in lung tissues and peripheral blood (PB) leukocytes from AH patients associated with SLE and other autoimmune diseases, and in the lungs and spleen from a pristane-induced C57BL/6 mouse AH model. SNHG16-overexpressed or -silenced alveolar and myelocytic cells were stimulated with lipopolysaccharide (LPS), a TLR4 agonist, for analyzing autophagy and NETosis, respectively. Pristane-injected mice received the intra-pulmonary delivery of lentivirus (LV)-SNHG16 for overexpression and prophylactic/therapeutic infusion of short hairpin RNA (shRNA) targeting SNHG16 to evaluate the effects on AH. Renal SNHG16 expression was also examined in lupus nephritis (LN) patients and a pristane-induced BALB/c mouse LN model. Results: Up-regulated SNHG16, TLR4 and TRAF6 expression with increased autophagy and NETosis was demonstrated in the SLE-AH lungs. In such patients, up-regulated SNHG16, TLR4 and TRAF6 expression was found in PB mononuclear cells with increased autophagy and in PB neutrophils with increased NETosis. There were up-regulated TLR4 expression and increased LPS-induced autophagy and NETosis in SNHG16-overexpressed cells, while down-regulated TLR4 expression and decreased LPS-induced autophagy and NETosis in SNHG16-silenced cells. Pristane-injected lung tissues had up-regulated SNHG16, TLR4/TRAF6 levels and increased in situ autophagy and NETosis formation. Intra-pulmonary LV-SNHG16 delivery enhanced AH through up-regulating TLR4/TRAF6 expression with increased cell death processes, while intra-pulmonary prophylactic and early therapeutic sh-SNHG16 delivery suppressed AH by down-regulating TLR4/TRAF6 expression with reduced such processes. In addition, there was decreased renal SNHG16 expression in LN patients and mice. Conclusions: Our results demonstrate that lncRNA SNHG16 regulates TLR4-mediated autophagy and NETosis formation in the human and mouse AH lungs, and provide a therapeutic potential of intra-pulmonary delivery of shRNA targeting SNHG16 in this SLE-related lethal manifestation. [ABSTRACT FROM AUTHOR]

Introduction: Systemic lupus erythematosus (SLE) is non-organ specific autoimmune disease with mainly skin, joint, and kidney involvement. SLE-related acute lung disease (ALD) is rare, poorly investigated and can lead to acute respiratory failure. We conducted a retrospective study aiming to describe clinical features, treatments and outcome of SLE-related APD. Methods: We retrospectively included all patients with SLE and ALD admitted from November 1996 and September 2018 to La Pitié-Salpêtrière Hospital, after exclusion of viral or bacterial lung infection, cardiac failure or any other alternate diagnosis. Results: During the time of the study, 14 patients with 16 episodes were admitted to our center: female 79%, mean age ± SD at admission 24 ± 11 years. ALD was inaugural of the SLE in 70% cases. SLE main organ involvement were: arthritis 93%, skin 79%, serositis 79%, hematological 79%, kidney 64%, neuropsychiatric 36% and cardiac 21%. 11 episodes required ICU admission for a median time of 8 days. Chest CT-scan revealed mostly basal consolidation and ground-glass opacities. When available, bronchoalveolar lavage mostly revealed a neutrophilic alveolitis with alveolar hemorrhage in 67% cases. Symptomatic respiratory treatments were: oxygen 81%, high-flow nasal canula oxygen 27%, non-invasive ventilation 36%, mechanical ventilation 64% and venovenous extracorporeal membrane oxygenation 18%. SLE-specific treatments were: corticosteroids 100%, cyclophosphamide 56% and plasma exchange 25%. All patients but one survived to ICU and hospital discharge. Two patients had a relapse of SLE-related ALD but none had interstitial lung disease during follow-up. Conclusion: Systemic lupus erythematosus-related acute respiratory failure is a severe event, mostly occurring at SLE onset, typical harboring a basal consolidation pattern on chest CT-scan and alveolar hemorrhage on BAL pathological examination. Mortality in our cohort is lower than previously reported but these results needs to be confirmed in further larger studies. [ABSTRACT FROM AUTHOR]

