BackgroundPeople living with dementia (PLWD) with advanced illness are prone to respiratory distress yet often cannot self-report dyspnea, delaying recognition and treatment. Near-field radio-frequency (NFRF) sensors offer touchless, covert cardiopulmonary monitoring that may be better tolerated than tethered devices.ObjectivesTo assess the feasibility and acceptability of NFRF bed sensor for home monitoring of PLWD and to estimate machine-learning (ML) performance for detecting respiratory distress.MethodsIn a 48-hour pilot study, PLWD were recruited from a geriatrics practice. A lab-designed NFRF bed sensor recorded cardiopulmonary waveforms. Recorded video enabled minute-level Respiratory Distress Observation Scale scoring as reference. Feasibility outcomes included adverse events, acceptability, and percentage of usable data. ML classifiers (eg, random forest, k-nearest neighbors) were evaluated using 5-fold cross-validation, and class imbalance was addressed through data augmentation.ResultsTen patient-legally authorized representative dyads were enrolled. No adverse events were reported, and no participants intentionally removed the sensor. Usable data averaged 52% (range 34-68%). Caregivers reported minimal burden and no patient distress. With augmented data, the random forest performed best, achieving 74.6% sensitivity and 95.5% specificity in detecting RDOS scores.ConclusionsNFRF bed sensors were feasible and acceptable to implement in the home setting with PLWD, with promising ML-based detection of respiratory distress. Larger, longer studies with a broader range of RDOS severity are needed to validate performance and refine deployment. As this technology develops and matures, it could provide a method for non-invasive continuous monitoring to detect respiratory distress in PLWD in palliative care settings.

A 66-year-old woman with a 6-month history of new-onset psoriasis after her first dose of COVID-19 vaccination recently progressed to acute erythroderma accompanied by fever and systemic inflammation. She was started on secukinumab for erythrodermic psoriasis (EP) after conventional therapies were contraindicated. On hospital day 6, her condition deteriorated with dyspnea, high fever, and edema. Laboratory evaluation revealed severe hypoalbuminemia and elevated inflammatory cytokines, with no evidence of infection. Imaging studies showed pulmonary edema and massive pleural effusions requiring therapeutic thoracentesis. After excluding sepsis, cardiogenic pulmonary edema, and allergic reactions, a diagnosis of systemic capillary leak syndrome (SCLS) complicating EP was established. Secukinumab was discontinued, and the patient received supportive care while being switched to apremilast. Her condition improved rapidly, with resolution of fever, reduction in pleural effusions, and significant diminishment of skin erythema. This case highlights a rare but life-threatening complication of severe acute EP, as both conditions are driven by a systemic cytokine storm. A single loading dose of secukinumab failed to effectively control the systemic cytokine storm in this patient, and the potential association between secukinumab administration and disease progression requires further investigation. We review the pathogenesis of EP, differentiate it from plaque psoriasis, identify the risk factors for SCLS, and discuss therapeutic considerations. Clinicians managing patients with severe psoriasis should remain vigilant for the potential occurrence of SCLS, particularly in those presenting with acute EP. Additionally, careful consideration should be given to the selection of biologic agents in high-risk patients.

The human lung normally accommodates exercise-induced cardiac output increases mainly via recruitment of non-concomitantly perfused pulmonary capillaries. Recruitment is detectable by measuring the first-pass transpulmonary metabolism of [3]H-benzoyl-Phe-Ala-Pro, providing an estimate of functional capillary surface area (FCSA). Pulmonary arterial hypertension (PAH) results from luminal narrowing of small precapillary arterioles, reducing downstream perfused FCSA. We hypothesized that exercising PAH patients would not be able to recruit FCSA normally. We studied two patients with severe PAH. Despite exercising to maximal dyspnea, neither could recruit FCSA. These limited data are the first direct measurements of FCSA in exercising PAH patients.

Eosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus characterized by dysphagia and food impaction. Although uncommon, spontaneous esophageal perforation may occur, most frequently involving the distal esophagus and the gastroesophageal junction. These perforations are typically managed with surgical or endoscopic interventions. Early diagnosis and prompt initiation of treatment within the first 24 hours significantly reduce morbidity and mortality. The aim of this report is to demonstrate that gastroesophageal junction perforation secondary to eosinophilic esophagitis can be successfully managed conservatively, even in delayed presentations, and to contribute to the understanding of treatment strategies for this rare but potentially life-threatening complication. We report the case of a 35-year-old male with a 12-year history of EoE who presented to the emergency department with retrosternal pain, dyspnea, and hematemesis. Five days prior to presentation, he developed a sore throat and cherry-colored diarrhea after consuming grilled chicken and self-administered ibuprofen for symptom relief. Contrast-enhanced imaging and upper endoscopy revealed a perforation at the gastroesophageal junction. Due to the location of the lesion, endoscopic stenting or clipping was considered inappropriate. In the absence of signs of acute abdomen, mediastinitis, or significant fluid collection, a conservative management strategy was adopted. The patient was admitted to the intensive care unit and initially treated with intravenous ceftriaxone (2 g/day) and metronidazole (1.5 g/day), which were later changed to piperacillin-tazobactam (4.5 g every 6 hours) following infectious disease consultation. The patient remained clinically stable, and oral intake was initiated on day 6. Antibiotic therapy was discontinued on day 10, and the patient was discharged without complications. At the three-month follow-up, the patient reported recurrent and progressively worsening dysphagia. Control endoscopy performed at the previously visited center revealed a distal esophageal stricture preventing passage of the gastroscope; therefore, a 12-cm fully covered self-expandable esophageal stent was placed. The stent was removed 20 days later, and the patient remained asymptomatic during the subsequent six-month follow-up period. Spontaneous esophageal perforation secondary to EoE is a rare but potentially life-threatening complication. This case highlights that conservative management may be a viable alternative to surgical or endoscopic intervention not only in early-detected cases but also in carefully selected delayed presentations managed in a multidisciplinary setting. Long-term follow-up remains essential for the early detection and treatment of late complications, such as stricture formation.

Left ventricular noncompaction (LVNC) is a rare primary cardiomyopathy characterized by a failure of myocardial morphogenesis, resulting in a prominent, characteristic "sponge-like" trabeculated endocardial layer. Clinical presentation is classical for heart failure, ventricular arrhythmias, and systemic thromboembolism, which defines its severity. Here, we describe a 34-year-old male with no prior medical history who presented with progressive dyspnea and volume overload. On initial evaluation, severe biventricular failure, stage 3b chronic kidney disease (type 2 cardiorenal syndrome), and significant hemodynamic impairment were noted. Subsequently, contrast-enhanced transthoracic echocardiography (TTE) was consistent with the diagnosis of LVNC and identified multiple mural thrombi, including a 2 cm mobile apical thrombus. Coronary angiography revealed normal coronary anatomy. Following these findings, the patient was stabilized with intravenous diuretics and initiated on guideline-directed medical therapy (GDMT). Due to the high risk of sudden cardiac death and persistent low ejection fraction, he was discharged with a wearable cardioverter defibrillator and referred for advanced heart failure and transplant evaluation. Shifting focus to the underlying pathophysiology, thrombus formation in LVNC is unique. It goes beyond global systolic dysfunction; the deep intertrabecular recesses create stasis that predisposes to fibrin deposition regardless of wall motion. This thrombogenicity necessitates a nuanced approach to anticoagulation. In summary, LVNC should be a primary consideration in young patients presenting with new-onset heart failure. This case underscores the necessity of imaging to identify obscured thrombi and highlights the evolving role of direct oral anticoagulants (DOACs) in managing the specific mechanical risks inherent to noncompacted myocardium.