Ear inflammation simulating those occurring in Relapsing Polychondritis may be secondary to an acute phylogenic or a chronic glaucomatous infectious process. The absence of regional lymphadenopathy should trigger the suspicion of a noninfectious process. It is important to note: The expression of auricular cellulitis and chondritis following even minor burns or trauma may be delayed. In some cases by weeks. Occurring at the sites that have long since healed.
TB
Trauma to the pinna
Trichoepithelioma
Toxic Epidermal Necrolysis
Auricular calcification-secondary to other conditions such as:
Addison disease
Diabetes Mellitus
Hypertension
Ochronosis
Acromegaly
or other conditions:
Benign nodular deformity - chondrodermatitis
chronica helices
over-exposure to:
sunlight
extreme cold
Inflammatory Arthritis
Collagen Vascular Disorder
Gonococcal Maturaopathy
Polyarthritis nodosa
Reiter's syndrome
Rheumatoid arthritis
Rheumatic fever
Wegener's granulomatosis
Eye Inflammation (Ocular)
Ocular inflammation, audiovestibular dysfunction, and polyarteritis may be seen in system narcotizing forms of vasculitis such as: Polyarthritis Nodosa, Wegener's Granulomatosis, Cogan's syndrome and Behcet's disease.
A useful differentiating feature is the absence of mucosal inflammation in Relasping Polychondritis..
Carinoma
Congenital Syphilis
Infectious Glaucomatous
Lesion
Infectious Perichondritis
Lethal Midline Granuloma
Lyphomatoid Granulomatosis
Lymphosarcoma
Wegener's Granulomatosis
Tracheal Involvement
Tracheal Obstruction
Prolonged Intubation
Sacroidosis
Trauma (e.g. Strangulation)
Wegener's Granulomatosis
Respiratory Tree Chondritis
Actinomycosis
Anthrax
Blast mycosis
Diptheria
Measles
Scarlet fever
Small Pox.
Tuberculosis
Typhus
Vincent Infection
Wegeners Granulomatosis
Airway narrowing can result from either an intrinsic lesion and/or extension or compression afforded by an extrinsic process.
Epiglottitis must always be considered when suspecting an upper airway obstruction. The cheif complaint is invariably the sudden onset of a severe sore throat in a previously healthy individual. Death may quickly ensue if the diagnosis is not promptly established and appropriate therapy instituted.
The larynx and tracheobronchial tree may be involved in the subglottic regions of the larynx in this disorder.
The larynx may rarely be involved in pemphigus valgarus, the suparglottic region having an erythematosus appearing ulcerated mucosa with a fibrinous exudate.
Larnygeal lesions have been reported in 10 percent having cicatricial pemphigoid.
Bullae or ulcers mainly occur on supraglottic structures and may be associated with odynophagia.
Infectious and nonifectious mediastinal lesions (such as tuberculosis, histoplasmosis and acidosis) may be associated with chronic inflammation, thickening and stenosis of the tracheal wall. Mediastinal lymphadenopathy has not been described in Relapsing Polychondritis..
Neoplastic disease
Rare tracheobronchapathia osteochondroplastica chartterized by Osseo artilaginous mucosal nodules which project into the lumen of the larrynx, trachea and bronchi.
Rhinoscleroma, a chronic glaucomatous disease caused by Klebsiella rhinoscleromatis, is endemic to Asia, Africa and South Africa. It may progress to a cicatricial stage with dense fibrotic narrowing of the larynx in this disorder.
Saber-sheath trachea associated with chronic obstruction pulmonary disease.
This page was last updated on: September 21, 2007
Relapsing Polychondritis is distinguished from other diseases by the co-existence of usually widespread potentially destructive inflammatory lesions involving cartilaginous structures throughout the body, organs of special sense, and the cardiovascular system. However, the variable, unpredictable expression of clinical features over time may make the diagnosis difficult to establish.
Deep chest wall burns (particularly of electrical origin)
Fungal infection
Pyogenic organisms
Tietze's Syndrome
Tuberculosis
Viral infection
Wegener'sGranulomatosis (WG)
May be particularly difficult to distinguish from RPC because of the potential of additional shared expressions of auricular chrondritis, saddle nose deformity, laryngotracheal broncial disease, glomerulonephritis, nervous system involvement, and the presence of ANCA. The correct diagnosis must be established by histologic means and by recognition of more specific clinical features such as cavitary lung lesions in WG, and diffuse dynamic tracheobronchial collapse and aortic aneurysms in RPC. An overlap is the most plausible explanation when discriminating data does not allow differentiation.
