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Communication Stations
Published in Adnan Darr, Karan Jolly, Jameel Muzaffar, ENT Vivas, 2023
Wai Sum Cho, Anna Slovick, Jameel Muzaffar, Adnan Darr
Part 2: Examination reveals a large septal perforation with friable mucosa and no ulceration. A saddle nose deformity is also notedPlease explain the next steps to the patient in terms of investigationPoints to cover: Blood testsUrinalysisChest X-rayPossible need for a biopsy depending on the results of the blood tests
Granulomatous Conditions of the Nose
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Topical nasal treatment such as douching, intranasal steroids and nasal lubricants may be helpful for symptomatic relief. Surgery is generally reserved for cases that are refractory to medical treatment, or for complications of GPA. Rhinoplasty to correct a saddle nose deformity should be deferred until the disease has been in remission for at least 1 year. Grommets are best avoided because of the risk of chronic otorrhoea.
Nose
Published in Ali Pirayesh, Dario Bertossi, Izolda Heydenrych, Aesthetic Facial Anatomy Essentials for Injections, 2020
Dario Bertossi, Fazıl Apaydın, Paul van der Eerden, Enrico Robotti, Riccardo Nocini, Paul S. Nassif
Saddle nose deformity: This can be a consequence of aggressive primary surgery. If a CT scan shows a structural connection of the nasal dorsum anatomy the shape can be corrected by illing the saddle area. First, define the tip projection; then filling runs from nasion to dorsum. The injection sequence is Nt, Na, Nd, St. If there are dorsal structural voids, such as exaggerated scarring or mucosal defects, filler should not be injected because of the deficiency of the structural integrity of the scaffold. The only procedure that can solve this complication is a secondary rhinoplasty.
Reconstructive rhinoplasty using cadaver cartilage in relapsing polychondritis
Published in Baylor University Medical Center Proceedings, 2023
Rishabh Shah, Eugene L. Alford
Relapsing polychondritis is a rare autoimmune disorder that primarily affects cartilaginous structures of the upper airways. It is characterized by recurrent episodes of inflammation leading to progressive anatomical deformation with cosmetic and functional impairment of the auricular cartilage, nasal cartilage, and respiratory tract.1 Patients may experience nasal stuffiness, rhinorrhea, and epistaxis. The bridge of the nose and surrounding tissue become erythematous, edematous, and tender and may collapse, producing a saddle nose deformity. The pathologic basis of the saddle nose is represented by a substantial loss of the dorsal height along with middle vault depression, internal nasal valve insufficiency, columellar retraction, loss of tip support, shortened vertical length, and overrotated tip.2 Nasal reconstruction can be challenging due to impaired wound healing and impaired graft integration that is caused both by the disease and by prolonged immunosuppressant treatment.3 Several types of reconstruction techniques have been used in the correction of saddle nose deformity, including autologous rib cartilage, fascia lata, and calvarial bone grafts. Costal and calvarial bone were the most used graft materials in an analysis done by Ezzat et al in 2017.4 In this case report, we present a patient with a history of relapsing polychondritis in whom cadaver cartilage was used for reconstruction.
Chronic Anterior Uveitis Associated with Relapsing Polychondritis: A Case Report
Published in Ocular Immunology and Inflammation, 2020
Yahui Wei, Ying Chi, Yuan Fang, Di Wu, Ronghua Qiao
It has been reported that the rate of misdiagnosis of RP is 47%, and the mean delay in the time from symptom onset until diagnosis is 14.4 months with a range of 8 days to 14 years.4 The ocular manifestations of RP were not characteristic. When RP presents with joint symptoms, it may be misdiagnosed as adjuvant arthritis or seronegative spondyloarthropathy. This patient presented with chronic anterior uveitis and additional joint symptoms with no characteristic findings; thus, making a prompt and proper clinical diagnosis was challenging. In this case, when the patient first presented to an ophthalmology outpatient clinic, important signs related to her saddle nose were overlooked. It is important for ophthalmology practitioners to be vigilant in observing the systematic manifestations of RP because the eyes are sometimes the initial organ involved. Early diagnosis and intervention may significantly improve the clinical outcome.
Relapsing polychondritis: state-of-the-art review with three case presentations
Published in Postgraduate Medicine, 2021
Bogna Grygiel-Górniak, Hamza Tariq, Jacob Mitchell, Azad Mohammed, Włodzimierz Samborski
Differentials depend on the organ involved in the course of RPC (Table 3). An auricular chondritis with sparing of the lobule is relatively unique to RPC. Infectious perichondritis can look similar except that the lobule is involved as well. The most common pathogen to cause it is due to Pseudomonas aeruginosa or Staphylococcus aureus [4,5]. The auricular deformation can be caused by trauma, leprosy, leishmaniasis, and frostbite[62]. Saddle nose deformity can be caused by trauma, leprosy, congenital syphilis, septal hematoma, perforation induced by cocaine inhalation, sarcoidosis, and granulomatosis with polyangiitis (GPA)[63]. Ocular inflammation can be seen in rheumatoid arthritis, polyarteritis nodosa, sarcoidosis, Behçet’s disease, systemic lupus erythematosus (SLE), seronegative spondyloarthropathies. Symptoms of respiratory tract involvement can be confused with asthma or bronchitis. The stenosis of the airway also occurs in GPA, sarcoidosis, and amyloidosis. Aortic or mitral regurgitation and aortic aneurysms can be present in several vasculitis diseases such as (giant cell arteritis, Takayasu’s disease, or Behçet’s disease), syphilis (syphilitic aortitis), genetic disorders (Marfan’s and Ehlers–Danlos syndrome)[10]. GPA and RPC are two conditions that overlap, and they can mimic the other in terms of clinical presentation (e.g. GPA can cause ocular inflammation, septal perforation, polyarticular arthritis, and hearing loss). Differentiating GPA features include sinusitis, parenchymal lung disease, renal involvement, c-ANCA positive serology, and epithelioid cell granulomas in biopsy [64,65].