The study was conducted in the Department of Forensic Medicine, Government Medical College, Thiruvananthapuram. The period of the study was from January 2013 to June 2014. 50 cases were included among which 25 cases were the hanging cases that survived for varying periods before death and 25 cases were from the non-survived victims of hanging. Macroscopic and microscopic changes in the lungs, were compared to find out the changes resulting from hypoxic insult. The cases were studied in detail and are described below. [ABSTRACT FROM AUTHOR]

Objective : Diffuse alveolar hemorrhage (DAH) is a severe pulmonary complication of numerous diseases, including rheumatic conditions. We have conducted an observational study using inpatient data from the National Inpatient Sample to study the relationship of DAH with rheumatic conditions along with their descriptive characteristics. Methods: An observational study was conducted on hospitalizations in 2016–2018 with a principal diagnosis of DAH from the United States National Inpatient Sample database. A multivariate logistic regression analysis was performed to calculate adjusted odds ratios (ORadj) for risk factors of DAH. Results: A total of 5420 DAH hospitalizations were identified among 90 million hospitalizations. Mortality in this group was found to be 24.3%. Majority of patients admitted with DAH were white and male, with a mean age of 61.8 years and a mean LOS of 10.6 days. Multivariate analysis showed that multiple rheumatic diseases were associated with DAH, including anti-neutrophil cytoplasmic antibody–associated vasculitis (AAV) (ORadj 72.56) (95% C.I. 50.607–104.043), antiphospholipid antibody syndrome (APLS) (ORadj 6.51) (95% C.I. 3.734–11.366), eosinophilic granulomatosis with polyangiitis (EGPA) (ORadj 7.13) (95% C.I. 1.886–26.926), Goodpasture's (ORadj 30.58) (95% C.I. 16.360–57.176), rheumatoid arthritis (RA) (ORadj 1.60) (95% C.I. 1.158–2.212), sarcoidosis (ORadj 3.99) (95% C.I. 2.300–6.926), and systemic lupus (SLE) (ORadj 5.82) (95% C.I. 3.993–8.481). Conclusion: Although DAH is a relatively rare entity, it carries a very high mortality. Multiple rheumatic diseases were associated with DAH hospitalizations including AAV, APLS, EGPA, Goodpasture's, RA, sarcoidosis, and SLE. Key points • It is known that DAH carries a high morbidity and mortality based on prior literature. However, large datasets on the association of rheumatic diseases with DAH are lacking • This study identifies the descriptive characteristics of patients admitted to the hospital with DAH • This study also identifies the strength of association of rheumatic diseases with DAH [ABSTRACT FROM AUTHOR]

Glycoprotein IIb/IIIa inhibitors play a key role in the treatment of patients who have acute coronary syndromes and undergone percutaneous coronary intervention. However, its serious complication is diffused alveolar hemorrhage. A 73-year-old diabetic woman presented with chest pain and dynamic ST elevation in ECG and positive troponin. She had occlusion in two coronary arteries and underwent percutaneous coronary intervention. The eptifibatide was administered. After hours, she showed respiratory symptoms, as well as drop of blood pressure and hemoglobin. All differential diagnoses suggested for her clinical presentation were evaluated, and finally, on the sixth day diffuse alveolar hemorrhage was diagnosed. Although respiratory symptoms such as hemoptysis and dyspnea may occur as complications of pulmonary edema and/or pneumonia, assumed clinical suspicion for pulmonary hemorrhage leading to early detection of it. Moreover, there is no definitive guideline for decreased bleeding complications and treatment of alveolar hemorrhage caused by glycoprotein IIb/IIIa receptor inhibitors.

