A healthy 55-year-old man without known medical problems presented for a routine physical examination and was found to have an abnormal ECG. He denied chest pain, dyspnea, palpitations, dizziness, or syncopal episodes. He also denied orthopnea, paroxysmal nocturnal dyspnea, and lower-extremity edema. His exercise capacity had been excellent. He was a lifelong nonsmoker and never had lung problems.

A 62-year-old man developed a scalp rash 2 months ago, followed by bilateral eyelid swelling. The nonpruritic rash then spread to involve most of his skin. He also had fatigue, muscle weakness, mild muscle soreness with activity, and dysphagia for solid foods for the last 3 weeks. He had no other symptoms. He had a 50 pack-year history of smoking and drank two to three shots of alcohol daily.

A 51-year-old man was admitted for evaluation of new-onset generalized seizures in the context of progressive and significant behavioral change. His medical history was only notable for previous outbreaks of genital herpes. He took no medications. He had occasional social alcohol use and no illicit drug use but was a 35-pack-year current smoker. The patient had no relevant occupational exposure history but had recently traveled to Panama. Initially, the patient's significant other noticed a progressive flattening of his affect. The patient then started to experience episodes of "passing out" that led to injuries prompting ED visits. He was prescribed antiseizure medications and scheduled for an outpatient workup. However, with progressive gait instability, lethargy, and an increase in frequency of generalized seizures, the patient was admitted for treatment of suspected viral encephalitis. Despite initiation of antimicrobial and antiviral therapy, the patient's level of alertness continued to decline, ultimately leading to intubation for airway protection.

The underlying cause of cystic fibrosis (CF) is the loss of epithelial chloride and bicarbonate transport due to mutations in the CF transmembrane conductance regulator (CFTR) gene encoding the CFTR protein. Ivacaftor is a gene-specific CFTR potentiator that augments in vivo chloride transport in CFTR mutations affecting channel gating. Originally approved for the G511D CFTR mutation, ivacaftor is now approved for eight additional alleles exhibiting gating defects and has also been tested in R117H, a CFTR mutation with residual function that exhibits abnormal gating. P67L is a class 4 conductance (nongating) mutation exhibiting residual CFTR function. We report marked clinical improvement, normalization of spirometry, and dramatic reduction in radiographic structural airway changes after > 1 year of treatment with ivacaftor in a young adult with the compound heterozygous genotype P67L/F508del CFTR. The case suggests that ivacaftor may have a potential benefit for patients with CF with nongating mutations.

Small pulmonary lesions can be difficult to locate intraoperatively. Preoperative CT scan-guided localization, for example with hookwire, is a popular method to help localize such lesions. However, the delay between CT scan localization with hookwire and surgery can lead to risks of pneumothorax and wire dislodgement. We describe a 56-year-old woman who underwent DynaCT-guided hookwire localization of a ground-glass opacity in the hybrid operating room followed immediately by single-port video-assisted thoracic surgery lobectomy. The advantages, disadvantages, and special considerations in adopting this approach are discussed.