Diffuse alveolar hemorrhage (DAH) is a rare but potentially life-threatening pulmonary condition that, while classically linked to autoimmune disorders, can occur in the setting of trauma. We report the case of a 20-year-old male who sustained polytrauma following a road traffic accident and initially had a normal chest radiograph. On the fourth day of hospitalization, he developed acute hypoxemia with new bilateral alveolar infiltrates; high-resolution computed tomography revealed diffuse ground-glass opacities with septal thickening. Bronchoalveolar lavage demonstrated progressively hemorrhagic return across aliquots, confirming DAH. Autoimmune markers were largely negative, and in the absence of systemic features, a multifactorial etiology involving trauma-related injury and anticoagulant use was considered. High-dose intravenous corticosteroids produced rapid clinical and radiological recovery. This case underscores the importance of considering DAH in trauma patients presenting with unexplained hypoxemia and bilateral infiltrates, even without hemoptysis, where early bronchoscopy and prompt treatment can be lifesaving.

Severe fever with thrombocytopenia syndrome (SFTS) is an emerging tick-borne viral infection that can rapidly progress to multiple organ failure with a high mortality rate. Pulmonary involvement has been reported, but the radiologic-pathologic correlation remains poorly understood. We report an autopsy-proven fatal case of SFTS in a 79-year-old man with pre-existing collagen vascular disease-associated interstitial lung disease. Serial chest computed tomography (CT) initially demonstrated subtle peripheral ground-glass opacities that progressively expanded over time. On the final CT examination obtained shortly before death, extensive bilateral consolidation with high attenuation on mediastinal window images was observed, suggestive of pulmonary hemorrhage. The patient developed severe thrombocytopenia, disseminated intravascular coagulation, and respiratory failure and died despite intensive treatment. Autopsy revealed diffuse pulmonary hemorrhage, alveolar septal thickening, focal diffuse alveolar damage with hyaline membrane formation, and prominent hemophagocytosis. Immunohistochemical staining demonstrated numerous SFTS virus-infected cells within the lung tissue. This case highlights the CT findings of pulmonary involvement in fatal SFTS and demonstrates a direct radiologic-pathologic correlation. Our findings suggest that cytokine storm and hemophagocytic syndrome play critical roles in the development of pulmonary hemorrhage and lung injury in SFTS.

Diffuse alveolar hemorrhage (DAH) is a life-threatening pulmonary condition characterized by widespread bleeding into the alveoli, leading to respiratory failure. It can result from various etiologies, including autoimmune disorders, drug reactions, and infections. Here is a rare case of a 37-year-old male who presented with progressive dyspnea, hemoptysis, and hypoxemia. Chest imaging and bronchoscopy confirmed the diagnosis of DAH, while laboratory tests revealed ANCA-associated vasculitis. On diagnosis, the patient with granulomatosis with polyangiitis was initiated on corticosteroids and cyclophosphamide. Early initiation of immunosuppressive therapy and supportive care plays a crucial role in disease management, reducing morbidity in such cases.

Diffuse alveolar hemorrhage (DAH) is a rare but life-threatening complication of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), with management largely extrapolated from broader AAV and ARDS literature. We conducted a review of studies published between 2000 and 2025 evaluating treatments and outcomes in AAV-associated DAH, synthesizing evidence across immunosuppressive, plasmapheresis, hemostatic, respiratory and hemodynamic, and infection prevention strategies. Glucocorticoids combined with rituximab or cyclophosphamide induce remission in most patients, although optimal steroid tapering and comparative efficacy in severe, ventilated DAH remain uncertain. Avacopan improves sustained remission and renal recovery in severe AAV and appears to be a feasible steroid-sparing adjunct in early DAH series. Large randomized trials demonstrate no survival benefit of plasma exchange. Local hemostatic therapies may provide rapid bleeding control, but evidence is limited. Respiratory outcomes are driven by hypoxemia severity and need for invasive ventilation or extracorporeal support. Lastly, infection prevention measures are strongly supported.

Pulmonary involvement (PI) in ANCA-associated vasculitis (AAV), especially interstitial lung disease (ILD) and diffuse alveolar hemorrhage (DAH), predicts poor outcomes, but a synthesis distinguishing these phenotypes is lacking. We searched seven databases up to April 1, 2026, and included observational studies. Using univariate and multivariate meta-analyses, we calculated pooled odds ratios (OR) or mean differences (MD). Nineteen studies (2,944 patients) were included. For ILD, robust independent risk factors were age > 65 years (OR = 3.60) and male gender (OR = 2.57). MPO-ANCA positivity was more frequent in the ILD group (OR = 2.29). Potential associated factors included smoking, D-dimer, ANA, low C4, and CA199. MPA subtype, cough, and dyspnea were more frequent in the ILD group. Factors associated with lower ILD frequency included GPA subtype, PR3-ANCA positivity, c-ANCA positivity, ENT involvement, gastrointestinal involvement, and a higher BVAS score. For DAH, potential associated factors included proteinuria, high BVAS score, Cr, BUN, PCT, decreased Hb, and low C3. PR3-ANCA positivity and hemoptysis were more frequent in the DAH group. For overall PI, independent risk factors were age (continuous OR = 1.04, > 65 years OR = 4.20), male gender (OR = 3.08), and high BVAS (OR = 3.03). MPO-ANCA positivity (OR = 2.55) was more frequent in the overall PI group, which largely overlapped with those for ILD, suggesting that ILD is the main driver of overall PI. This first meta-analysis combining univariate and multivariate approaches with an evidence-grading framework for ILD demonstrates distinct clinical patterns for ILD versus DAH, offering a clinically actionable tool for risk stratification and personalized management of PI in AAV.

