A 33-year-old male farmer residing in the Kendujhar district (central part) of Odisha state, India, with a 3-year history of type 2 diabetes mellitus that was not well-controlled, presented with a 4-month history of recurrent fever, dyspnea, left-sided pleuritic chest pain, loss of appetite, and significant loss of weight. Despite multiple hospital admissions and several courses of antibiotics during this period, he showed no sustained clinical improvement, with only brief asymptomatic intervals followed by symptom recurrence.

Pancreaticopleural fistula (PPF) is a rare complication of acute or chronic pancreatitis, resulting from the disruption of the pancreatic duct and abnormal communication between the pancreas and the pleural cavity. Patients often present with respiratory symptoms rather than abdominal complaints, making diagnosis challenging and frequently delayed. We report a case of PPF presenting as a rapidly recurrent right-sided pleural effusion in a patient with recurrent alcohol-related pancreatitis. A 48-year-old man with a history of recurrent alcoholic pancreatitis presented with progressive dyspnea and pleuritic chest pain. Chest radiography demonstrated a moderate-to-large right pleural effusion. Diagnostic thoracentesis yielded 2 L of dark maroon exudative fluid with a markedly elevated amylase level of 70,476 U/L. Drainage was performed in a symptom-guided manner, with the procedure terminated after symptom improvement, and the patient was monitored for re-expansion pulmonary edema. Despite initial symptomatic improvement, the patient developed rapid reaccumulation of effusion within 24 hours, necessitating pigtail chest tube placement. Due to persistent loculated pleural collections and inadequate drainage, intrapleural alteplase and dornase alfa were administered. Magnetic resonance cholangiopancreatography demonstrated a fluid tract extending from the pancreas into the right pleural cavity, raising suspicion for a PPF. Endoscopic retrograde cholangiopancreatography revealed chronic pancreatitis with obstructing pancreatic duct stones and a ductal defect. Complete stone extraction, pancreatic sphincterotomy, and pancreatic duct stent placement were successfully performed. The patient experienced complete resolution of the pleural effusion, with no recurrence following stent removal. This case highlights the importance of considering PPF in patients with recurrent pleural effusions and a history of pancreatitis, particularly when pleural fluid amylase levels are markedly elevated. Early recognition and endoscopic intervention can facilitate definitive treatment, prevent recurrent hospitalizations, and avoid repeated invasive pleural procedures.

A man in his early 30s presented with a 4-month history of low-grade fever and chronic dry cough. Three months before admission, he developed persistent low-grade fever, rash and bilateral cervical lymphadenopathy. He was diagnosed with HIV infection and started on tenofovir/lamivudine/dolutegravir. Two weeks before admission, he developed right-sided pleuritic chest pain. Chest CT revealed bilateral pleural effusions and generalised lymphadenopathy involving the lower cervical, mediastinal and axillary regions. An excisional biopsy of a right lower cervical lymph node demonstrated hyaline-vascular architecture, including 'lollipop' lesions and onion-skinning of the mantle zones. Immunohistochemistry showed human herpesvirus 8 (HHV-8)-positive plasmacytoid cells within the mantle zones, without malignant features, consistent with HHV-8-associated multicentric Castleman disease (MCD). The patient continued antiretroviral therapy and received rituximab 375 mg/m[2] every week for four cycles. He achieved complete resolution of the pleural effusions. This case illustrates the variable clinical presentation of HHV-8-associated MCD in a patient living with HIV.

A 41-year-old incarcerated male with multiple comorbidities presented with severe constitutional symptoms, including persistent fever, pleuritic chest pain, and significant unintentional weight loss. Diagnostic evaluation revealed a large, irregular posterior mediastinal mass on chest CT, characterized by calcifications, heterogeneous low-attenuation areas, and internal air locules extending to the subcarinal region adjacent to the lower thoracic esophagus. These findings initially raised concerns for an esophageal pathology complicated by potential perforation; however, an esophagram excluded esophageal rupture. Laboratory studies demonstrated persistent thrombocytosis, hypoalbuminemia, anemia, elevated inflammatory markers, and a low-positive Histoplasma antibody titer (1:8), suggestive of fungal involvement. Further evaluation with endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) obtained purulent material from an enlarged subcarinal lymph node, supporting the presence of an active bacterial infection. Microbiological analysis demonstrated moderate growth of viridans group streptococci, which correlated with Gram-stain findings of Gram-positive cocci in chains. Although scant Staphylococcus epidermidis was also recovered, it was considered likely to represent contamination and was therefore not regarded as the primary pathogen. Treatment with broad-spectrum intravenous antibiotics alongside systemic antifungal therapy led to significant clinical and radiological improvement. Follow-up CT imaging demonstrated marked reduction of the mediastinal mass, resolution of internal air locules, and improvement in lymphadenopathy and pleural effusions. This case report emphasizes the diagnostic complexity of infectious mediastinal masses that closely mimic malignancies. It further highlights the importance of integrating comprehensive clinical, radiological, serological, and microbiological data to establish an accurate diagnosis and guide appropriate targeted treatment.

