4 Nasal Perforation Etiology

10.1055/b-0037-145023

4 Nasal Perforation Etiology

Mauricio López-Chacón, Arturo Cordero Castillo, Cristobal Langdon, Francesca Jaume, Isam Alobid

Summary

The etiology of nasal septal perforation (NSP) is very variable; the most common cause is traumatic postsurgical procedure. However, the presence of an NSP could also be the first clinical manifestation of a systemic inflammatory disease such as granulomatous polyangiitis, sarcoidosis, lupus erythematosus, neoplasia, or infection. An adequate medical history and physical examination are the most relevant tools when establishing the differential diagnosis. Complementary tests that can also aid in the diagnosis include laboratory tests (complete blood cell count [CBC], specific antibodies), imaging tests (computed tomographic [CT] scans), or biopsies.

4.1 Introduction

Nasal septal perforation (NSP) is defined as a communication between the two nasal cavities secondary to a defect in any portion of the mucosa, submucosa, and the perichondrium, as well as in the osteocartilage septum (Fig. 4‑1). NSP can have an iatrogenic or pathological origin. ¹ ^, ²

Fig. 4.1 Endoscopic view of nasal septal perforation.

Previous studies report that the approximate prevalence of NSP in the general population is 1%, although its exact prevalence is difficult to determine. ³ ^, ⁴ Between 15 and 39% of patients with NSP do not experience any symptoms and are diagnosed during a routine ENT (ear-nose-throat) examination. ¹ ^, ⁵ The localization and the size of the perforation can influence in the presence of symptomatology. ¹

Regarding the localization of the nasal perforations, 92% are located in the anterior portion of the septum and 8% are either posterior or superior. ⁴ Anterior perforations are more frequently caused by trauma and are usually associated with more symptomatology, whereas posterior or superior perforations are mostly associated with systemic diseases.

The most frequent symptoms associated with NSP include epistaxis (58%), crusting (43%), obstruction (39%), pain (17%), and whistling (15%). ¹ ^, ⁴

The etiology of NSP is very variable. The most common are traumatic secondary to bilateral laceration of the septal mucosa during septoplasty. ² ^, ⁵ ^, ⁶ However, the presence of an NSP could also be the first clinical manifestation of a systemic inflammatory disease such as granulomatous polyangiitis, sarcoidosis, lupus erythematosus, neoplasia, or infeccions. ³ ^, ⁶ ^, ⁷ ^, ⁸ Nowadays there has been an increase in NSP prevalence secondary to the consumption of licit and illicit intranasal drugs. ³

The authors discuss the pathogenesis and principal causes of NSP, including traumatic, nasal drug use, occupational exposure, and neoplasia. Systemic causes are discussed in greater detail in s. Kap..

4.2 Pathogenesis

The nasal septal mucoperichondrium is in charge of providing blood supply to the quadrangular cartilage. NSP usually occurs when there has been an interruption in the vascular supply in both sides of the septal mucosa at almost the same location. ¹ ^, ⁴ ^, ⁵ ^, ⁸

Four stages have been described in the development of NSP. The first stage consists in mucosal irritation accompanied with rhinorrhea. During the second stage, a blanching occurs at the anterior-inferior portion of the septal mucosa at the Kiesselbach area, which has less vascularization and increased adherence to the cartilage. This inflammatory process leads to the production of crusting and nasal picking, which increases the risk of infection in the affected area. During these initial steps there is also a loss of the mucosal and submucosal layer, without affecting the perichondrial layer. If the mucosal layer does not regenerate adequately, a loss of the perichondrial layer occurs followed by ulceration and necrosis of the septal cartilage. The borders of the perforation are covered with atrophic epithelium that is more susceptible to bleeding and crust formation. This is also affected by the change in airflow. If no other insults occur, the border cicatrization is produced in approximately 3 months. ¹ ^, ⁴ ^, ⁵ ^, ⁸

4.3 Etiology

In the following paragraphs the different local etiologies associated with NSP are discussed in greater detail. As shown in Table 4‑1, the etiologies can be grouped in traumatic, intranasal drugs use and neoplasms. Systemic diseases (inflammatory and infectious) are discussed in s. Kap..

Table 4.1 Causes of nasal septal ulcerations (modified from ⁴ ^, ⁸ )
Nasal septal perforation
Traumatic/iatrogenic	Septal surgery Chemical cautery Nasal packing Nasogastric probe Nasal fracture Foreign body Self-inflicted
Nasal drug abuse	Decongestant Corticoids Cocaine
Occupational exposure	Chemical irritants Physical irritants Heavy metal
Inflammatory	Wegener’s granulomatosis Sarcoidosis Systemic lupus erythematosus Rheumatoid arthritis Crohn’s disease Dermatomyositis Sarcoidosis
Infectious	Syphilis HIV Fungal infections Leprosy Tuberculosis
Neoplasms	Non-Hodgkin lymphoma Squamous cell carcinoma Adenoid cystic carcinoma Basal cell carcinoma Esthesioneuroblastoma Rhabdomyosarcoma
Abbreviation: HIV, human immunodeficiency virus.

4.3.1 Traumatic Causes

Some studies report that the prevalence of traumatic NSP is around 39% of the total amount of NSP. ⁵ Self-inflicted trauma, accidental trauma, or medical procedure-related trauma are the most common causes. ⁵

Approximately 1 to 8% of nasal septoplasties are complicated with NSP. ⁹ It should be highlighted that a higher percentage (~17%) has been reported with submucosal nasal septum resection technique. ⁶

Studies performed in cadavers have determined that the major mechanical tensile strength of the septal lining is localized in the perichondrial layer. Therefore, a correct dissection of the subperichondrial plane during septal surgery provides a stronger septal flap and may prevent the development of NSP during nasal surgery. ¹⁰

Other important factors that should be taken into account during a septoplasty is the precarious irrigation of the quadrangular cartilage, because the risk of NSP increases if the blood supply is disrupted on both sides of the mucosa in approximately the same area. ¹

Allergic rhinitis (AR) has also been associated with an increased risk of NSP following septoplasty due to the mucosal epithelial damage during the allergic season. However, this has not been proven when comparing the incidence of NSP after septoplasty between patients with and without AR. ¹¹

Different suture techniques have been developed to prevent postsurgical complication after nasal packing and nasal splints. ¹² Many studies have concluded that the risk of synechiae, and hematomas are lower when using nasal splints and suturing compared with nasal packings. ¹² However, those studies have not found significant differences when comparing the use of nasal packing, haemostatic suturing techniques, and nasal splints to prevent the formation of NSP or infections. ⁹ ^, ¹²

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