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4
Medical Management of Rhinologic
Disorders in the Rhinoplasty Patient
C. Spencer Cochran Bradley F. Marple
Although some patients undergo rhinoplasty for cosmetic reasons, many pa-
tients seek initial surgical evaluation for correction of functional problems with
the nose, such as nasal obstruction or congestion. e nose performs six key
functions of the upper airway: respiration, olfaction, humidication, temperature modication, particle ltration, and phonation. Any of these nasal functions
can be altered or impaired by structural or functional abnormalities arising from
sinonasal disease processes, and functions that are aected by mucosal disease
are particularly important to the rhinoplasty surgeon.
A thorough understanding of nasal function and the impact of rhinologic disease
processes is crucial to the overall success of the rhinoplasty surgeon.
Nasal Disorders
Inammatory Disorders
Acute rhinosinusitis
Adenoid hypertrophy
Allergic fungal rhinosinusitis
Allergic rhinitis
Chronic rhinosinusitis
Deviated septum
Internal/external valve collapse
Nasal polyposis
Structural abnormalities
Turbinate hypertrophy
Noninammatory Disorders
Atrophic rhinitis
Nonallergic rhinitis
Rhinitis medicamentosa
Vasomotor rhinitis
Other or Systemic Disorders
Cocaine-induced destructive lesions
Sarcoidosis
Wegner’s granulomatosis
45
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INFLAMMATORY DISORDERS OF THE NOSE
AND PARANASAL SINUSES
e nasal mucosa and its mucociliary blanket act as the initial barrier to infection and environmental insult. us the intranasal mucosa and paranasal sinuses
are frequent sites of both allergic and nonallergic inammation. Nasal mucus
is a complex aqueous mixture of glycoproteins, lipids, salts, and other cellular
constituents that normally protects nasal epithelia. Aside from its function as a
simple mechanical barrier, nasal mucus likely plays an active role through inactivation of many substances that gain access to the nose. Understanding the
underlying pathophysiology of the inammatory disorders can improve the selection of treatments of these conditions and their impact on rhinoplasty patients
and outcomes.
Allergic Rhinitis
Allergic rhinitis has been estimated to aect million Americans, with health
care–related expenditures in the billions of dollars. Allergic rhinitis is a type
I allergic reaction in which allergen-specic immunoglobulin E (IgE) bound
to nasal mast cells interacts with an inhalant allergen to produce the following
symptoms of allergic rhinitis: sneezing, pruritus, congestion, rhinorrhea, and
nasal discharge. Although allergic rhinitis is still only partially understood, key
elements of its pathophysiology have been elucidated. Initially, an individual
who is susceptible to the development of allergic disease encounters a potential
allergen. Sensitization is the process in which the immune system is triggered to
recognize an allergen, ultimately leading to the development of T-lymphocytes,
B-lymphocytes, and allergen-specic IgE. On subsequent exposures, the same
allergen can simultaneously bind to two adjacent allergen-specic IgE molecules
on the surface of a mast cell, triggering degranulation of the cell and release of
histamine and other inammatory mediators. is reaction is referred to as
the early phase response and leads to the immediate onset of symptoms, such as
sneezing, rhinorrhea, and congestion. is process, in turn, leads to further recruitment of neutrophils, lymphocytes, and eosinophils. Once at the site of the
initial degranulation of the mast cell, these inammatory cells give rise to a selfsustaining inammatory reaction known as the late phase response, which is less
severe but more prolonged than the early phase response.
Treatment of allergic rhinitis begins with identication of and avoidance of the
allergen, which precludes the formation of antigen-specic IgE and eliminates the
initiation point of the allergic cascade. In reality, avoidance is dicult to achieve,
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Pharmacologic Agents for Allergic Rhinitis
Target erapy
Anticholinergics
Antihistamines
Antileukotrienes
Decongestants
Mast cell stabilizers
Mucolytic
Immunomodulation
Immunotherapy
Intranasal steroids
Systemic steroids
and patients must rely on medical management to treat their allergy symptoms.