Cardiac etiologies of hemoptysis are less common. One such etiology includes mitral regurgitation. In patients with hemoptysis and unilateral consolidation, careful chest auscultation and cardiac assessment may assist in making an early diagnosis. [ABSTRACT FROM AUTHOR]

Copyright of Salud, Ciencia y Tecnología is the property of Fundacion Salud, Ciencia y Tecnologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Leptospirosis is a common zoonotic disease with a wide range of clinical manifestations, specifically in tropical regions. Weil's disease is considered a severe form of leptospirosis seen in a minority of leptospirosis cases with considerable mortality. These patients typically developed the triad of acute renal injury, jaundice, and hemorrhages. Herein, we reported a case of a 28-year-old male transferred to our intensive care unit due to severe leptospirosis with diffuse alveolar hemorrhage, cholestatic jaundice, acute respiratory distress, and renal injury. The patient was successfully managed with appropriate antimicrobial treatment and other supportive management, including mechanical ventilation, vasopressor, and corticosteroid therapy. Ten days after admission, the patient unexpectedly developed uncontrollable massive upper gastrointestinal bleeding, requiring immediate surgical interventions. Splenectomy, partial gastrectomy, along with gastro-esophageal anastomosis were performed. Following a prolonged hospitalization, the patient fully recovered and was discharged home with excellent clinical outcomes. This fulminant leptospirosis case described here should assist in informing medical professionals of the clinical significance of this serious, occasionally fatal illness. Moreover, leptospirosis should be considered in any location wherever risk factors are present, not just in epidemic and tropical areas. In this case, we pointed out that serious complications of leptospirosis, such as hemorrhage, may happen despite their rarity. In such cases, adopting an integrated multidisciplinary team approach is essential to prevent complications and reduce mortality.

Abstract Cardiac etiologies of hemoptysis are less common. One such etiology includes mitral regurgitation. In patients with hemoptysis and unilateral consolidation, careful chest auscultation and cardiac assessment may assist in making an early diagnosis.

Diffuse alveolar hemorrhage secondary to sevoflurane inhalation is a rare condition. It should be considered in postoperative patients presenting symptoms of hemoptysis, hypoxemia, or radiographic alveolar infiltrates. We present the case of a 42-year-old man who experienced a diffuse alveolar hemorrhage following sedation with sevoflurane during a low-risk orthopedic procedure. Initially, the patient presented hemoptysis, hypoxemia, and dyspnea. X-ray findings suggested alveolar hemorrhage and the diagnosis was confirmed with fiberoptic bronchoscopy. The patient improved under the care of the pulmonary service and was discharged. Early identification and management of this respiratory complication were crucial for a successful recovery.

Human COPA mutations affecting retrograde Golgi-to-endoplasmic reticulum (ER) protein transport cause diffuse alveolar hemorrhage (DAH) and ER stress ("COPA syndrome"). Patients with SLE also can develop DAH. C57BL/6 (B6) mice with pristaneinduced lupus develop monocyte-dependent DAH indistinguishable from human DAH, whereas BALB/c mice are resistant. We examined Copa and ER stress in pristane-induced lupus. Copa expression, ER stress, vascular injury, and apoptosis were assessed in mice and COPA was quantified in blood from patients with SLE. Copa mRNA and protein expression were impaired in B6 mice with pristane-induced DAH, but not in pristane-treated BALB/c mice. An ER stress response (increased Hsp5a/BiP, Ddit3/CHOP, Eif2a, and spliced Xbp1) was seen in lungs from pristane-treated B6, but not BALB/c, mice. Resistance of BALB/c mice to DAH was overcome by treating them with low-dose thapsigargin plus pristane. CB6F1 mice did not develop DAH or ER stress, suggesting that susceptibility was recessive. Increased pulmonary expression of von Willebrand factor (Vwf), a marker of endothelial injury, and the chemokine Ccl2 in DAH suggested that pristane promotes lung microvascular injury and monocyte recruitment. Consistent with that possibility, lung endothelial cells and infiltrating bone marrow-derived cells from pristane-treated B6 mice expressed BiP and showed evidence of apoptosis (annexin-V and activated caspase-3 staining). COPA expression also was low in patients with SLE with lung involvement. Pristane-induced DAH may be initiated by endothelial injury, resulting in ER stress, apoptosis of lung endothelial cells, and recruitment of myeloid cells that propagate lung injury. The pathogenesis of DAH in SLE and COPA syndrome may overlap. [ABSTRACT FROM AUTHOR]