Pulmonary lymphangitic carcinomatosis (PLC) and pulmonary tumor embolism (PTE) are rare manifestations of metastatic malignancy that may mimic more common causes of dyspnea and pulmonary hypertension, often leading to delayed diagnosis. Both conditions are associated with poor prognosis and may present with rapidly progressive right ventricular failure. A 45-year-old female lifelong non-smoker with no significant past medical history presented with a two-week history of cough, pleuritic chest pain, and worsening fatigue. CT pulmonary angiography was negative for central macrovascular pulmonary embolism but demonstrated interlobular septal thickening, ground-glass opacities, pulmonary nodules, and vertebral lesions. Initial echocardiography showed mild to moderate pulmonary hypertension with preserved right ventricular function. Despite supportive management, the patient experienced rapid clinical deterioration, progressing to severe pulmonary hypertension, right ventricular failure, cardiogenic shock, and pulseless electrical activity arrest. Post-mortem examination revealed invasive pulmonary adenocarcinoma with extensive lymphovascular invasion and metastatic disease, consistent with PLC and PTE. This case emphasizes the need to take into account PLC and PTE in patients with rapidly progressive pulmonary hypertension despite negative pulmonary embolism imaging. Recognition of subtle radiographic clues may facilitate earlier diagnosis, although prognosis remains poor once right ventricular failure develops.

Pulmonary artery pseudoaneurysm (PAP) is a rare but potentially fatal vascular lesion resulting from focal disruption of the pulmonary arterial wall. Although hemoptysis from the pulmonary arterial system is uncommon, PAP carries a high risk of rupture, with reported mortality rates up to 50%. PAP is most often caused by trauma or infection, with pyogenic bacteria and fungi as typical pathogens, while Streptococcus constellatus is an exceptionally rare cause. A 60-year-old woman with well-controlled type 2 diabetes presented with recurrent massive hemoptysis, fever, and right-sided pleuritic chest pain, without prior lung disease or trauma. She initially underwent emergency bronchial artery embolization (BAE) and antibiotic therapy for necrotizing pneumonia-associated hemoptysis, with no clinical improvement. Following the second BAE for recurrent massive hemoptysis, a PAP, possibly related to a bronchial-pulmonary arterial shunt, was suspected in the right lower lobe on angiography and subsequently confirmed on contrast-enhanced computed tomography. Despite optimal medical therapy, repeated BAE, and coil embolization of the PAP, hemoptysis persisted, and respiratory status deteriorated. The patient ultimately underwent video-assisted thoracoscopic right lower lobectomy, with intraoperative cultures of lung tissue and pleural fluid confirming S. constellatus, and achieved complete recovery without recurrent hemoptysis. PAP is a rare but potentially fatal cause of hemoptysis that requires a high index of suspicion. Although endovascular intervention is effective for initial hemorrhage control, persistent infection or refractory hemoptysis may necessitate surgical resection to achieve definitive management. This case highlights S. constellatus as an exceptionally rare infectious cause of PAP and underscores the importance of a multidisciplinary approach in complex, antibiotic-resistant cases.

Post-traumatic pericarditis is a subtype of post-cardiac injury syndrome (PCIS) that occurs after non-iatrogenic cardiac trauma. Post-traumatic pericarditis is rare and difficult to diagnose. We present a case of post-traumatic pericarditis progressing to transient constrictive pericarditis following a penetrating stab wound to both ventricles, illustrating the role of multimodal imaging in diagnosis and follow-up. A 22-year-old male presented with a two-day history of severe pleuritic chest pain, six weeks after surviving a penetrating stab injury to the left and right ventricles. Initial evaluation revealed no fever, a normal cardiovascular examination, and stable vital signs. Inflammatory markers were raised, and electrocardiography (ECG) showed anterolateral T-wave inversion without PR depression or ST elevation. CT pulmonary angiography demonstrated moderate pericardial effusion and mild pleural effusion. Echocardiography showed a small pericardial effusion with septal bounce, suggesting early constriction. Cardiac magnetic resonance imaging (MRI) demonstrated pericardial thickening, prominent septal bounce and flattening, and circumferential late gadolinium enhancement, in keeping with acute transient constrictive pericarditis. The patient was treated with colchicine, ibuprofen, and prednisolone. Serial follow-up MRI showed resolution of the pericardial inflammation. This case highlights post-traumatic pericarditis as a rare complication of life-threatening penetrating cardiac trauma. Serial multimodal imaging, particularly cardiac MRI, may support the diagnosis and help monitor the response to anti-inflammatory therapy.

