A 62-year-old woman with a long-term smoking history was evaluated at our lung cancer clinic for a new 2.5-cm lung nodule. She had a history of well-controlled COPD and hypertension. She was in overall good health until 3 weeks before her evaluation in an ED for new-onset exertional dyspnea. Her physical examination was unremarkable, except for diffuse hyperpigmented scaly scalp lesions that coalesced into plaques. Her subjective symptoms were nonproductive cough, exertional dyspnea, unintentional weight loss of 10 lb, and fatigue that had started 2 months earlier. She did not have fever or night sweats.

A 33-year-old man with obesity, systemic arterial hypertension, and psoriasis who had been treated previously with little success by a pulmonologist for chronic unproductive irritant cough came to the outpatient pulmonary department because of profuse cough and short syncope (probably cough-induced). Chest radiography revealed widened mediastinum with lobular, polycyclic contours that was suspected to be a large mediastinal lymphadenopathy or mediastinal mass.

A 74-year-old man presented to the ED with acute chronic exertional dyspnea of 5-day duration. As part of his previous evaluation, 5 months earlier, he had undergone cardiopulmonary stress testing, routine laboratory evaluation, and chest radiography that were unremarkable. Over the subsequent months, he had waxing and waning exercise capacity until his incident hospitalization; the exercise was limited to < 40 meters. He reported associated nonproductive cough, 15-pound unintentional weight loss over the past 5 months, night sweats, easy fatigability, and early satiety. A chest radiograph was performed that showed a left hilar, mass-like consolidation with loss of the left heart border that was associated left-sided pleural effusion and left lower lung zone consolidation. On physical examination, he was afebrile and normotensive with a sinus tachycardia of 125 beats per minute. He was noted to be tachypneic with a respiratory rate of 24 breaths per minute and saturation of 95% on room air. Examination of the chest showed diminished breath sounds over left lower lung fields with scattered end expiratory wheezing.

A 37-year-old woman presented to the ED in Singapore with a 6-month history of chronic cough and dyspnea that was associated with small volume hemoptysis, night sweats and occasional fever. Of note, she had no sick contacts or recent travel. Systemic review revealed no loss of weight or appetite and no autoimmune features. She had no other medical history and was a lifelong nonsmoker and was not an alcoholic.

A 32-year-old man was admitted to the hospital because of dyspnea on exertion for 2 months. Dyspnea occurred in both inspiration and expiration with an associated wheeze that was more pronounced with exertion. He had no other medical history or allergies. The patient was a current one-pack-a-day smoker for the past 5 years. He denied any close personal contact or recent exposure to any patients with active TB. He denied any current symptoms of chest pain, cough, fever, or changes in weight. On a prior admission for similar symptoms, the patient had been diagnosed with asthma and treated with an inhaled corticosteroid/long-acting beta-agonist with no change or improvement in symptoms.

A 27-year-old man with a history of bronchiolitis obliterans caused by a severe viral illness during early childhood that necessitated lung transplantation who was receiving tacrolimus therapy presented with rapidly worsening mental status. Prior to his change in mental status, his postoperative course was complicated by severe primary graft dysfunction and acute renal failure due to acute tubular necrosis that required continuous renal replacement therapy (CRRT). The patient had a prolonged intubation that required periodic BAL for mucous plugging. He ultimately was weaned to high-flow nasal cannula and subsequently 2 L/min by nasal cannula to maintain oxyhemoglobin saturations at >90%. On the night before mental status change, the patient experienced day/night inversion. After arousing that morning, the patient became combative, violent, and confused. This altered mentation progressed throughout the day to somnolence and lethargy, necessitating endotracheal intubation for airway protection. The patient experienced subsequent hypotension that necessitated low-dose epinephrine and vasopressin infusions.

A 34-year-old man presented to Queen Elizabeth Central Hospital in Blantyre, Malawi with multiple enlarged right cervical lymph nodes. He had no associated constitutional symptoms. Fine-needle aspirate (FNA) of one of the lymph nodes was negative for acid-fast bacilli (AFB) by smear microscopy. The FNA specimen was not sent for histological examination. Mycobacterial culture and Xpert MTB/RIF were not available at the time. He tested positive for HIV but CD4 T-cell count was not requested at the time of HIV diagnosis, and he did not start antiretroviral therapy (ART) pending confirmation of the cause of lymphadenopathy. Excision biopsy of the lymph nodes was planned; however, the patient was lost to follow-up before the procedure was performed.

Immersion pulmonary edema, more commonly referred to as swimming-induced pulmonary edema (SIPE), is a well-documented condition believed to be a result of immersion physiologic condition that is characterized by a peripheral-to-central redistribution of blood volume. It disproportionally affects young, healthy athletes with no clinically overt cardiovascular or pulmonary conditions. We present four cases of healthy athletes with previously documented SIPE, who participated in Institutional Review Board-approved clinical studies that examined the pathophysiologic condition and prevention of SIPE. During standard recumbent echocardiography, trivial mitral regurgitation was observed in all four individuals. Acute exacerbation of their mitral regurgitation was observed during immersion with both immersed resting and immersed exercise echocardiography, contributing to the development of SIPE. These observations demonstrate that the occurrence of subclinical or trivial mitral valve regurgitation during dry rest is a novel risk factor for SIPE. We propose the use of immersion echocardiography as a useful investigative tool for otherwise healthy individuals with SIPE and no previously explainable cause.