Severe pulmonary leptospirosis (SPFL), characterized by diffuse alveolar haemorrhage (DAH) and acute respiratory distress syndrome (ARDS), carries a high mortality, often due to diagnostic delays and complex management. We report a case of a 42-year-old male with outdoor occupational exposure who presented with fever and hemoptysis, rapidly progressing to severe respiratory failure and thrombocytopenia. Chest imaging confirmed DAH/ARDS. For refractory hypoxemia, veno-venous extracorporeal membrane oxygenation (VV-ECMO) was initiated without systemic anticoagulation due to active pulmonary haemorrhage. Metagenomic next-generation sequencing (mNGS) of bronchoalveolar lavage fluid rapidly identified Leptospira interrogans, enabling targeted antimicrobial therapy alongside multidisciplinary support. The patient gradually improved, was successfully weaned from ECMO and ventilator support, and was discharged without residual organ dysfunction. This case demonstrates that early application of anticoagulation-free VV-ECMO combined with mNGS-based rapid diagnosis and multidisciplinary care can improve outcomes in SPFL, highlighting the importance of considering this diagnosis in febrile patients with DAH and environmental exposure.

Invasive pulmonary aspergillosis (IPA) is a fulminant fungal infection that predominantly occurs in immunocompromised patients; however, it may occasionally be encountered in immunocompetent individuals, often leading to diagnostic delay and unfavorable outcomes. We describe a case of invasive pulmonary aspergillosis (IPA) in an immunocompetent woman in her mid-20s who presented with productive cough, hemoptysis, low-grade fever, and pleuritic chest pain, closely resembling pulmonary tuberculosis at initial evaluation. While the chest x-ray was normal, high-resolution computed tomography of the chest demonstrated a characteristic halo sign in the right middle lobe. Further evaluation with bronchoscopy and bronchoalveolar lavage revealed a markedly elevated galactomannan index, and fungal culture grew Aspergillus flavus. Hence the patient was initiated on oral voriconazole in accordance with Infectious Diseases Society of America guidelines, resulting in complete clinico-radiological resolution. In immunocompetent patients with persistent respiratory symptoms and suggestive imaging results, this report emphasizes the significance of maintaining a high index of suspicion for IPA. It also emphasizes the importance of early intervention in the form of bronchoscopic evaluation and prompt antifungal therapy in achieving favorable outcomes.

We present a 19-year-old female, eight weeks postpartum, with a seven-week history of migratory arthralgias followed by progressive dyspnea and pleuritic chest pain. A large mass in her right lower lobe was discovered on computed tomography. Laboratory evaluation demonstrated elevated anti-proteinase 3 (PR3) antibody, along with elevated inflammatory markers. The bronchoalveolar lavage culture grew Cryptococcus neoformans, and serum cryptococcal antigen was positive. The patient was diagnosed with pulmonary cryptococcosis and treated with amphotericin and flucytosine, given the severity of her illness. Granulomatosis with polyangiitis was a part of the initial differential but was not diagnosed until she later developed transient hemoptysis, recurrent epistaxis, skin rash, and significant proteinuria. The skin biopsy was consistent with cutaneous vasculitis, and the kidney biopsy was positive for glomerulonephritis, confirming postpartum systemic vasculitis masked by a concurrent pulmonary cryptococcal infection.

Hiccups are commonly benign, self-limiting events often triggered by transient gastrointestinal or central nervous system irritants. However, when persistent, they may indicate underlying pathology involving the thoracic, gastrointestinal, or neurological systems. We report the case of a 65-year-old male smoker who presented with a 4-day history of persistent hiccups. He denied fever, chest pain, hemoptysis, or other systemic symptoms. Physical examination was largely unremarkable except for decreased air entry in the right middle and lower lung zones. Initial investigations, including gastroscopy and tumor markers, ruled out gastrointestinal causes. CT scan of the chest revealed a right lower lobe consolidation and cavitation with air fluid level and adjacent ground-glass opacities, along with enlarged subcarinal lymph nodes. Differential diagnoses included lung abscess, pneumonia, and tuberculosis cavitation. The patient was admitted for suspected lung abscess and received antibiotics. Bronchoscopy with bronchoalveolar lavage revealed no endobronchial lesions, and PCR testing and culture of the fluid was negative for tuberculosis but positive for klebsiella pneumonia. Despite radiologic regression of pneumonia, the cavitary lesion and lymphadenopathy persisted initially, but later started to regress. This case highlights an unusual presentation of lung abscess manifesting solely as persistent hiccups, without classic respiratory or systemic signs. We aim to emphasize the need to consider thoracic causes in patients with otherwise unexplained persistent hiccups, and undergo further evaluation in such cases.

