Posterior Nasal Neurectomy for Vasomotor Rhinitis

LITERATURE REVIEW III

Diajukan Oleh :
dr. Odhi Anggani
16/408083/PKU/16559

Pembimbing :
Dr. dr. Luh Putu Lusy Indrawati, M.Kes., Sp. T.H.T.K.L (K)

Department of Otorhinolaryngology Head and Neck Surgery Faculty of Medicine,

Public Health, and Nursing Gadjah Mada University/Dr. Sardjito
General Hospital Yogyakarta 2019
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 TABLE OF CONTENT

Cover Page .......................................................................................................................... i

Approval ............................................................................................................................. ii

Table of Content .................................................................................................................. iii

CHAPTER I. INTRODUCTION ........................................................................................ 1

A. Background ............................................................................................................. 1

B. Problem Statement .................................................................................................. 2

C. Objective ................................................................................................................. 2

CHAPTER II. LITERATURE REVIEW ............................................................................ 3

A. Anatomy .................................................................................................................. 3

B. Pathophysiology of Vasomotor Rhinitis ................................................................. 4

C. Diagnosis and Treatment of Vasomotor Rhinitis .................................................... 10

D. Surgical Technique of Posterior Nasal Neurectomy ............................................... 21

CHAPTER III. CONCLUSION .......................................................................................... 30

REFERENCES .................................................................................................................... 31

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 CHAPTER I

INTRODUCTION

A. Background

Vasomotor rhinitis (VMR) is cited as the most prevalent cause of nonallergic rhinitis

(NAR). Studies have estimated that 14 million people in the United States are affected by

VMR and that this disease process costs $2–3 billion annually. Allergic rhinitis (AR) remains

the most prevalent form of rhinitis with a ratio of 3:1 (AR/ NAR); however, 60% of patients

with AR will develop nasal symptoms in response to nonallergic environmental triggers. Thus,

VMR is responsible for a significant portion of rhinitis symptoms at a considerable annual cost.

As mentioned previously, VMR is in the category of NAR and the triggers are nonallergic

and noninfectious in nature. Common triggers for VMR include changes in barometric

pressure, temperature, humidity, strong odors, tobacco smoke, ingestion of alcohol, and

changes in menstrual-related hormones. Symptoms include nasal obstruction/congestion,

rhinorrhea, postnasal drip, throat clearing, and cough and can be perennial, seasonal, persistent,

or intermittent. The triggers of changing barometric pressure, temperature, and humidity can

result in a more “seasonal-type” picture because all of these components change along with the

seasons, which makes VMR sometimes difficult to differentiate from AR. Allergy testing (skin

prick or blood testing) will differentiate between the two. The possible hormonal component

is supported by the fact that female subjects are more commonly affected by VMR than male

subjects at a 2:1 ratio.

It is largely felt that the etiology of VMR is in part caused by either nociceptive

dysfunction, autonomic dysfunction, or both. Both nociceptive dysfunction and autonomic

dysfunction carry at their core an underlying pathology including a hyperactive

parasympathetic nervous system, hypoactive sympathetic nervous system, or imbalance

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between the parasympathetic and sympathetic nervous systems. Until the pathophysiology has

been better elucidated and specific testing created for the diagnosis of VMR, diagnosis

currently consists of the clinical history, physical exam, and the exclusion of other possible

causes.

First-line treatment of VMR is medical therapy in the form of topical therapy. Surgical

intervention should be considered in the event that maximal medical therapy has failed to

control a patient’s symptoms. (Halderman & Sindwani, 2015)

B. Problem Statement

In recent years there are many surgical intervention option that can be considered for

treating vasomotor rhinitis. Inferior turbinate reduction, vidian nerve neurectomy, posterior

nasal neurectomy, and cryoablation of the posterior nasal nerve are the example of it. This

literature review will be focused especially for the posterior nasal neurectomy as one treatment

modality for vasomotor rhinitis.

C. Objective

The objectives of this study were to examine the available literature about posterior

nasal neurectomy for treatment of vasomotor rhinitis.

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 CHAPTER II

LITERATURE REVIEW

A. Anatomy

The vidian nerve carries parasympathetic nerve fibers from the facial nerve to the

sphenopalatine ganglion. At the sphenopalatine ganglion, the parasympathetic fibers synapse.

