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Refers to a communication between the nasal passageways.
It is usually discovered incidentally during clinical or radiological examination.
The communication occurs between nasal passageways via the cartilaginous or bony portions of the nasal septum.
Most patients are a symptomatic, as the process is mostly indolent, as demonstrated an NSP prevalence of 2% in an urban population undergoing computed tomography scans for other indications
Symptoms include nasal crusting and epistaxis commonly present in children, while in adults rhinorrhea and obstruction may manifest.
Its presentation varies with the size and location.
Anterior perforations commonly associated with whistling noise.
Posterior perforation is more likely to form asymptomatic scar tissue.
Most cases of NSP are iatrogenic, related to nasal surgery or procedures.
The nasal septum is made up of a trapezoidal plate of bone and cartilage with an overlying mucosal that extends posteriorly from the nasal vestibule to the choanae and lies perpendicular to the hard palate in the sagittal plane.
An anterior cartilaginous portion of the nasal septum abuts the posterior bony portion of the septum.
Anteriorly, the septal quadrangular cartilage lies superior to the small vomeronasal cartilage, whereas the perpendicular plate of the ethmoid bone sits above the vomer bone posteriorly.
Bony crests from the maxilla and palatine bone contribute to the posterior-inferior bony septum.
The septum comprises the nasal mucosa overlying the anterior and posterior perichondrium.
Diagnose of an NSP is best achieved with direct visualization of the perforation.
Caudal nasal perforations can be seen directly with anterior rhinoscopy.
Illumination of one nostril with a flashlight and observation of the light beam in the other nostril increases the yield of this finding.
Perforation of the septum can result from any injury that separates the mucosa from the perichondrium or interferes with the tenuous blood supply of the septum.
The largest group of adult patients with symptomatic perforation have no obvious etiology, iatrogenic causes, especially septoplasty and nasal cautery/packing, account for most cases where a cause is identified.
Causes include:
Trauma
Surgical complications
Nose-picking
Placement of foreign objects.
Drugs and Toxins
Cocaine
Methamphetamine
Ketamine
Vasoconstrictors
Intranasal corticosteroids
Industrial irritants
Soda ash
Bevacizumab
Neoplasms
Nasal carcinoma
Multiple myeloma
Non-Hodgkin lymphoma
Natural killer cell/nasal cell lymphoma
Autoimmune and Inflammatory causes
Systemic lupus erythematosus
Granulomatosis with polyangiitis
Relapsing polychondritis
Immunoglobulin G4-related disease
Pyoderma gangrenosum
Takayasu arteritis
Rheumatoid arthritis
Mixed connective tissue disorder
Psoriatic arthritis.
Systemic sclerosis
Cryoglobulinemia
Crohn’s disease
Dermatomyositis
Sarcoidosis
Infections
Leprosy
Tuberculosis
Nontuberculous mycobacteria
HIV/AIDS
Histoplasmosis
Aspergillosis
Mucor
Environmental molds
Mucocutaneous leishmaniasis
Syphilis
Congenital Defects of Nasal Bones
Aside from surgery, nose-picking and its associated compulsive behavior, rhinotillexomania, is described in up to 17% of certain adolescent populations.
Septal hematomas due to trauma and posttraumatic abscesses are found predominantly in children.
Foreign bodies, are rarely associated with NSP.
Many drugs are linked with NSP, caused from vasoconstrictive ischemia to direct cytotoxicity.
Cocaine use is the most common etiology of NSP.
Chronic vasoconstriction leads to tissue necrosis of the perichondrium and periosteum.
Chemical substances used to cut cocaine may further contribute to septum damage.
Methamphetamine and ketamine, can also lead to NSP.
Septal perforation is associated with prolonged use of phenylephrine and oxymetazoline nasal decongestants, causing local vasoconstriction.
Bevacizumab, a monoclonal antibody that inhibits the expression of vascular endothelial growth factor A, is associated with NSP.
The prolonged use of nasal decongestants for more than5 days can induce rhinitis medicamentosa, and chronic use can induce nasal polyps and ethmoiditis.
Intranasal corticosteroids use May be associated with NSP, especially in female patients.
Beclomethasone is the intranasal corticosteroid that commonly causes crusting and epistaxis before perforation.
The exposure to industrial agents chromium compounds, copper, arsenic, soda ash and nickel may cause NSP.
Non-Hodgkin lymphomas, skin carcinomas, melanoma have been described as causes of NSP.
Autoimmune disorders associated with vasculitis of the nasal mucoperichondrium and periosteum, can lead to NSP.
Among the autoimmune processes Granulomatosis with polyangiitis (GPA) is the leading cause of perforations, followed by relapsing polychondritis,and systemic lupus erythematosus, accounting for 48%, 26% and 6%, respectively.
An extreme form of NSP is the saddle-nose deformity, which occurs when the nasal bridge support mechanisms are eroded and external deformity results.
Immunoglobulin G4-related disease May be associated with sinonasal compromise.
Mycobacterium leprae is the most common mycobacterium causing NSP, with the nasal mucosa being involved in up to 95% of patients with leprosy.
Clinical manifestations of leprosy can range from epistaxis to NSP to total destruction of the nasal septum.
Primary nasal tuberculosis has been a rare event.
AID related NSP due to infections.
Rarely, tertiary syphilis can destroy the cartilaginous portion of the septum.
The History and physical examination are the most diagnose its presence.
History obtained regarding prior surgeries, trauma to the nose, drug use, and any rheumatologic/autoimmune symptoms.
Direct visualization is usually diagnostic.
Biopsy of the edge of a septal perforation has value, but the correlation between clinical and histological findings in patients with NSP or ulcers is poor.
In appropriate clinical setting, chest radiography, rheumatological or infectious diseases laboratory tests, and serum levels of IgG4 may be valuable to diagnose the etiology of NSP.
Management: Asymptomatic NSP with stable lesion usually requires no intervention.
Prevention of progression of the initial disease process.
Surgical repair of the septal defect. Asymptomatic NSP with stable size usually requires no intervention.
Treatment with cyclophosphamide and prednisone can frequently cause disease remission in patients with sinonasal and systemic manifestations of Granulomatosis with polyangiitis.
High-dose prednisolone in combination with oral corticosteroid maintenance has resulted in response in patients with IgG4-RD.
Surgical repair of septal perforation is mainly reserved for patients with obstructive symptoms, airflow disturbances, and nasal whistling.
Surgical techniques include septal repair ranging from conservative therapy with nasal saline, topical petroleum jelly, saline irrigation to aggressive repair with vascularized local flaps to restore continuity of intranasal contours and reducing turbulent airflow.