Medical management of allergic rhinitis involves both target therapy and immunomodulation. Targeted forms of therapy (antihistamines, decongestants,
mucolytics, anticholinergics, antileukotrienes, and mast cell stabilizers) address
the mediator eects of allergy, whereas immunomodulation (topical or systemic
steroids, immunotherapy, and potentially monoclonal antibodies) prevents initiation and downregulates the allergic response.
Allergy may present as a single rhinologic disease, or it may coexist with or contribute to other rhinologic disease processes. For example, allergy produces mucosal edema, which may lead to sinusitis via ostial obstruction and set the stage
for secondary bacterial infection.
Allergic rhinitis may present as a single rhinologic disease, or it may coexist with
or contribute to other rhinologic disease processes.
Acute Rhinosinusitis
Acute rhinosinusitis (ARS) is an inammatory state involving the paranasal sinuses and intranasal mucosa. It is dened as a discrete infectious process that
lasts less than weeks. e diagnosis of ARS is established by a strong history
of two or more major factors, one major factor plus two minor factors, or nasal
purulence on examination. Allergy, structural abnormalities, cystic brosis, cilia
defects, viral or bacterial infections, and immunosuppression can contribute to
the development of ARS. Antibiotics and decongestants are the mainstays of
treatment for bacterial ARS.
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Acute Rhinosinusitis: Diagnostic Criteria
Major Criteria
Facial pain/pressure
Fever
Hyposmia/anosmia
Nasal discharge
Nasal obstruction
Purulence in nasal cavity
Minor Criteria
Headache
Dental pain
Fatigue
Fever
Halitosis
Otalgia/pressure/fullness
Rhinoplasty is generally contraindicated in the presence of active infection.
Chronic Rhinosinusitis
Chronic rhinosinusitis (CRS), an inammatory state diering in duration from
ARS, was formally dened in by the Task Force for Dening Chronic Rhinosinusitis as a “group of disorders characterized by inammation of the mucosa
of the nose and paranasal sinuses of at least weeks’ duration.” Although infection certainly may represent a component of CRS, it is becoming increasingly
clear that there is a multifactorial causation and interrelationship among many
of the inammatory disorders of the nose and paranasal sinuses. Treatment of
CRS is medical, with functional endoscopic sinus surgery (FESS) reserved for
treatment failures. Several studies indicate that sinus surgery at the time of rhinoplasty may be a viable option if there are no signs of infection.
Allergic Fungal Rhinosinusitis
Allergic fungal rhinosinusitis (AFS) is an immunologically mediated sinonasal
disease process rather than an infectious process. e inammation associated
with AFS is probably related to eosinophil chemotaxis and degranulation. e
diagnosis of AFS is established by the characteristics of IgE-mediated hypersensitivity, nasal polyposis, characteristic CT or MRI ndings, allergic fungal mucin, and positive fungal stain of sinonasal contents. Long-term control of allergic
fungal sinusitis requires both elimination of fungal antigen (usually requiring
surgery) and control of its recurrence through either immunomodulation (immunotherapy or corticosteroids) or fungistatic antimicrobials.
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Nasal Polyposis
Nasal polyposis is the end result of intranasal inammation and may present as
an isolated phenomenon, referred to as idiopathic nasal polyposis, or as a compo-
nent of other rhinologic diseases such as allergic fungal sinusitis. Samter’s triad
refers to nasal polyposis in addition to asthma and allergy or sensitivity to aspirin. Inammatory nasal polyposis is usually a bilateral disease and when unilateral
may signify a neoplastic process.
Treatment of nasal polyposis entails administration of antileukotrienes, topical
steroids, systemic corticosteroids, and oen debulking in a functional endoscopic
sinus surgical procedure. Although steroid nasal sprays are eective for the treat
ment of small nasal polyps and prevention of polyp regrowth aer nasal and sinus surgery, large polyp masses that essentially block the nasal passage will not
generally yield to topical therapy.