Postsynaptic parasympathetic fibers form 3 branches in the pterygopalatine fossa. These nerve

branches innervate the nasal mucosa as the nasal nerve, the lacrimal gland as the lacrimal nerve,

and the palate as the greater palatine nerve.

The parasympathetic nerve fibers of the nose enter the nose through the sphenopalatine

foramen. These are called the posterior superior nasal nerves (Figure 1). The posterior superior

nasal nerves divide further to become the lateral and the medial posterior superior nasal nerves.

The lateral posterior superior nasal nerves innervate the superior, middle, and inferior conchae

and the superior and middle meatus.

Other parasympathetic nerve fibers of the nose branch off from the greater palatine nerve

and enter the nasal cavity through the canaliculi of the perpendicular plate of the palatine bone

as the posterior inferior nasal nerves. These nerves innervate the inferior turbinate and the

inferior meatus. (Kikawada, 2007)

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Figure 1 The bony structure of the right side composing the sphenopalatine foramen (left) and
parasympathetic nerve passing through the sphenopalatine foramen (right). SB, sphenoid
bone; PB, palatine bone; PC, pterygoid canal; SPF, sphenopalatine foramen; EC, ethmoidal
crest for middle concha; CC, conchal crest for inferior concha; SM, posterior part of superior
meatus; MM, posterior part of middle meatus; VN, vidian nerve; PPG, pterygopalatine
ganglion; LN, lacrimal nerve; PSNN, posterior superior nasal nerve; SPA, sphenopalatine
artery.

B. Pathophysiology of Vasomotor Rhinitis

Nonallergic noninfectious perennial rhinitis (NANIPER), is a heterogeneous disease,

which is characterized by nasal hyperreactivity that results in symptoms of nasal blockage,

rhinorrhoea, and sneezing, which are often indistinguishable from nasal symptoms of allergic

rhinitis. Diagnosis of the disease is established on the basis of persistent symptoms throughout

the year after exclusion of infection (as indicated by a clear and watery nasal discharge, as

compared with a purulent discharge produced in infectious rhinitis), any anatomical or medical

disorder of the nose, and negative skin prick testing for IgE-mediated sensitivity to relevant

aeroallergens.

Although negative skin prick testing is necessary to confirm diagnosis of nonallergic

rhinitis, it is important to note that irrelevant aeroallergens may occasionally result in positive

skin prick testing.

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 NANIPER comprises several forms of rhinitis, in which the aetiology and/or

pathophysiology is established only for some minor forms of the disease, in particular drug-

induced rhinitis and nonallergic rhinitis with eosinophilia syndrome (NARES). In contrast, the

aetiology is largely unknown for a majority of about 75–80% of the individuals, in whom the

disease is classified as being idiopathic or vasomotor rhinitis. Although other more minor forms

of rhinitis (e.g. occupational rhinitis, nonallergic hormonal rhinitis, food-induced rhinitis,

emotioninduced rhinitis, physical/chemical irritant-induced rhinitis, and rhinitis of the elderly)

have also been defined on the basis of limited information on aetiological and pathological

factors.

Unlike drug-induced rhinitis and the other minor forms of nonallergic rhinitis

(occupational, nonallergic hormonal, food-induced, emotion-induced rhinitis and physical/

chemical irritant-induced rhinitis) for which there is some aetiological information, the

aetiology of idiopathic rhinitis is unknown and diagnosis is generally established by exclusion.

It has, however, been demonstrated that careful determination of the intensity of symptoms

combined with modern diagnostic tools such as nasal provocation with cold dry air, which

results in increased mucus production and nasal blockage in a dose–dependent manner in

idiopathic rhinitis patients, can be used to discriminate between idiopathic rhinitis patients and

normal healthy subjects.

Several mechanisms have been postulated to explain the pathophysiology of idiopathic

rhinitis, of which: (i) increased permeability of the nasal epithelium; (ii) non-IgE-mediated

inflammatory responses; and (iii) neurogenic responses are the most plausible. It has been

suggested that an increase in the nasal epithelial permeability, resulting as a consequence of

epithelial damage by irritants, infection or cellular components such as eosinophilMBP/ECP,

might lead to increased access of stimuli to the sensory nerve endings, vessels and secretory

glands and become manifest as the symptoms of rhinitis. However, many of these events are

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not different from those observed in the bronchi of asthmatics, and are thus unlikely to

exclusively explain the pathological features of idiopathic rhinitis.

