Abstract:

Acute rhinosinusitis (ARS) is an acute, diffuse inflammation of the mucosa lining the 
nasal cavity and paranasal sinuses (sphenoidal, maxillary, frontal). It is commonly caused by 
infectious agents (viruses and bacteria), but can also have allergic, vasomotor, toxic, or chemical 
origins. ARS is a significant cause of morbidity in the pediatric population, with a healthy child 
suffering from upper respiratory tract infections (URTIs) 6 to 10 times a year. The primary 
pathogenic mechanism in ARS is the partial or complete obstruction of the sinonasal ostia. Stenosis 
disrupts mucociliary clearance and ventilation. This blockage results from arterial vasodilation and 
an active cellular reaction, leading to hyperemia, edema of the nasopharyngeal and paranasal 
mucosa, and glandular hypersecretion. These processes are precisely orchestrated by biologically 
active substances (BAS), known as inflammatory mediators. These mediators are of cellular 
(histamine, serotonin, chemotactic factors, Arachidonic acid metabolites including Pg, TX, LT, and 
interferon gamma) or plasma origin. Many are activated in a cascade, multiplying their effects. 
Detailed knowledge of the stages and mediators of acute inflammation is essential for ensuring 
adequate pathogenetic and symptomatic treatment. In children, ARS presents with local symptoms 
such as nasal obstruction, rhinorrhea, cough, reduced smell, and periorbital puffiness. General 
symptoms like fever and headache may also be present. Since these symptoms overlap with other 
childhood conditions (e.g., adenoid vegetation, allergic rhinitis, viral infection), differential 
diagnosis is necessary. Diagnosis is based on detailed history, physical status, paraclinical tests 
(CBC, CRP, ESR), virological/microbiological analysis of secretions, and imaging.

 
Keywords: Acute rhinosinusitis, pathophysiology, children, inflammation mediators, nasal 
obstruction.  

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