NONINFLAMMATORY RHINOLOGIC DISORDERS
Rhinitis Medicamentosa
-
Rhinitis medicamentosa refers to rebound rhinitis and congestion of the nasal
mucosa resulting from the sudden cessation of topical decongestants aer prolonged use. Treatment is supportive and entails absolute abstinence from further
topical decongestants. Topical steroid sprays and even systemic steroids may be
benecial to attenuate the mucosal hyperemia and edema.
Postrhinoplasty Rhinitis
Aer rhinoplasty, some patients complain of nasal obstruction. Beekhuis reported a % incidence of symptomatic nasal obstruction in his series of rhinoplasty patients. Treatment is oen expectant, but oral decongestants, topical nasal
steroid sprays, and nasal saline irrigation may be of use.
Atrophic Rhinitis
Overresection of intranasal structures such as the middle or inferior turbinate
can lead to atrophy of the nasal mucosa with subsequent symptoms of dryness,
crusting, and nasal obstruction. Nasal saline solution may provide symptomatic
relief.
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PHARMACOLOGIC AGENTS
Antihistamines
e histamine that is released from mast cells in the allergic response causes
vasodilation and an increase in vascular permeability. Early phase reactions to
histamine produce symptoms such as sneezing, rhinorrhea, and congestion. Late
phase reactions include eosinophil recruitment, cellular adhesion, and leukotriene eects.
Antihistamines are agents that have been developed to block the histamine that is
released in response to exposure to an allergen. First-generation antihistamines
competitively bind H-receptors and eectively attenuate the local eects of histamine. Unfortunately, their lipophilic nature allows them to cross the bloodbrain barrier and produce central nervous system side eects such as sedation,
decreased cognitive performance, decreased motor coordination, and impairment in central interpretation of vestibular input. In addition, rst-generation
antihistamines have anticholinergic eects such as xerostomia and urinary retention. Paradoxical stimulation by antihistamines may be seen in infants and
older patients.
e newer second- and third-generation antihistamines bind H-receptors noncompetitively, are lipophobic, and have minimal anticholinergic activity. As a
result, they are associated with fewer side eects, including less sedation, less
psychomotor depression, and fewer anticholinergic eects. ey do not demonstrate the phenomenon of antihistamine tolerance, or “tachyphylaxis,” which
had been observed with rst-generation compounds. Additionally, newer antihistamines also act directly on inammatory mediators, diminishing their production or negating their eects. Ecacy proles of later generation antihistamines
are similar to those of the sedating antihistamines with regard to the attenuation
of the irritative symptoms of allergic rhinitis, which include sneezing, pruritus,
and rhinorrhea; however, neither is ecacious in alleviating congestion.
,
For
this reason, antihistamines and decongestants such as pseudoephedrine are fre
quently combined.
Oral Antihistamines
First-Generation
Chlorpheniramine
Clemastine
Diphenhydramine
Hydroxyzine
Promethazine
Second- and ird-Generation
Cetirizine
Fexofenadine
Loratadine
Desloratadine
Norastemizole
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A move toward topical preparations in the treatment of allergic rhinitis has included the development of several antihistamines delivered in this fashion. e
rst intranasal antihistamine introduced in the United States was azelastine,
which appears to be equivalent to other antihistamines in potency. Unfortunately, a high incidence of taste perversion has been noted among patients using it. Topical nasal formulations of levocabastine have been introduced in the
United States, Canada, and Mexico. is preparation is said to be , times
more potent than chlorpheniramine, with duration of eect of hours or more
and few if any side eects.
Because of similar ecacy among older and newer generation antihistamines,
selection should be based on safety, cost, physician’s experience, and individual
preference.
Rhinoplasty patients who have symptomatic allergic rhinitis and who take antihistamines should continue their medication regimen in the perioperative period.