Although non-IgE-mediated inflammatory responses have been shown to be present in

the nasal airways of idiopathic rhinitis patients by some authors, others have not been able to

demonstrate inflammation in their group of patients. Also a major difficulty with the few

studies demonstrating inflammation in nonallergic rhinitis has been that a clear distinction was

not made between idiopathic rhinitis and NARES in the patient groups investigated, of which

the latter could account for the observed inflammation. Similarly, inconsistent results have

been demonstrated for the efficacy of antiinflammatory treatments such as corticosteroids and

antihistamines in the treatment of this condition, suggesting that inflammation may not be an

important underlying mechanism.

In contrast, there is increasing evidence that neurogenic mechanisms are likely to be

involved in the pathophysiology of rhinitis symptoms. Neural regulation in the upper airways

is maintained by the sensory (peptidergic), sympathetic (adrenergic), and parasympathetic

(cholinergic) nervous systems, which innervate and interact in the nasal mucosa to regulate

epithelial, vascular, and glandular processes in particular. Under normal conditions the

sympathetic nervous system constitutes the main vasoactive mechanism, ensuring vascular

tone. The sympathetic nerve fibres that innervate the nose originate from the first and second

thoracic segments of the spinal cord and synapse in the superior cervical ganglion. Post-

ganglionic fibres enter the nose accompanying branches of the carotid artery and innervate

mainly the vasculature and to a lesser extent the secretory glands, where they discharge

norepinephrine (Nor) and NPY to cause predominantly vasoconstriction and a decrease in nasal

secretion (Fig. 2a). This normal sympathetic tone has the net effect of increasing nasal patency.

In contrast, preganglionic parasympathetic fibres leave the superior salivatory nucleus

and join the postganglionic sympathetic fibres to form the vidian nerve, prior to synapsing with

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the sphenopalatine ganglion. Post-ganglionic parasympathetic fibres then innervate both the

blood vessels and the exocrine (seromucous and serous) glands of the nasal mucosa, of which

innervation of the glands appears to be more important. The parasympathetic nerve fibres

release predominantly acetylcholine (Ach), and other neuropeptide transmitters such as

vasoactive intestinal peptide (VIP), which increase nasal secretion and vasorelaxation, leading

to nasal congestion under extreme conditions (Fig. 2b). Although the parasympathetic tone is

not as prominent as the sympathetic tone under normal conditions, it has been demonstrated

that, in conjunction with sensory neurons, the parasympathetic neurons play an essential role

in ‘‘protective’’ nasal clearing reflexes such as sneezing, secretion and congestion, in response

to exogenous noxious stimuli. Stimulation of sensory mechanoreceptors and/or chemo-

sensitive receptors in the nose leads to excitation of the parasympathetic reflex, via stimulation

of the trigeminal nerve connected to the central nervous system (Fig. 2c).

However, it has been suggested that there is a balance between the sympathetic and

parasympathetic tones, which under normal conditions is biased towards the sympathetic tone

and results in increased nasal patency and low mucus production. In contrast, some mechanistic

studies in idiopathic rhinitis have suggested that this balance becomes biased towards the

parasympathetic system, i.e., hypo-reactivity of the sympathetic system and hyper-reactivity of

the parasympathetic system; resulting in functional abnormality of the nasal end organs in these

patients.

Other studies have suggested that the functional abnormality in idiopathic rhinitis may

be associated with abnormal sensory afferent nerves and/or C-fibre stimulation. C-fibres are

unmyelinated parts of the sensory neurons that originate from the ethmoidal and posterior

nerves and innervate the vessels, glands and epithelium of the mucosa. C-fibres are

unspecialized sensory nerve endings, which induce local antidromic spreading of the action

potential in peripheral branches of the sensory neurons and local release of neuropeptides on

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stimulation by noxious agents. Neuropeptides such as substance P (SP), in particular, and

calcitonin generelated protein (CGRP) are released from C-fibres and cause a localized

increase in vascular permeability and nasal secretion. Under normal conditions this acts as a

protective nose clearing reflex mechanism similar to that described above for the

parasympathetic reflex. However, there are several reports, which suggest that increased C-

fibre activity may lead to nasal dysfunction in idiopathic rhinitis. Several studies have

demonstrated that capsaicin, the pungent agent in red peppers, predominantly stimulates C-

fibres to induce burning, rhinorrhoea, and nasal congestion. Similarly, several studies have

demonstrated that repeated nasal provocation with capsaicin significantly reduces nasal

complaints in patients with idiopathic rhinitis.

