A 62-year-old African American man was admitted to the hospital with hemoptysis. He had a complicated medical history significant for active tobacco use (>50 pack-year history), coronary artery disease, and heart failure with reduced ejection fraction. He reported intermittent episodes of coughing up streaks of blood in the sputum for the past 3 years. For the past few days before this presentation, he had multiple episodes of coughing up over a tablespoon of only blood. He was not on any anticoagulant agents. There were no risk factors for TB, nor was there a history of fevers, chills, shortness of breath, leg swelling, changes in his urine color and frequency or urgency, or unintended weight loss. On admission, he was noted to be breathing comfortably. Vital signs revealed a temperature of 36.6ºC, BP of 138/70 mm Hg, heart rate of 66 beats/min, respiratory of rate of 18 breaths/min, and a blood oxygen saturation level of 98% on room air. Physical examination was significant for decreased bilateral breath sounds with no wheezing, crackles, or rhonchi. Cardiovascular examination revealed normal cardiac rhythm without murmur, rubs, or gallops. There was no clubbing or edema on his extremities.

An 84-year-old physician was seen in the pulmonary clinic with 10 days of progressive exertional dyspnea, night sweats, and dry cough. For the past 5 months, he had been taking ibuprofen for lumbar radiculopathy from spinal stenosis. Ten days earlier, ibuprofen was switched to naproxen 250 mg twice daily because of its longer half-life. He denied fever, weight loss, rash, dysphagia, proximal muscle weakness, wheeze, sinus congestion, and peripheral numbness/tingling. Medical history included paroxysmal atrial fibrillation, hypertension, Hashimoto's thyroiditis, and OSA. Long-term medications included aspirin, flecainide, atorvastatin, amlodipine, levothyroxine, and candesartan. He was a lifelong nonsmoker. There was no history of recent travel.

A 43-year-old man experienced sudden onset of chest pain and shortness of breath onboard a domestic flight. After consultation with the airline's operations center, a decision was made to land the plane in its destination airport. After landing, an ambulance was ready, and the patient was transferred to the ED in our facility. Patient evaluation was immediately started, and oxygen supply and venous access were secured.

A 26-year-old man presented with a 2-week history of productive cough and a 1-year history of effort-related dyspnea. His medical history was significant for hay fever and exertion-triggered asthma. He was not taking medicines regularly but was using inhaled salbutamol as needed. He was an ex-smoker, with a previous history of 2-pack years.

A 67-year-old woman presented to her primary physician with a year of periumbilical abdominal discomfort with diarrhea, bloating, and unintentional weight loss. While undergoing workup for the abdominal pain, she presented to the ED with dyspnea that worsened over a few weeks. She had no associated chest pain, lower extremity edema, fevers, or chills, but endorsed orthopnea. The patient's medical history included hypothyroidism and diabetes mellitus. Her family history was significant for coronary disease in her father and hypertension in her mother. She had no recent travel; she is a nonsmoker and rare alcohol drinker. She worked in administration.

A 74-year-old man was referred to a pulmonologist for evaluation of a 1-year history of nonproductive cough and progressive exertional dyspnea. He was initially evaluated by his primary care physician, where he had spirometry that was negative for any obstructive or restrictive lung disease. An echocardiogram showed a normal left ventricular ejection fraction, with no wall motion abnormality or valvular heart disease. He had an outpatient chest radiograph performed (Fig 1), and he was subsequently treated empirically for a COPD exacerbation with 5 days of oral prednisone and azithromycin. He was eventually referred to a pulmonologist because of a lack of clinical improvement. On seeing his pulmonary physician, he described the same exertional dyspnea and a nonproductive cough. A review of systems was negative for fever, chills, wheezing, angina, arthralgia, myalgia, rash, or leg swelling. He denied any medical illness and was not taking any medications. He was currently retired and had worked as a cashier his entire adult life. He had no occupational exposure to asbestos, coal dust, beryllium, silica dust, or dust from hard metal objects, such as cobalt. However, he had smoked approximately 1 to 2 packs of cigarettes per day and had done so for the past 50 years. His vital signs were unremarkable, aside from an oxygen saturation of 94% on room air. His physical examination revealed bibasilar "velcro-like" inspiratory crackles on lung examination. There was no digital clubbing, nor was there peripheral edema in his lower extremities. He had no muscle tenderness and demonstrated normal muscle strength against resistance.

High spinal cord injured patients (SCI) are susceptible to respiratory muscle impairments. Transcranial direct current stimulation (tDCS) and peripheral electrical stimulation (PES) may influence the diaphragm's central control, but until now they are not described as a therapeutic resource for difficult weaning. We present two case reports of SCI patients (P1 and P2) with long-term tracheostomy (>40 days) and hospital stay (>50 days). In association with respiratory exercise, P1 received a combined application of anodal tDCS over the supplementary motor area plus sensory PES in the thoracic-abdominal muscles, and P2 received isolated excitatory PES in the abdominal muscles, applied daily except on weekends. Maximum inspiratory/expiratory pressure, peak cough flow, diaphragm excursion, and thickening fraction were measured in the first and last days of the protocol. Both patients had improvements, with clinical impact such as cough effectiveness, decannulated after 15 applications of stimulation. Augmentation of neural respiratory drive and corticospinal excitability is suggested.

Niemann-Pick Disease type B (NPDB) is a rare autosomal recessive disease belonging to the family of lysosomal storage disorders. NPDB is caused by mutations of sphingomyelin phosphodiesterase 1 gene (SMPD1) and is characterized by hepatosplenomegaly, interstitial lung disease, recurrent pulmonary infections, and neurologic disorders. Bronchiectasis are atypical. Until now, only three cases of lung transplantation for severe respiratory impairment have been reported. We describe a case of NPDB that was diagnosed after lung transplantation for cystic bronchiectasis. In 2016, a 31-year-old woman who was experiencing hypoxemic respiratory failure and recurrent pulmonary infections due to cystic bronchiectasis received a double-lung-transplantation. Histopathologic study on removed lungs revealed clusters of CD68 foamy lipid-laden macrophages with concentric and palisade arrangement, compatible with the diagnosis of NPDB, which was confirmed after SMPD1 genetic sequencing. Twenty-three months after transplantation, allograft function is stable (FEV1 was 100% of best-FEV1). The singularity of this case lies in the presence of bronchiectasis, which is an unprecedently described phenotype of NPDB. This finding was accompanied by the detection of a novel SMPD1 mutation (p.Ala46=) of uncertain meaning.