The acetazolamide challenge test is frequently performed to evaluate cerebral blood flow and reserve capacity in cerebrovascular disease. Most of its side effects are mild and transient. Acute pulmonary edema (PE) has never been reported to occur after acetazolamide challenge tests. Here, we present a case of acute noncardiogenic PE triggered by an acetazolamide challenge test. A 62-year-old man with carotid artery stenosis underwent an acetazolamide challenge test during an arterial spin labeling (ASL) magnetic resonance (MR) imaging study. The patient showed stable vital signs and no neurologic abnormalities. The patient had no pulmonary or cardiac problems that could induce acute PE. Routine laboratory findings, electrocardiography, and chest X-ray also produced normal findings. An acetazolamide challenge ASL MR study was performed with intravenous administration of 1 g of acetazolamide. Two hours after acetazolamide administration, sudden dyspnea and hypoxemia developed, and chest X-ray and computed tomography revealed diffuse PE. Immediately, the oxygen supply and furosemide treatment were initiated. The following day, the dyspnea and PE improved and the patient recovered completely. To the best of our knowledge, this is the first case report of acute noncardiogenic PE triggered by intravenous acetazolamide administration in an acetazolamide challenge test.

We present the case of a 22-year-old female with a history of systemic lupus erythematosus and antiphospholipid syndrome, complicated by recurrent deep vein thrombosis of the lower extremities and pulmonary embolism, who subsequently developed chronic thromboembolic pulmonary hypertension. The patient presented with progressive dyspnea, ultimately limiting daily activities, and was managed with long-term anticoagulation and pulmonary vasodilator therapy. Diagnostic workup, including imaging and hemodynamic assessment, revealed multiple bilateral segmental perfusion defects, right heart dilation, and significantly elevated pulmonary pressures with increased pulmonary vascular resistance, consistent with operable chronic thromboembolic disease. The patient underwent pulmonary endarterectomy via median sternotomy under cardiopulmonary bypass with deep hypothermia and intermittent total circulatory arrest. Two periods of circulatory arrest, of 19 and 18 minutes, were utilized during the procedure. Organized thromboembolic material was successfully removed from both pulmonary arteries, achieving adequate endarterectomy planes without major intraoperative complications. In the immediate postoperative period, the patient remained hemodynamically stable, with expected improvement in right ventricular afterload and pulmonary hemodynamics. This case highlights the importance of recognizing chronic thromboembolic pulmonary hypertension in young patients with autoimmune disease and recurrent thrombotic events, as well as the role of pulmonary endarterectomy as a potentially curative treatment when performed in specialized centers.

Giant goiters can lead to tracheal compression with acute respiratory failure. We present a case with a giant goiter as well as acute respiratory failure, which required urgent surgery. We report the case of a 36-year-old female patient who presented to the emergency room with a giant goiter, which had been present for 12 years and had become compressive for one month, as well as laryngeal dyspnea. For this compressive goiter, she benefited from an emergency thyroidectomy. After histological analysis of the specimen, it was found to be cancerous. Giant goiters can cause compression of the critical structures of the neck. In cases of compressive goiter, dyspnea is the most common sign of compression and can constitute a life-threatening emergency requiring emergency thyroidectomy. Multi-nodular goiter and thyroid cancers are the two main etiologies found in the literature to be responsible for acute dyspnea due to tracheal compression. Emergency thyroidectomy is the appropriate treatment for asphyxial goiter.

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.

This study aims to compare the efficacy and safety of catheter-directed mechanical thrombectomy using the Tendvia system versus systemic thrombolysis in patients with intermediate-to-high-risk acute pulmonary embolism.

This case report describes a female in her late 80s who presented with progressive dyspnoea and marked hypoxia. Notably, the hypoxia was refractory to high-flow supplemental oxygen. Her medical history included myeloperoxidase (MPO) positive vasculitis, vitamin B12 deficiency with a baseline haemoglobin of 88g/dL and well-controlled hypertension. A venous blood gas showed a MetHb of 10.2% [< 2%], which was initially overlooked. She was admitted to the ward and remained refractory to supplementary oxygen. A subsequent arterial blood gas (ABG) revealed an oxygen saturation (SaO2) of 95% and a methaemoglobin (MetHb) level of 10.7%. On review of her drug history, it was noted that she was taking 100 mg of dapsone once daily for Pneumocystis jirovecii pneumonia (PCP) prophylaxis. Dapsone was discontinued; her symptoms and hypoxia rapidly improved, and she was discharged 48 hours later.