Figure 3 suggesting that this may be a consequence of either C-fibre desensitization or

degeneration, although this remains to be confirmed in human models. However, reports on

the involvement of C-fibre-mediated inflammatory processes as underlying mechanisms are

conflicting, because although some studies have demonstrated capsaicin-induced neurogenic

inflammation in patients with allergic rhinitis, this has been shown not to be the case in

idiopathic rhinitis. (Garay, 2004)

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Figure 2. Effects of: (A) sympathetic innervation; (B) parasympathetic innervation; and (C)
nasal reflex on nasal function.

Figure 3. Effect of repeated provocation with capsaicin or placebo on nasal complaints in

idiopathic rhinitis patients, as indicated by a symptom score measured on a VAS of 0–10 cm.
(Modified from Blom et al. 1997 (23) and reprinted with kind permission.)

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C. Diagnosis and Treatment of Vasomotor Rhinitis

Nonallergic rhinitis (NAR) describes chronic symptoms of nasal congestion, obstruction,

and rhinorrhea unrelated to a specific allergen based on skin or serum testing. NAR affects

approximately 30 million Americans, and more than 200 million worldwide. Although NAR

can present with symptoms similar to those found in allergic rhinitis (AR), NAR tends to have

an older age of onset, typically presenting between 30 and 60 years of life. Patients with NAR

are more commonly women, have decreased eosinophil response, and suffer from more

frequent headaches and olfactory dysfunction, but less sneezing and pruritus. The predominant

symptom of NAR, nasal congestion, can have a significant impact on quality of life,

contributing to sleep disturbances, daytime somnolence, and decreased productivity at work.

Additionally, patients may have a combination of AR and NAR, known as mixed rhinitis (MR).

The use of an irritant index questionnaire has helped to reclassify patients with NAR, AR, or

MR based on their symptoms in response to nonallergic triggers and aeroallergen skin prick

tests, as well as to stratify them according to low or high irritant burdens. Patients with NAR

are often misdiagnosed as having sinusitis and are treated with multiple courses of antibiotics

without resolution of symptoms. In recent years, NAR has been divided into several different

subtypes, including rhinitis that is drug-induced, gustatory, hormonal, or senile; vasomotor

rhinitis (VMR); NAR with eosinophilia; and atrophic rhinitis. VMR is the most frequent form

of NAR and is characterized by nasal symptoms usually triggered by changes in environmental

conditions, weather, strong emotions, smells, and hormones.

Brandt and Bernstein6 developed a validated questionnaire that helps diagnose VMR.

Unlike AR, VMR is a clinical diagnosis based on a patient’s symptoms and triggers. To best

appreciate the treatment options for NAR, we need to first evaluate the pathophysiology of

NAR. Although the etiology is not well understood, there is thought to be a dysregulation of

sympathetic, parasympathetic, and nociceptive nerves innervating the nasal mucosa resulting

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in increased vascular permeability and mucus release from submucosal nasal glands. Mucus

secretion is controlled primarily by the parasympathetic nervous system, whereas the

sympathetic system controls the vascular tone. Acetylcholine is the main parasympathetic

neurotransmitter that regulates nasal mucus secretion and rhinorrhea, a common symptom of

rhinitis.

Noradrenaline and neuropeptide Y are sympathetic neurotransmitters that modulate the

secretions initiated by the parasympathetic system. In addition, sensory neuropeptides and

nociceptive type C-fibers of the trigeminal nerve contribute to mast cell degranulation and the

itching and sneezing reflexes. The first-line treatment for VMR is medical therapy in the form

of topical corticosteroid and topical antihistamine sprays (which are indicated for NAR as well

as AR).

Ipratropium bromide (0.03%) is the only topical anticholinergic approved for treatment of

NAR with no systemic side effects except for occasional dryness and epistaxis. Topical

capsaicin has been shown to be an efficacious treatment for NAR based on its modulating

effects on C-fibers, but because of its irritant qualities, its use is often limited by patient

intolerance. There are no oral antihistamines or anticholinergics currently approved for NAR.