Glycoprotein IIb/IIIa inhibitors play a key role in the treatment of patients who have acute coronary syndromes and undergone percutaneous coronary intervention. However, its serious complication is diffused alveolar hemorrhage. A 73-year-old diabetic woman presented with chest pain and dynamic ST elevation in ECG and positive troponin. She had occlusion in two coronary arteries and underwent percutaneous coronary intervention. The eptifibatide was administered. After hours, she showed respiratory symptoms, as well as drop of blood pressure and hemoglobin. All differential diagnoses suggested for her clinical presentation were evaluated, and finally, on the sixth day diffuse alveolar hemorrhage was diagnosed. Although respiratory symptoms such as hemoptysis and dyspnea may occur as complications of pulmonary edema and/or pneumonia, assumed clinical suspicion for pulmonary hemorrhage leading to early detection of it. Moreover, there is no definitive guideline for decreased bleeding complications and treatment of alveolar hemorrhage caused by glycoprotein IIb/IIIa receptor inhibitors. [ABSTRACT FROM AUTHOR]

Imtinene Ben Mrad,1 Melek Ben Mrad,2 Zeineb Oumaya,1 Ihsen Zairi,1 Boutheina Besbes,1 Khalil Ouaghlani,1 Sofien kamoun,1 Sobhi Mleyhi,2 Rim Miri,2 khadija Mzoughi,1 Sondos Kraiem1 1Cardiology Department, Habib Thameur Hospital, Tunis, Tunisia; 2Cardiovascular Surgery Department, Rabta Hospital, Tunis, TunisiaCorrespondence: Imtinene Ben MradCardiology Department, Habib Thameur Hospital, App 2b, Bloc 12, cite Olympique, Tunis, 1003, TunisiaTel +011 216 20156852Email imtinenebenmrad12@gmail.comAbstract: Alveolar hemorrhage (AH) is a heterogeneous clinical syndrome with a high mortality rate, characterized by extensive bleeding into the alveolar spaces. AH secondary to systemic thrombolysis treatment in the setting of acute myocardial infarction is an uncommon complication, but potentially fatal and can lead to acute respiratory failure. This entity is rarely reported in the literature. We report two cases of acute AH after intravenous thrombolysis for acute myocardial infarction, which could contribute to the literature on the subject, and discuss the risk factors as well as the clinical and radiological findings supporting the diagnosis. We overview also the rare previous published case reports in this context, and we contrast our findings with those reported in the literature.Keywords: hemoptysis, alveolar hemorrhage, myocardial infarction, fibrinolytic therapy, streptokinase

Objective: To evaluate histomorphological effects of Soybean oil supplementation on lung tissue injury and alveolar hemorrhage induced by Bisphenol A (BPA). Study Design: Laboratory-based experimental study. Place and Duration of Study: Anatomy department, Army Medical College, Rawalpindi and National Institute of Health, Islamabad, from Nov 2015 to Nov 2016. Methodology: Forty (40) healthy BALB/c mice of 9-11 weeks of age, weighing between 30-37gm were housed in a controlled environment at National Institute of Health. Group 1 (10) was control group. Group 2 (10) was given a daily dose of 50 milligram/kilogram body weight of Bisphenol A and group 3 (10) was given a daily dose of 500 milligram of Soybean oil and group 4 (10) was concurrently given Bisphenol A and Soybean oil with daily doses of 50 milligram/kilogram body weight and 500 milligrams. After a period of 8 weeks, animals were dissected 24 hours after receiving the last dosage. Lung wet weight, animal weight and relative body tissue weight index (RTBWI) were calculated. Tissue processing & staining was done. Alveolar hemorrhage was histomorphologically and statistically analysed using SPSS-21. Results: On microscopic examination, alveolar hemorrhage (AH) was observed in 10 (100%) group 2 specimens with increase in RTBWI and whereas only 5 (50%) of group 4 specimens had alveolar hemorrhage with slight improvement in relative body tissue weight index (RTBWI). Conclusion: Bisphenol A (BPA) induced lung injury as evident by intraalveolar hemorrhage, blood vessel congestion and increased RTBWI ratio were ameliorated by concomitant administration of Soybean oil.

