Pharyngolaryngeal dysfunction associated with myopathy is not well characterized. We present a case of toxic or inflammatory myopathy causing severe vocal fold hypomobility and dysphagia, with complete recovery. A 47-year-old female with tuberous sclerosis, lymphangioleiomyomatosis, and a recent upper respiratory infection, taking atorvastatin and, until recently, everolimus, presented with several weeks of myalgias and 10 days of dyspnea. Examination demonstrated full extremity strength and inspiratory stridor. Flexible laryngoscopy revealed severely hypomobile bilateral vocal folds with pooled pharyngeal secretions. Creatine phosphokinase (CK) was >40,000 U/L at presentation. Rheumatology workup was negative. Magnetic resonance imaging of the brain demonstrated enhancement of facial and cervical musculature. Computed tomography of the neck showed new laryngeal muscle heterogeneity. Neither identified vagal or laryngeal nerve pathology. Treatment included high-dose dexamethasone, racemic epinephrine, albuterol, intravenous fluids, a temporary feeding tube, and discontinuation of atorvastatin and lisinopril. By hospital day 14, CK decreased to 1,420 U/L, and vocal fold motion had significantly improved. At one-month follow-up, vocal fold mobility normalized, symptoms resolved, and CK was 320 U/L. Extended myositis antibody panel at four-month follow-up was negative. Recovery was sustained at seven months. This case suggests pharyngolaryngeal musculature can be preferentially affected in acute myopathy.

Ganglioneuromas are uncommon benign tumours derived from neural crest cells and composed of mature ganglion and Schwannian stromal elements. They most frequently arise in the posterior mediastinum and retroperitoneum, while cervical involvement is rare. Although ganglioneuroma may occur in association with neurofibromatosis type 1, such presentations are infrequently reported. Surgical excision is generally curative; however, postoperative sympathetic dysfunction, including Horner syndrome, may occur because of the close anatomical relationship of these tumours to the cervical sympathetic chain. We report the case of a 24-year-old woman with sporadic neurofibromatosis type 1 who presented with right-sided neck pain and temporomandibular discomfort. Clinical examination revealed a firm, non-tender, non-pulsatile mass in the right anterior cervical triangle, with preserved vocal cord mobility on flexible nasoendoscopy. Magnetic resonance imaging demonstrated a well-circumscribed fusiform lesion within the right carotid space extending from C1 to C6, with anterolateral displacement of the common carotid artery and splaying of the carotid bifurcation, consistent with a neurogenic tumour. Following multidisciplinary discussion, the lesion was excised via a transcervical approach. Histopathological examination confirmed ganglioneuroma with degenerative changes and no malignant features. Postoperatively, the patient developed ipsilateral ptosis and miosis consistent with Horner syndrome. Ophthalmological assessment confirmed sympathetic dysfunction. Her symptoms gradually resolved, with complete recovery by six months. Follow-up magnetic resonance imaging demonstrated no residual or recurrent disease, and serial imaging over four years showed no recurrence and stability of a smaller contralateral lesion. This case highlights cervical ganglioneuroma as a rare differential diagnosis for carotid space masses in patients with neurofibromatosis type 1. Although complete excision offers an excellent prognosis, careful preoperative counselling and operative planning are essential because of the risk of temporary sympathetic chain dysfunction, particularly in lesions extending toward the skull base.

Severe asthma represents a clinically challenging proportion of the asthma population, characterized by persistent symptoms, frequent exacerbations, and a higher healthcare burden. To address the complexity of uncontrolled disease, specialized severe asthma clinics have emerged as key models for delivering precision medicine through multidimensional assessment and tailored interventions. This paper describes the organization, clinical approach, and multidisciplinary framework of a tertiary Severe Asthma Centre established in Northern Italy in 2017. The center integrates prioritized outpatient access with a structured day-hospital program (Complex Outpatient Macro Activity, MAC), enabling accelerated diagnostic work-up, comprehensive phenotyping/endotyping, and repeated educational interventions. Central elements include confirmation of diagnosis, assessment of type 2 inflammatory biomarkers (FeNO, IgE, blood and sputum eosinophils), evaluation of airway inflammation, and systematic identification of pulmonary and extrapulmonary treatable traits. A broad multidisciplinary network supports the management of comorbidities such as allergic rhinitis, chronic rhinosinusitis, hypereosinophilic disorders, allergic bronchopulmonary aspergillosis, metabolic and endocrine complications, gastroesophageal reflux disease, and vocal cord dysfunction. Pulmonary rehabilitation is integrated as an adjunctive intervention, particularly for patients with severe disease. Our severe asthma clinic implements precision medicine and the treatable traits approach in clinical practice to optimize outcomes, rationalize biologic therapy use, and reduce glucocorticoid exposure. Future perspectives include expansion toward a "united airways disease" clinic, integrating upper and lower airway management to further improve care for complex inflammatory airway diseases.

Peri-extubation airway complications such as coughing, laryngospasm and oxygen desaturation remain common during emergence from general anaesthesia and may contribute to postoperative morbidity. Lidocaine is widely used to reduce airway reactivity during extubation; however, evidence comparing intravenous and topical administration routes in adults remains limited. In particular, little evidence exists regarding topical lidocaine gel applied at the time of endotracheal intubation. This trial aims to compare intravenous lidocaine with topical lidocaine gel for prevention of peri-extubation airway complications in adults undergoing elective orthopaedic surgery.

Interscalene brachial plexus block (ISB) is commonly used for shoulder surgery and is associated with predictable complications such as phrenic nerve palsy due to its proximity to adjacent neural structures. While the spread of local anesthetic may involve the recurrent laryngeal nerve, resulting in vocal cord dysfunction, which is uncommon, progression to bilateral vocal cord paralysis, causing acute airway obstruction, is exceedingly rare. A 74-year-old obese female underwent elective outpatient right shoulder arthroscopy under ultrasound-guided interscalene block with bupivacaine. Within hours postoperatively, she developed progressive respiratory distress. Despite high-flow oxygen and bag-valve-mask ventilation, oxygen saturation declined into the 60s with marked resistance to ventilation. Emergent intubation resulted in immediate improvement. Point-of-care ultrasound demonstrated diffuse B-lines without right heart strain, and imaging confirmed pulmonary edema. Workup did not reveal a primary pulmonary or obstructive cardiac etiology; however, troponin elevation consistent with type 2 myocardial infarction was identified. The patient improved rapidly with ventilatory support and diuresis, was extubated within 48 hours, and was discharged without recurrence. This case demonstrates a rare complication of ISB involving sequential spread of local anesthetic, potentially facilitated by arthroscopic fluid extravasation, leading to phrenic nerve involvement and bilateral recurrent laryngeal nerve dysfunction. Resultant airway obstruction caused negative pressure pulmonary edema and secondary demand ischemia. Resistance to ventilation and refractory hypoxemia after ISB should raise concern for upper airway obstruction. Early airway management is critical to improve outcomes.