Oropouche virus (OROV) is an emerging orthobunyavirus that causes increasingly severe and deadly disease in Brazil. However, coinfection with influenza A(H1N1)pdm09 has not been previously described in the published literature, to our knowledge. We report the first documented fatal case of OROV and influenza A(H1N1)pdm09 coinfection in a previously healthy 16-year-old female from rural Maranhão, Brazil. The patient presented with dyspnea, odynophagia, and hemoptysis and deteriorated rapidly, requiring orotracheal intubation on day three of illness due to massive endobronchial hemorrhage, followed by fatal hemodynamic collapse. Autopsy revealed bilateral serosanguineous pleural effusion, diffuse alveolar hemorrhage, pericardial petechiae, acute tubular necrosis, and cerebral edema with tonsillar herniation. Real-time reverse-transcriptase polymerase chain reaction confirmed OROV in lung, liver, spleen, and lymph node tissues, and influenza A(H1N1)pdm09 in both nasal swab and lung tissue; all other arboviruses and respiratory pathogens tested negative. The histopathological findings provide, to our knowledge, the first histopathological characterization of OROV-associated microvascular injury and suggest synergistic thromboinflammatory pathways with influenza A. This case broadens the recognized clinical spectrum of OROV and highlights the need for systematic coinfection screening and coagulation monitoring in severe arboviral presentations, even in young patients without comorbidities.

Hemorrhagic pneumonia is a severe and often fatal disease in captive forest musk deer (Moschus berezovskii), but the pathogen remains incompletely understood. Based on incomplete statistics, the estimated incidence in captive populations ranges from 20% to 80%, with the disease occurring mainly in autumn, winter, and early spring. The disease has an acute onset and rapid progression. Due to the species' strong stress response, affected animals rarely show behavioral changes, making early detection difficult. In this study, we investigated a mortality case presenting with oral bleeding and hematemesis on a forest musk deer farm. Postmortem examination revealed diffuse hemorrhagic pneumonia, and lung tissue samples were collected for histopathology, bacterial isolation, full-length 16S rRNA gene sequencing, and DNA/RNA virome sequencing. Histological examination showed extensive alveolar hemorrhage, fibrinous exudate, and macrophage infiltration. Bacterial culture and 16S rRNA gene sequencing identified Bergeyella zoohelcum as the predominant bacterium, accounting for 100% of the bacterial community in the lung tissue. Virome analysis revealed predominantly DNA bacteriophages (e.g., Cirlivirales, Cremevirales, Microviridae) and no known pathogenic RNA viruses; only seven low-abundance, unclassified RNA viral contigs of low completeness were detected. These results indicate that B. zoohelcum is the likely causative agent of hemorrhagic pneumonia in this case, with no evidence of viral involvement. This study provides the first direct association of B. zoohelcum with hemorrhagic pneumonia in forest musk deer, highlighting its pathogenic potential and the importance of monitoring this bacterium in captive populations.

Diffuse Alveolar Hemorrhage (DAH) is a life-threatening condition characterized by widespread bleeding within the alveoli, often resulting from pulmonary capillaritis, bland pulmonary hemorrhage, or diffuse alveolar damage. It presents with hemoptysis, dyspnea, hypoxemia, and anemia, and can lead to respiratory failure. This case report highlights a rare instance of DAH in a pregnant woman with untreated Graves' disease, emphasizing the importance of considering uncommon etiologies in the absence of typical triggers.

Pulmonary tumor thrombotic microangiopathy (PTTM) is a severe complication of malignancy, characterized by rapidly progressive pulmonary hypertension and a dismal prognosis. This report describes the case of a 71-year-old woman with a history of estrogen receptor (ER)-positive left breast cancer who developed PTTM. She presented with exertional dyspnea and a cough. Arterial blood gas analysis revealed hypoxemia with an elevated alveolar-arterial oxygen gradient. Chest computed tomography (CT) showed diffuse ground-glass and nodular opacities without obvious pulmonary embolism (PE). Echocardiography revealed right ventricular enlargement and moderate pulmonary hypertension. Right heart catheterization confirmed severe pulmonary hypertension with a mean pulmonary artery pressure of 46 mmHg and pulmonary vascular resistance of 844 dynes/sec/cm[5]. After transbronchial lung biopsy (TBLB) and bronchoalveolar lavage (BAL) failed to yield a diagnosis, PTTM was confirmed by detecting malignant cells via cytology of blood aspirated from the pulmonary artery during catheterization. The administration of systemic chemotherapy resulted in a marked improvement in hemodynamics, radiological findings, and symptoms, allowing her to be weaned from home oxygen therapy.