Massive haemothorax is a life-threatening condition most commonly associated with thoracic trauma, malignancy, or iatrogenic injury. Anticoagulation, while essential for thromboembolic disease management, may precipitate or exacerbate occult bleeding complications. We report the case of a 69-year-old woman who presented with pleuritic chest pain, productive cough, and progressive dyspnoea following a recent fall and long-haul travel. CT pulmonary angiography confirmed segmental and subsegmental pulmonary emboli with bilateral consolidation, and therapeutic low-molecular-weight heparin was initiated. On the third hospital day, she developed sudden hypoxia, left-sided chest pain, and a significant haemoglobin decline. Repeat imaging demonstrated a massive left haemothorax with lung collapse and mediastinal shift, together with previously unrecognised right-sided rib fractures. Anticoagulation was immediately discontinued and reversed, and the patient underwent blood transfusion and chest drainage, yielding over 2.4 L of blood. Residual loculated haemothorax was successfully managed using image-guided catheter drainage without surgical intervention. This case highlights the rare occurrence of delayed contralateral haemothorax complicating anticoagulation and underscores the importance of recognising atypical bleeding presentations and balancing thrombotic and haemorrhagic risk through multidisciplinary decision-making.

Giant cavernous hepatic hemangiomas may occasionally demonstrate atypical imaging characteristics that mimic malignant or infectious hepatic lesions, creating diagnostic uncertainty and increasing the risk of anchoring bias. We report the case of a 41-year-old male who presented with fever, pleuritic chest pain, leukocytosis, and a large right pleural effusion following CT-guided lung biopsy. Imaging revealed a large hepatic lesion with atypical radiographic features concerning for malignancy or disseminated infection, along with pulmonary inflammatory changes and empyema. Thoracentesis yielded pleural fluid concerning for empyema. Given the constellation of findings, the hepatic lesion initially dominated diagnostic reasoning and raised concern for a unifying metastatic or infectious process. However, liver biopsy ultimately confirmed cavernous hepatic hemangioma, while pulmonary biopsy demonstrated inflammatory changes without evidence of malignancy. Histopathologic evaluation established that the hepatic lesion was incidental and unrelated to the patient's acute illness, whereas the empyema was most likely secondary to the recent thoracic intervention. This case highlights the importance of avoiding anchoring bias and recognizing concurrent but unrelated disease processes when evaluating complex clinical presentations.

Pericarditis is a common disease caused by various factors such as viral infections, systemic diseases, or drugs. A diagnosis of pericarditis is rendered in up to 5% of Emergency Room (ER) visits for non-ischemic chest pain. It is diagnosed when pleuritic chest pain is present, accentuated in the supine position, accompanied by ECG changes comprising new extensive ST-segment elevation and PR depression, a pericardial friction rub, and new or increased pericardial effusion on echocardiography. In North America and Western Europe, the most common causes of acute pericarditis are idiopathic or viral, followed by post-procedural (iatrogenic) pericarditis, radiation therapy, and cardiac surgery. Tuberculosis is the most common cause of pericarditis in endemic areas and is managed with antituberculosis therapy, with corticosteroids used when there is concurrent constrictive pericarditis. New diagnostic techniques have aided the sampling and analysis of pericardial fluid and in determining its cause. Treatment of pericarditis comprises high-dose Non-Steroidal AntiInflammatory Drugs (NSAIDs) for uncomplicated cases, with doses tapered when symptoms have subsided and C-reactive protein level has normalized, typically over several weeks. Colchicine (often a 3-6-month course) is needed to both alleviate symptoms and decrease recurrences, while glucocorticoids and newer therapies with interleukin-1 blockers are reserved for recurrences and/or failures of prior therapies. Integrated use of new imaging methods facilitates more precise detection and better management of complications such as pericardial effusion or constriction. The diagnostic yield of extensive laboratory evaluation and pericardiocentesis remains low; hence, invasive procedures should be limited mostly to patients in whom a therapeutic intervention is needed. The majority of pericardial effusions can be safely drained with an echo-guided percutaneous technique. Pericardiectomy remains the definitive treatment for constrictive pericarditis and provides symptomatic relief in most cases. Importantly, differentiation of constrictive pericarditis from restrictive cardiomyopathy remains a clinical challenge, but is facilitated by tissue Doppler and colour M-mode echocardiography. All these issues are reviewed herein.