We present here a case of diffuse alveolar hemorrhage (DAH) following exposure to inhaled anesthetic sevoflurane. A 29-year-old male was admitted to the plastic surgery department with gynecomastia. Surgery was performed without complication under general anesthesia with intravenously administered midazolam (4mg), fentanyl and inhaled sevoflurane. Immediate hypoxemia and massive hemorrhage was detected at the end of the operation, and a chest radiography revealed bilateral widespread alveolar infiltrates. The serum hemoglobin level dropped by 2.5 g/dl (from 13 to 10.5 gr) in the postoperative setting. The patient was treated with methylprednisolone (1 gr) administered intravenously daily for 3 days. The hypoxemia resolved and alveolar infiltrates on the chest radiograph disappeared on the 4th day. There is limited data in literature reporting on the association between sevoflurane and DAH. None of the predisposing factors or causative reasons for DAH were detected in our case, and so it can be concluded that the use of sevoflurane as an inhaled anesthetic was responsible for the DAH. [ABSTRACT FROM AUTHOR]

Since the coronavirus disease 2019 (COVID-19) pandemic continues and a new variant of the virus has emerged, the COVID-19 vaccination campaign has progressed. Rare but severe adverse outcomes of COVID-19 vaccination such as anaphylaxis and myocarditis have begun to be noticed. Of note, several cases of new-onset antineutrophil cytoplasmic antibody-associated vasculitis (AAV) after COVID-19 mRNA vaccination have been reported. However, relapse of AAV in remission has not been recognized enough as an adverse outcome of COVID-19 vaccination. We report, to our knowledge, a first case of renal-limited AAV in remission using every 6-month rituximab administration that relapsed with pulmonary hemorrhage, but not glomerulonephritis, following the first dose of the Pfizer-BioNTech COVID-19 vaccine. The patient received the COVID-19 vaccine more than 6 months after the last dose of rituximab according to the recommendations. However, his CD19+ B cell counts were found to be increased after admission, indicating that our case might have been prone to relapse after COVID-19 vaccination. Although our case cannot establish causality between AAV relapse and COVID-19 mRNA vaccination, a high level of clinical vigilance for relapse of AAV especially in patients undergoing rituximab maintenance therapy following COVID-19 vaccination should be maintained. Furthermore, elapsed time between rituximab administration and COVID-19 mRNA vaccination should be carefully adjusted based on AAV disease-activity.

Systemic lupus erythematosus (SLE) is an autoimmune disease that affects multiple organs. SLE can affect the lung, the pulmonary vasculature, and the pleura. A 38-year-old female with limb pain and ecchymosis who later developed pulmonary thromboembolism and alveolar hemorrhage is presented here. Clinical, imaging, laboratory, and histopathological evidence is presented. The patient met the European League Against Rheumatism (EULAR) and the American College of Rheumatology (ACR) criteria for SLE. Furthermore, the patient had a Systemic Lupus Erythematosus Disease Activity Index 2000 (SLEDAI-2K) score of 35; thus, indicating severe disease. This case is an example of concomitant venous and arterial lung complications in an SLE patient. [ABSTRACT FROM AUTHOR]

Introduction. Alveolar hemorrhage syndrome is a severe condition, with a high-risk of death. A timely diagnosis and therapy may be life-saving. The “gold-standard” method for diagnosing alveolar hemorrhage is bronchoscopy with bronchiolo-alveolar lavage. Pulmonary function tests are useful to appreciate the severity of alveolar hemorrhage. The objective of the study was to measure the impact of alveolar hemorrhage on lung function tests and to detect useful associations between Golde score value and the type of alveolitis with spirometry tests, lung diffusing capacity for carbon monoxide (DLCO) and carbon monoxide transfer coefficient (KCOc), and six minutes walking test (6MWT). Material and methods. We conducted a retrospective study on a sample of 60 patients diagnosed with alveolar hemorrhage syndrome, hospitalized in The National Institute of Pneumology “Marius Nasta” Bucharest, Romania, between June 2010 and February 2019. Results. The results of bronchiolo-alveolar lavage show that macrophage alveolitis is associated with moderate-severe alveolar hemorrhage syndrome, while neutrophilic and lymphocytic alveolitis are associated with mild to moderate alveolar hemorrhage syndrome. Pulmonary function tests (spirometry and complex respiratory tests) showed that only Tiffeneau index, maximal expiratory flow at 50% of vital flow capacity and DLCOc were influenced by the presence of moderate to severe alveolar hemorrhage. The degree of desaturation measured at the end of 6MWT did not correlate with the degree of alveolar hemorrhage severity. Conclusions. An abnormal gas transfer is common in alveolar hemorrhage, an increase of DLCOc value being a sensitive marker for the disease.