When medical management does not adequately control a patient’s symptoms, surgical

interventions may be considered (Fig. 4).

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 Figure 4. Surgical targets in vasomotor rhinitis

1. Inferior Turbinate Reduction

Inferior turbinate hypertrophy contributes to chronic rhinitis symptomatology by

hypersecretion and nasal obstruction. Patients with NAR have been shown to benefit from

surgical corrections of nasal obstruction with improvements in the patientreported sino-nasal

outcome test (SNOT-22), global nasal function tests, and objective nasal peak inspiratory flow.

Many different surgical techniques have been developed for inferior turbinate reduction

(ITR). The total inferior turbinectomy, historically performed to improve nasal obstruction, has

long fallen out of favor, as it can lead to potential complications, including atrophic rhinitis and

paradoxic nasal obstruction, characteristic of empty nose syndrome. Mucosal-sparing and

turbinate-sparing techniques are now favored to preserve physiologic function of the turbinate;

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they include submucosal microdebrider reduction of soft tissue, submucosal resection of bone,

electrocautery, radiofrequency ablation, coblation, laser ablation, cryotherapy, direct

microdebridement, and lateral bone outfracture. The pros and cons of each technique are well

studied and described. In general, there is abundant level 3 and 4 evidence supporting the

benefit of various modalities of turbinate reduction in patients with VMR. However, no true

standard of care exists because robust side-by-side comparisons of turbinate reduction

techniques have not been done.

In one study attempting such a comparison, Passali et al. (2003) performed one of the few

randomized control trials evaluating 6 surgical techniques for inferior turbinate reduction with

a 6-year follow-up period. The investigators compared traditional turbinate resection, laser

cautery, electrocautery, cryotherapy, submucosal resection, and submucosal resection with

lateral bone displacement. Of the 6 options, only submucosal resection resulted in stable

subjective symptom improvement in nasal obstruction and discharge as well as objective

improved mucociliary clearance and nasal volumes. The addition of lateral bony displacement

further improved long-term results. More recently, Harju et al. (2018) conducted a randomized

placebo-controlled trial of turbinate reduction techniques, comparing radiofrequency ablation,

diode laser, and microdebrider-assisted inferior turbinoplasty, as well as a sham procedure.

Although the sham procedure was associated with a notable placebo effect of patient-reported

improvement, all 3 surgical techniques provided statistically significant additional reductions

in severity of nasal obstruction compared with the sham procedure. There was no superior

technique among the 3 tested. Regardless of the technique, the overarching goal in inferior

turbinate surgery remains to improve the nasal airway and decrease mucosal edema while

preserving turbinate function.

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 2. Botulinum Toxin

Botulinum toxin (BTX) has been shown to have a potential role in treatment of NAR

through its anticholinergic effect on nasal mucosa. BTX inhibits the release of acetylcholine

from the presynaptic nerve terminal; of the available serotypes, BTX-A has the greatest

anticholinergic effect. The injection of BTX-A (4 U) into the head of the inferior (2 U) and

middle turbinates (2 U) in patients with VMR decreases rhinorrhea, but the improvement is

typically short-lived, lasting only 4 weeks. Injection of higher doses of BTX-A (20 U)

decreases symptoms of nasal obstruction, sneezing, nasal discharge, and nasal itching for up to

12 weeks. BTX also can be safely injected into the septum at higher doses (80 U), but the

improvement in nasal symptoms is short-lived at only 2 weeks. All studies have shown BTX

injection to be safe and without significant side effects. However, BTX may not be a practical

option for most patients with VMR, given that the symptom benefits are only temporary. In

addition, only the rhinorrhea symptom of VMR is reduced by BTX. Furthermore, not all

patients see an improvement with BTX, likely due to the multifactorial causes of rhinitis that

are not mediated by acetylcholine.

3. Vidian Neurectomy

Therapeutic transection of the vidian nerve is a well-described surgical option that aims to

disrupt the autonomic supply to the nasal cavity, thereby decreasing nasal secretions. The

vidian nerve is formed by the joining of the greater superficial petrosal and deep petrosal

nerves. The deep petrosal nerve contains sympathetic fibers, whereas the greater superficial

petrosal nerve contains preganglionic parasympathetic secretomotor fibers for the lacrimal,

palatine, and nasal glands, as well as the vasodilator nerves for the nasal mucous membranes.