Decongestants
Decongestants exert a sympathomimetic eect via a-- and a--receptor stimulation. ey displace norepinephrine from presynaptic sympathetic receptors and
block the reuptake of norepinephrine, resulting in smooth muscle contraction
and vasoconstriction. Decongestants are available as topical agents or systemic
agents. Systemic formulations (pseudoephedrine and phenylpropanolamine)
achieve peak levels in to hours and have a half-life of to hours. ey are
administered alone or as a component in many over-the-counter cold and allergy
preparations. Additionally, decongestants may be formulated with prescription
antihistamines (for example, Allegra-D) to relieve nasal congestion, the allergic
symptom complex that is not addressed by antihistamines alone. As is the case
with over-the-counter combinations, the decongestant most commonly combined with an antihistamine is pseudoephedrine, in a total daily dose of to
mg.
Decongestants are not without their side eects. e most common side eect of
systemically administered decongestants is cardiovascular stimulation. Pseudoephedrine may produce somewhat less blood pressure elevation than the other
available systemic decongestants, although any decongestant may be used (albeit
with caution) in patients with stable, treated hypertension.
lar stimulatory eects of these drugs include tachycardia, palpitations, and even
arrhythmias. e central nervous system stimulation produced by decongestants
is generally manifested as anxiety and insomnia. Additionally, the stimulatory
side eects of systemic decongestants are enhanced by tricyclic antidepressants
,
Other cardiovascu-
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and MAO inhibitors. e potentiation by MAO inhibitors may persist for up to
weeks aer these drugs have been discontinued. us systemic decongestants
should be administered cautiously and in reduced doses in patients with hypertension, atherosclerotic coronary artery disease, and/or hyperthyroidism, in patients taking MAO inhibitors, and in patients with urinary retention.
Topical decongestants (oxymetazoline and phenylephrine) have an onset of action of minutes and a duration of more than hours. ey have a greater local
potency and fewer systemic eects compared with systemic decongestants. A
frequently encountered problem associated with prolonged use of topical decongestants is rhinitis medicamentosa; however, the risk of rhinitis medicamentosa
can be minimized by limiting topical decongestant use to just to days.
Topical and systemic decongestants may be a benecial symptomatic treatment
modality for patients aer septorhinoplasty to help reduce postoperative congestion and nasal obstruction.
e risk of rhinitis medicamentosa can be minimized by limiting topical decongestant use to just 3 to 5 days.
Nasal Saline Solution
Topical nasal saline solution has been used as an adjunct in the treatment of multiple rhinologic disorders as well as in the postoperative care of patients undergoing rhinoplasty or endoscopic sinus surgery. Saline facilitates the removal of
blood clots and secretions, particularly when nasal splints are in place. Anecdotal
evidence supports the ecacy of nasal saline solution. Although there have not
been many scientic studies addressing the use of nasal saline, Tomooka et al
reported a statistically signicant improvement in nasal symptoms in patients
with sinonasal disease who used nasal irrigation.
Anticholinergics
Topical anticholinergic preparations (ipratropium bromide) decrease parasympathetic tone locally to decrease watery rhinorrhea, a common complaint in patients with allergic rhinitis. However, anticholinergics do not reduce congestion,
irritation, itching, or sneezing. Ipratropium bromide is now available in .%
and .% strengths in a metered-dose pump spray for intranasal use. e .%
strength is primarily used to alleviate the initial rhinorrhea of the common cold,
whereas the .% concentration is used to control rhinorrhea caused by va-
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somotor rhinitis, perennial nonallergic rhinitis, perennial allergic rhinitis, and
gustatory rhinitis.
,
e most important factor is a sucient dose early in the day to control symptoms, with additional dosing as necessary. e recommended dosing regimen
is two sprays in each nostril in the morning on arising, with subsequent doses
of two sprays in midaernoon and in the evening, if needed. Oen the morning
dose alone suces. In these circumstances, the use of a topical anticholinergic
is not curative but will oen control symptoms that are extremely bothersome
to the patient. Side eects from topical nasal ipratropium are minimal, and its
long-term use does not appear thus far to present a problem.