Broncholithiasis refers to the presence of calcified or ossified material within the tracheobronchial tree. This rare condition is more frequently reported in regions endemic for tuberculosis and histoplasmosis, where necrotizing granulomatous lymphadenitis may lead to dystrophic calcification and eventual erosion of calcified lymph nodes into the bronchial lumen. Clinical presentation is heterogeneous and ranges from incidental findings to hemoptysis, chronic cough, recurrent infection, and post-obstructive complications. We conducted a retrospective review of five patients diagnosed with broncholithiasis at our tertiary care center. Clinical records were reviewed for demographic characteristics, presenting symptoms, imaging findings, bronchoscopic interventions, microbiologic data when available, and short-term follow-up outcomes. Two patients presented primarily with hemoptysis, one with chronic cough and severe infectious complications, one with recurrent pneumonia and lobar collapse, and one was incidentally referred with an obstructing broncholith. All five cases were managed bronchoscopically using combinations of rigid or flexible bronchoscopy, forceps, balloon dilation, cryotherapy, topical hemostatic measures, and argon plasma coagulation when needed. Two patients also required video-assisted thoracoscopic surgery for empyema management rather than for broncholith extraction itself. Where available, microbiologic findings included Actinomyces and mixed molds, highlighting the risk of post-obstructive infection. These cases underscore the heterogeneous clinical spectrum of broncholithiasis and support bronchoscopy as the primary diagnostic and therapeutic modality in appropriately selected patients. Early recognition, multidisciplinary management, and attention to associated infectious complications may improve outcomes.

Introduction: Tuberculous aneurysm of the thoracic aorta (TBAA) is an extremely rare but potentially fatal manifestation of tuberculosis (TB). Clinical presentation may include hemoptysis in the absence of parenchymal lung abnormalities. Case report: We presented a 62-year-old male with cough, chest pain, and minimal hemoptysis. Diagnostic evaluation confirmed an aneurysm of the descending thoracic aorta at a site previously treated with endovascular repair, with no imaging findings suggestive of pulmonary TB. Bronchoscopy revealed blood in the main bronchi without an identifiable endobronchial source. The diagnosis of TB was established by polymerase chain reaction (PCR) testing of bronchial aspirate obtained during bronchoscopy. Emergency surgical intervention was recommended because of an impending aortic rupture, but the patient declined surgery. Standard antituberculous therapy was initiated, and the patient subsequently developed drug-induced liver injury, prompting temporary cessation of treatment. The clinical course was later complicated by the development of an aortoesophageal fistula (AEF), with significant implications for prognosis. Conclusions: Early recognition of TBAA, along with a multidisciplinary approach that integrates advanced diagnostic modalities, timely vascular intervention, and carefully managed antituberculous therapy, is essential to reduce mortality and optimize treatment outcomes.

Background: Influenza is a common cause of hospitalization in young children, particularly infants. While most infections are self-limited, severe and life-threatening complications may occur. Diffuse alveolar hemorrhage (DAH) is a rare pulmonary manifestation of influenza, predominantly reported in adults, and is exceedingly uncommon in immunocompetent infants. Case Presentation: We report the case of an 8-month-old previously healthy female infant who presented with influenza A infection and rapidly progressed to acute respiratory failure and shock despite antiviral therapy. Bleeding was noted from the nasal cavity prior to clinical deterioration, and during emergent endotracheal intubation, blood was observed flooding the bronchial tree, consistent with massive pulmonary hemorrhage. Flexible bronchoscopy showed diffusely erythematous and friable airway mucosa without an identifiable focal bleeding source, and early bronchoalveolar lavage was nondiagnostic. Nasopharyngeal testing confirmed influenza A (H3). Laboratory findings revealed severe systemic inflammation, leukopenia with neutropenia, and anemia with normal coagulation parameters. Chest imaging demonstrated bilateral pulmonary infiltrates. After exclusion of autoimmune, coagulation, immunodeficiency, and alternative infectious causes, a diagnosis of diffuse alveolar hemorrhage secondary to influenza A infection was established. The patient was successfully managed with supportive care, antiviral therapy, tranexamic acid, and empiric antibiotics, without corticosteroid treatment, and made a full recovery. Conclusions: This case emphasizes that influenza-associated DAH in infants may occur without overt hemoptysis and may not demonstrate classical BAL findings early in the disease course. Clinicians should maintain a high index of suspicion in rapidly deteriorating infants with influenza and diffuse pulmonary infiltrates. The optimal role of corticosteroids remains uncertain and should be individualized.

