A 33-year-old teacher from Ghana with no medical comorbidities and no relevant family history came to our pulmonology department with progressive difficulty in breathing, wheezing, and stridor for 6 months. Similar episodes had been treated previously as bronchial asthma. She was being treated with high-dose inhaled corticosteroids and bronchodilators but had no relief. The patient also described two episodes of large quantities of hemoptysis (> 150 mL) in the previous week. A general physical examination revealed a tachypneic young woman with an audible inspiratory wheeze. Her BP was 128/80 mm Hg; pulse, 90 beats/min; and respiratory rate, 32 breaths/min. There was a hard, minimally tender, nodular swelling of 3 × 3 cm in the midline neck felt just below the cricoid cartilage, moving with deglutition and protrusion of the tongue, with no retrosternal extension. There was no cervical or axillary lymphadenopathy. Laryngeal crepitus was present.

A 52-year-old White man, who currently smokes, was admitted to the medical ICU with worsening shortness of breath. The patient was dyspneic for a month and had been clinically diagnosed with COPD by his primary care doctor and started on bronchodilators and supplemental oxygen. He had no known medical history or recent illness. His dyspnea worsened rapidly over the next month, prompting admission to the medical ICU. He was on high-flow oxygen followed by noninvasive positive pressure ventilation and then mechanical ventilation. He denied cough, fever, night sweats, or weight loss at the time of admission. There was no history of work-related or occupational exposures, drug intake, or recent travel. Review of systems was negative for arthralgia, myalgia, or skin rash.

A 39-year-old man with a history of arteriovenous malformation in the upper right limb that was complicated with vascular-type ulcers and repeated soft tissue infection and who had needed a supracondylar amputation of the limb when he was 27 years old presented a new soft tissue infection that manifested with fever, chills, increase in the diameter of the stump with local skin erythema, and painful necrotic ulcers. The patient reported mild dyspnea for 3 months (World Health Organization functional class II/IV) that had worsened during the last week (World Health Organization functional class III/IV) with chest tightness and bilateral lower limb edema.

A 37-year-old man attended a medical clinic at the confluence of the Appalachian and the St. Lawrence Valley after 2 weeks of coughing greenish sputum and progressive dyspnea on exertion. In addition, he reported fatigue, fevers, and chills. He had quit smoking a year earlier and was not a drug user. He recently had spent most of his free time outdoors, mountain biking, but had not travelled outside of Canada. Medical history was unremarkable. He did not take any medication. Upper airway samples taken for SARS-CoV-2 proved negative; he was prescribed cefprozil and doxycycline for presumed community-acquired pneumonia. He returned to the emergency room 1 week later with mild hypoxemia, persisting fever, and a chest radiography consistent with lobar pneumonia. The patient was admitted to his local community hospital, and broad-spectrum antibiotics were added to the regimen. Unfortunately, his condition deteriorated over the following week, and he experienced hypoxic respiratory failure for which he required mechanical ventilation before his transfer to our medical center.

Fat embolism syndrome describes a constellation of symptoms that follow an insult and that results in a triad of respiratory distress, neurologic symptoms, and petechia. The antecedent insult usually entails trauma or orthopedic procedure, most frequently involving long bone (especially the femur) and pelvic fractures. The underlying mechanism of injury remains unknown but entails biphasic vascular injury with vascular obstruction from fat emboli followed by an inflammatory response. We present an unusual case of a pediatric patient with acute onset of altered mental status, respiratory distress, hypoxemia, and subsequent retinal vascular occlusions after knee arthroscopy and lysis of adhesions. Diagnostic findings most supportive of the fat embolism syndrome included anemia, thrombocytopenia, pulmonary parenchymal, and cerebral pathologic findings on imaging studies. This case highlights the importance of fat embolism syndrome as a diagnostic consideration after an orthopedic procedure, even absent major trauma or long bone fracture.

Modern sleep specialists are taught that, before the twentieth century, sleep was universally classified as a passive phenomenon with minimal to no brain activity. However, these assertions are made on the basis of particular readings and reconstructions of the history of sleep, using Western European medical works and ignoring works composed in other parts of the world. In this first of two articles on Arabic medical discussions on sleep, I shall show that sleep was not understood to be a purely passive phenomenon, at least from the time of Ibn Sīnā (lat. Avicenna, d. 1037) onward. Building on the earlier Greek medical tradition, Ibn Sīnā provided a new pneumatic understanding of sleep that allowed him to explain previously recorded phenomena associated with sleep, while providing a way to capture how certain parts of the brain (and body) can even increase their activities during sleep.