A 32-year-old man who had worked as a welder for 13 years was hospitalized for a fever and hemosputum with dyspnea. He was diagnosed with welding fume-associated lung disease with alveolar hemorrhaging and acute respiratory failure. Despite surviving the acute phase with corticosteroid therapy, hypoxemia persisted after a month and a half, requiring home oxygen therapy. As a result of the introduction of nintedanib, his clinical findings gradually improved, and the patient was weaned from oxygen therapy after six months. Inhalation of a large amount of welding fumes in a short period can cause alveolar hemorrhaging and prolonged pulmonary dysfunction.

Background and objectives: Bronchoalveolar lavage (BAL) is commonly performed to evaluate diffuse lung disease and occasionally to identify alveolar hemorrhage. However, the clinical impact of alveolar hemorrhage and its risk factors in patients with diffuse lung disease have not been clarified. Materials and Methods: We retrospectively analyzed the medical records of all patients who underwent BAL to evaluate diffuse lung disease from January 2017 to December 2020. Alveolar hemorrhage was defined as progressive hemorrhagic BAL fluid or the presence of ≥20% hemosiderin-laden macrophages in the BAL fluid. Logistic regression analysis was performed to assess the association between alveolar hemorrhage and other factors. Results: Sixty subjects were enrolled in this study. Alveolar hemorrhage was observed in 19 subjects (31.7%) with idiopathic interstitial pneumonia, acute respiratory distress syndrome, interstitial pneumonia with autoimmune features, drug-induced lung injury, eosinophilic pneumonia, adenocarcinoma, and systemic lupus erythematosus. The use of anticoagulants was a significant risk factor for alveolar hemorrhage (odds ratio 7.57, p = 0.049). Patients with alveolar hemorrhage required intubated mechanical ventilation more frequently (63.2% vs. 24.4%, p = 0.005) and had higher in-hospital mortality rates (26.3% vs. 4.9%, p = 0.028) than those without alveolar hemorrhage. Conclusions: Alveolar hemorrhage was observed in various etiologies. The use of anticoagulants was a significant risk factor for alveolar hemorrhage. Patients with alveolar hemorrhage showed more severe respiratory failure and had higher in-hospital mortality than those without alveolar hemorrhage. [ABSTRACT FROM AUTHOR]

Objective: To evaluate histomorphological effects of Soybean oil supplementation on lung tissue injury and alveolar hemorrhage induced by Bisphenol A (BPA). Study Design: Laboratory-based experimental study. Place and Duration of Study: Anatomy department, Army Medical College, Rawalpindi and National Institute of Health, Islamabad, from Nov 2015 to Nov 2016. Methodology: Forty (40) healthy BALB/c mice of 9-11 weeks of age, weighing between 30-37gm were housed in a controlled environment at National Institute of Health. Group 1 (10) was control group. Group 2 (10) was given a daily dose of 50 milligram/kilogram body weight of Bisphenol A and group 3 (10) was given a daily dose of 500 milligram of Soybean oil and group 4 (10) was concurrently given Bisphenol A and Soybean oil with daily doses of 50 milligram/kilogram body weight and 500 milligrams. After a period of 8 weeks, animals were dissected 24 hours after receiving the last dosage. Lung wet weight, animal weight and relative body tissue weight index (RTBWI) were calculated. Tissue processing & staining was done. Alveolar hemorrhage was histomorphologically and statistically analysed using SPSS-21. Results: On microscopic examination, alveolar hemorrhage (AH) was observed in 10 (100%) group 2 specimens with increase in RTBWI and whereas only 5 (50%) of group 4 specimens had alveolar hemorrhage with slight improvement in relative body tissue weight index (RTBWI). Conclusion: Bisphenol A (BPA) induced lung injury as evident by intraalveolar hemorrhage, blood vessel congestion and increased RTBWI ratio were ameliorated by concomitant administration of Soybean oil. [ABSTRACT FROM AUTHOR]

