Pathophysiology of nasal congestion

Abstract

Nasal congestion is a common symptom in rhinitis (both allergic and nonallergic), rhinosinusitis and nasal polyposis. Congestion can also be caused by physical obstruction of nasal passages and/or modulation of sensory perception. Mucosal inflammation underlies many of the specific and interrelated factors that contribute to nasal congestion, as well as other symptoms of both allergic rhinitis and rhinosinusitis. A wide range of biologically active agents (eg, histamine, tumor necrosis factor-alpha, interleukins, cell adhesion molecules) and cell types contribute to inflammation, which can manifest as venous engorgement, increased nasal secretions and tissue swelling/edema, ultimately leading to impaired airflow and the sensation of nasal congestion. Inflammation-induced changes in the properties of sensory afferents (eg, expression of peptides and receptors) that innervate the nose can also contribute to altered sensory perception, which may result in a subjective feeling of congestion. Increased understanding of the mechanisms underlying inflammation can facilitate improved treatment selection and the development of new therapies for congestion.

Keywords: allergic rhinitis; congestion; obstruction; pathophysiology; rhinosinusitis.

Figure 1

Clinical data support a role for leukotrienes as mediators of congestion in allergic rhinitis. A) Cysteinyl leukotrienes (cys-LT) can be recovered at elevated levels in nasal secretions with increased allergen dose exposure in patients with allergic rhinitis. ^aVersus baseline. ^bVersus previous pollen dose and baseline. Adapted with permission from Creticos PS, Peters SP, Adkinson NF Jr, Naclerio RM, Hayes EC, Norman PS. Peptide leukotriene release after antigen challenge in patients sensitive to ragweed. N Engl J Med. 1984;310(25):1626–1630. Copyright © 1984 Massachusetts Medical Society. All rights reserved. B) Challenge with cysteinyl leukotriene increases nasal airway resistance (NAR). ^aP < 0.05 vs baseline. Adapted with permission from Okuda M, Watase T, Mezawa A, Liu CM. The role of leukotriene D4 in allergic rhinitis. Ann Allergy. 1988;60(6):537–540. Copyright © 1988 American College of Allergy, Asthma and Immunology.

Figure 2

Increased levels of inflammatory cytokines and total protein are found in nasal lavage fluids from patients with acute rhinosinusitis compared with healthy controls. ^aP ≤ 0.011 vs controls. Drawn from data of Repka-Ramirez et al.

Figure 3

Inflammation associated with chronic rhinosinusitis (CRS) and chronic rhinosinusitis with nasal polyps (CRS-NP). A) Levels of eicosanoid leukotrienes C₄, D₄, and E₄ (LTC₄/D₄/E₄) were significantly higher in nasal tissue taken from CRS and CRS-NP patients compared with healthy controls. ^aP < 0.05 vs controls. ^bP < 0.05 vs CRS. B) Levels of eosinophil cationic protein (ECP), a marker of eosinophilic inflammation, were significantly higher in nasal tissue taken from CRS and CRS-NP patients compared with healthy controls. ^aP < 0.05 vs controls. ^bP < 0.02 vs controls. Drawn from data of Pérez-Novo et al.

Figure 4

Inflammatory mediators and markers of nasal congestion in inferior turbinate tissue of control (those without polyps) and nasal polyposis (NP) patients. A) Patients with NP show significantly increased levels of interleukin (IL)-5, a proinflammatory cytokine, compared with controls. B) Patients with NP have increased levels of eosinophil cationic protein (ECP), a marker of eosinophilic inflammation, compared with controls. NP patients were grouped on the basis of the presence of specific immunoglobulin E (IgE) antibodies in tissue: NP I, undetectable specific IgE; NP II, selected specific IgE; and NP III, multiclonal IgE. The box-and-whisker plot represents the median, the lower to upper quartile, and the minimum to the maximum value, excluding outside and far-out values, which are displayed as separate points. Adapted from J Allergy Clin Immunol, Vol 107, Bachert C, Gevaert P, Holtappels G, Johansson SG, van Cauwenberge P, Total and specific IgE in nasal polyps is related to local eosinophilic inflammation. Pages 607–614. Copyright © 2001, with permission from Elsevier.

Figure 5

Generation of nasal symptoms through neural pathways. Sensory nerves can be stimulated by products of allergic reactions and by external physical and chemical irritants. Signals are transmitted to the central nervous system (CNS), where they can trigger sensations (pruritus) and can further travel through secondary synapses to activate efferent motor (sneezing) and autonomic neurons. Action potentials traveling through parasympathetic efferent nerves can lead to glandular activation and rhinorrhea, as well as to some vasodilatation. Suppression of sympathetic neural output, on the other hand, results in vasodilatation and nasal congestion. Antidromic stimulation of sensory nerves with release of tachykinins and other neuropeptides at the nasal mucosa contributes to symptom development with glandular activation, vasodilatation, and plasma extravasation. Neuropeptide release can also lead to leukocyte recruitment and activation. Collectively, events generated by the antidromic stimulation of sensory nerves constitute the phenomenon of “neurogenic inflammation”. Reprinted from J Allergy Clin Immunol, Vol 118, Sarin S, Undem B, Sanico A, Togias A, The role of the nervous system in rhinitis, Pages 999–1016, Copyright 2006, with permission from American Academy of Allergy, Asthma and Immunology.