Leukotriene Receptor Antagonists
Although histamine plays a signicant role as the primary culprit of the allergic
reaction, leukotrienes are a group of inammatory mediators that play a supporting role in sinonasal inammation. Leukotrienes, formerly referred to collectively
as slow-reacting substances of anaphylaxis, were isolated in and consist of a
family of inammatory mediators that are end-products of the arachidonic acid
cascade produced in response to degranulation of mast cells.
e biologic eects of the cysteinyl leukotrienes (LTC, LTD, LTE) can act to
trigger a number of processes important to inammation of respiratory mucosa,
including chemotaxis of inammatory cells (for example, neutrophils, lymphocytes, eosinophils), increased permeability of vessels, and vasodilation.
,
Identication of the leukotrienes as an important mediator of allergic inammation piqued interest in the potential that blocking their eect might have on the
allergic response. Leukotriene-modifying agents were rst found to have a positive eect in the control of asthma and then a benecial rhinologic application in
treating allergic rhinitis, aspirin sensitivity (Samter’s triad), and idiopathic nasal
polyposis. Several studies have proved their ecacy in alleviating the congestive
symptoms of allergic rhinitis as well as sneezing and rhinorrhea. Because they
improve mucus production and congestion, the treatment eect of a leukotriene
inhibitor with an H-antagonist may be additive.
Montelukast, a leukotriene receptor antagonist, acts to inhibit the action of leukotrienes at the end-organ receptor site. Studies comparing this preparation to
placebo have demonstrated a statistically signicant impact on both daytime and
nighttime symptoms of allergy. Moreover, this class of medications has demonstrated the ability to decrease the number of activated eosinophils resident within
inamed mucosa. Given the relatively novel state of this class of medications
and the limited amount of data that are currently available regarding their impact
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on allergic rhinitis, there is much to learn about how this class of medications
may be used to positively aect patient outcomes. Initial information appears
to support the use of leukotriene receptor antagonists in the treatment of symptomatic allergy, especially for symptoms of rhinorrhea and nasal congestion. e
potential impact of this class of medications on eosinophils may also suggest a
broader role in the treatment of inammatory disorders of the nose and paranasal sinuses in the future.
Mast Cell Stabilizers
Cromolyn sodium (Nasalcrom, Intal) and nedocromil (Tilade) exert direct eects
on mast cells by inhibiting their calcium-dependent degranulation in response
to allergen exposure, although the exact mechanism of its action remains a matter of conjecture. e result is prevention of an allergic reaction when it is used
before exposure to an antigen. ese agents may also exert a late phase inhibition of eosinophils and neutrophils. Although they are ineective if administered
immediately aer allergen exposure, they are good for anticipated situational allergy if used to days before exposure to the inciting antigen.
Of course, to be eective, cromolyn (or any intranasally administered drug) must
adequately reach the nasal mucosa. is means that it may not be appropriate
for use in patients with severe septal deviation and/or marked turbinate hypertrophy. Not only will polyps prevent cromolyn from achieving adequate contact
with nasal mucosa, but also the cromolyn has no eect on the polyps. Rather, it
prevents the allergic event when applied beforehand, and to a much lesser degree
may ameliorate symptoms of an allergic event in progress. It must be reapplied
every to hours to remain eective. Despite these shortcomings, cromolyn
is especially eective for patients with allergy to well-dened inhalants that are
unavoidable and are not encountered on a continuous basis. Also, cromolyn is
exceptionally safe and is probably one of the best methods of providing relief for
pregnant women with mild to moderate symptoms of allergic rhinitis.
Mucolytics
Mucolytics, such as guaifenesin, decrease the viscosity of mucus and increase
its volume via a vagal nerve−mediated increase in parasympathetic tone. Wawrose et al found a signicant decrease in congestion and thinner postnasal drip
among patients with CRS, and Morgan and Petty showed improvement in the
frequency of cough and chest discomfort in patients with chronic obstructive
pulmonary disease. However, Druce found no support for the ability of guaifenesin to reduce viscosity. e role of mucolytics as a symptomatic adjunct to
treatment of sinonasal disorders and in postoperative care remains unclear.
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