Rasmussen aneurysm is a pulmonary artery pseudoaneurysm adjacent to a cavitatory lung lesion, classically presenting in tuberculosis; remains to be rare reported in non-tuberculous-mycobacterium (NTM). We illustrate a case of massive hemoptysis secondary to Rasmussen aneurysm in mycobacterium avium complex (MAC) infection.

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitides are rare disorders characterized by inflammation of small blood vessels, including capillaries, venules, and arterioles. The three main subtypes of primary ANCA-associated vasculitides (i.e., granulomatosis with polyangiitis, microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis) can present with diverse and nonspecific symptoms, making diagnosis difficult. We report the case of secondary, drug-induced ANCA vasculitis in a female patient who presented with hemoptysis and dyspnea complicated by acute kidney injury and severe anemia. Serologic testing and renal biopsy confirmed the diagnosis of ANCA-associated vasculitis (AAV). Her hospital course was complicated by multiple gastrointestinal bleeds requiring two interventional radiology procedures, first on her gastroduodenal artery and later on her inferior pancreaticoduodenal artery. The patient was treated with cyclophosphamide and plasma exchange during hospitalization and was transitioned to rituximab and intravenous steroids, resulting in an eventual recovery. This case highlights the intricacies of diagnosing AAV and the potential severe, life-threatening complications, such as gastrointestinal hemorrhage. Early recognition and a multidisciplinary approach are critical to evaluate and treat as well as to improve outcomes in patients with this rare but serious condition.

Pulmonary arteriovenous malformations (PAVMs) are abnormal communications between an artery and a vein without an intervening capillary component. Most PAVMs are congenital, caused by hereditary hemorrhagic telangiectasia, but around 20% are acquired. The most common presenting symptom is dyspnoea on exertion, but patients can be completely asymptomatic. Furthermore, Gestational trophoblastic neoplasia (GTN) is a group of rare tumors that arise from abnormal growth of trophoblastic tissue which includes invasive mole, choriocarcinoma, placental site trophoblastic tumor, and epithelioid trophoblastic tumor can progress, invade, metastasize, and lead to death if left untreated. In the majority of GTNs, the disease is limited to the uterus where the abnormal trophoblast proliferation and localized hCG production may lead to focal vascular changes, including the formation of AVMs. Most patients with GTN present with abnormal vaginal bleeding but they can also present with bleeding from metastatic sites. Symptoms of pulmonary metastasis from GTN often include cough, hemoptysis, and chest pain. However, PAVMs are not typically listed as a direct consequence of this metastatic spread. Here, we report a rare case of metastatic GTN initially presented with pulmonary vascular malformation.

Libman-Sacks endocarditis (LSE), characterized by sterile valvular vegetations, is a recognized complication of systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). However, its occurrence as the initial manifestation of previously undiagnosed autoimmune disease is uncommon and may create significant diagnostic uncertainty. A 27-year-old female presented to the emergency department with acute-onset exertional dyspnea, cough, and severe anemia, with a history of three consecutive first-trimester miscarriages. Initial evaluation revealed severe mitral regurgitation with valvular masses, raising suspicion for infective endocarditis. Further workup demonstrated elevated inflammatory markers, autoimmune hemolytic anemia, nephrotic-range proteinuria, and positive autoimmune serology, including antinuclear antibodies, anti-double-stranded DNA, anticardiolipin IgG, anti-β2-glycoprotein I IgG, and lupus anticoagulant. Transthoracic echocardiography showed severe mitral regurgitation with valvular masses and reduced left ventricular ejection fraction, while transesophageal echocardiography confirmed Libman-Sacks vegetations. Computed tomography of the chest revealed diffuse alveolar hemorrhage. The patient was diagnosed with new-onset SLE and APS, presenting with LSE and multisystem involvement. Management included pulse methylprednisolone therapy, hydroxychloroquine, cyclophosphamide, therapeutic anticoagulation, and plasma exchange for alveolar hemorrhage, resulting in clinical improvement with resolution of hemoptysis and improvement in cardiac function. This case is particularly notable because severe valvular disease led to the initial recognition of previously undiagnosed SLE and APS in the setting of simultaneous pulmonary, hematologic, renal, and obstetric manifestations. It highlights the importance of considering autoimmune etiologies in young patients with unexplained valvular heart disease, particularly in the presence of suggestive systemic features.