Valproic acid (VPA) is an antiepileptic drug that is widely used in various seizure disorders both in adults and in children. Hematological and coagulation abnormality is a well-known adverse effect associated with VPA. However, VPA-induced diffuse alveolar hemorrhage is a rare entity. We are reporting one such case of VPA-associated diffuse alveolar hemorrhage.

Main Teaching Point: Diagnosing acute ascending aortic dissection in patients with equivocal radiologic data may rely on associated findings such as pulmonary artery intramural hematoma. The immediate diagnosis of aortic dissection is paramount in its management. Its diagnosis may be challenging on computed tomography when the intimal flap, pathognomonic of dissection, is not readily visualized. Pulmonary artery intramural hematoma may arise from rupture of the posterior wall of the ascending aorta into the common aortopulmonary adventitia as a result of acute dissection. The clinical significance of pulmonary artery hematoma is unknown, but its presence may facilitate the diagnosis of acute dissection when other radiologic findings are equivocal. Herein, we present four cases of pulmonary artery intramural hematoma associated with Stanford type A acute aortic dissection, among whom patient outcomes depended mainly on the prompt treatment the dissection.

Major targets of microscopic polyangiitis(MPA) are small blood vessels in the lungs and kidneys. The presence of lung lesions and old age are known to be poor prognostic factors. A 71-year-old woman was admitted to hospital for general malaise and edema. She had acute renal failure and was started on dialysis. MPO-ANCA was positive. One week later, acute respiratory failure with alveolar hemorrhage occurred, requiring intubation and mechanical ventilation. She was treated with immunosuppressive therapy and plasma exchange. On the 8th day after intubation, alveolar hemorrhage resolved and she was taken off mechanical ventilation. Five days later, respiratory failure recurred and she died. The cause of death according to autopsy was respiratory failure due to alveolar hemorrhage, interstitial pneumonia, pulmonary capillary inflammation, and organizing pneumonia arising from diffuse alveolar damage. Despite the patient's age, we performed intensive treatment, but postmortem results indicated that immunosuppression was insufficient. On the other hand, evidence to support more intense immunosuppressive therapy is lacking, and such therapy may increase the risk of infection. New clinical standards are needed to optimize immunosuppressive efficacy while minimizing risk. [ABSTRACT FROM AUTHOR]

We described a case of alveolar hemorrhage (AH) after marijuana smoking using a water pipe made with plastic bottle (bong) before making a narrative review of the literature. A 19-year-old male was admitted for hemoptysis and dyspnea evolving since the previous day. He smoked marijuana ten times a day using bongs. Computed tomography scan of the chest (chest CT-scan) evidenced ground glass opacities involving upper lobes with crazy-paving pattern. Bronchoalveolar lavage (BAL) yielded fluid becoming progressively bloody suggestive of AH. Screening of drug metabolites ruled out the presence of cocaine degradation products. Treatment with prednisone was prescribed and oxygen requirements decreased rapidly. The patient accepted to stop bongs, but kept on smoking marijuana using joints. He was asymptomatic 2 months later; all ground glass opacities had vanished. Four cases described exactly the same circumstances as ours. All were young male patients containing ground glass opacities with diffuse or bilateral pattern in their chest CT-scan. The explanation suggested by the authors of these cases was the potential concomitant inhalation of acid anhydrides derived from use of heated plastic bottle. No acid anhydrides were experimentally evidenced after thermodesorption of heated polyethylene terephthalate (PET) (in which a majority of plastic bottles are made) we performed, but other compounds were. E-cigarette, or vaping, product use-associated lung injuries cases share some chest CT-scan patterns with those of AH following bong use and we tried to draw a parallel between these two latter before discussing a physiopathological hypothesis. [ABSTRACT FROM AUTHOR]