The first vidian neurectomy was described by Golding-Wood in 1961 through a transantral

approach. Others described performing neurectomies using transpalatal, transethmoidal, and

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transnasal techniques. However, these initial surgeries suffered from significant morbidity due

to postoperative bleeding, facial and palate numbness, and ocular injuries.

Recurrent symptoms from incomplete nerve section was common due to poor visualization

afforded by these approaches. The popularity of the vidian neurectomy diminished until the

application of endoscopic techniques, which have improved visualization and decreased

complications. El Shazly (1991) described one of the earliest reports of endoscopic vidian

neurectomy with successful resolution of secretomotor rhinitis symptoms. Robinson and

Wormald subsequently described their retrograde endoscopic technique by which a mucosal

incision is made over the sphenopalatine foramen and the sphenopalatine artery is cauterized.

A mucosal flap is elevated posteriorly to the anterior face of the sphenoid and the periosteum

and fat of the pterygopalatine fossa is exposed. The vidian nerve, which travels along the

sphenoid floor, is identified emerging through the pterygoid canal (Fig. 5). The nerve is isolated

and sharply resected and cauterized. Another technique proposed by Su et al. (2011) uses an

anterograde transsphenoidal approach to the vidian nerve by first creating a large

sphenoidotomy and removing the sphenoid process of the palatine bone until the vidian canal

is identified inferolaterally. This anterograde approach obviates the need to ligate the

sphenopalatine artery. Both techniques recommend resection of a 2-mm to 3-mm segment of

the vidian nerve in addition to cautery of the nerve stump to prevent reinnervation. Endoscopic

vidian neurectomy has benefited from an improvement in intraoperative visualization, yielding

increased success rates. Rates of successful control of rhinitis and of patient satisfaction have

been reported as high as 91% after vidian neurectomy. A recent systematic review by Marshak

et al. (2016) reported that all published case series that used the endoscopic technique for VMR

had an improvement in rhinorrhea and nasal obstruction. In one of the only prospective case

series published, Zhang et al. (2015) showed improvement in patients’ reported Sinusitis

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Symptom Questionnaire scores and SNOT-22 scores, particularly in the subdomains of

rhinorrhea and nasal congestion.

Despite favorable success rates with vidian neurectomy, there can be notable

complications associated with the procedure. The most commonly cited complication is

postoperative dry eyes due to collateral injury of the postganglionic secretomotory fibers

innervating the lacrimal gland. Halderman and Sindwani (2015) systematically reviewed 6

studies that described endoscopic vidian neurectomies. The rate of dry eyes ranged from 23.8%

to 100.0% with an aggregate rate of 48.0%. The second most common complication was cheek,

palate, and gingival numbness that ranged from 2.97% to 22.2% in reviewed studies.29

However, most of the symptoms were temporary, with dry eyes resolving in 1 to 6 months and

cheek/palate numbness resolving between 2 weeks and 1 year.

Figure 5. (A) Endoscopic view of the vidian canal drilled along its medial and inferior
borders (blue arrows), beginning at its opening in the posterior pterygopalatine fossa (black
arrow). Axial (B) and coronal (C) computed tomography views of the vidian canal (blue
arrows) at the base of the sphenoid sinus.

4. Posterior Nasal Neurectomy

In light of concerns regarding complications that may be associated with vidian

neurectomy, the posterior nasal nerve has emerged as an alternative surgical target. The vidian

nerve travels through the pterygoid canal as a single bundle until its parasympathetic fibers

synapse at the sphenopalatine ganglion. The postganglionic fibers consist of multiple efferent

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rami that project from the pterygopalatine ganglion toseparately innervate the orbit, palate, and

nasal mucosa. The postsynaptic parasympathetic fibers that give rise to the posterior nasal

nerve travel with the sphenopalatine artery, entering the nasal cavity via the sphenopalatine

foramen. Because the posterior nasal nerve traverses distal to the branching point for nerves

innervating the lacrimal gland and palate, selective transnasal sectioning of the posterior nasal

nerve does not carry a risk of eye dryness or palate numbness. In rat models, transection of the

posterior nasal nerve results in depletion of choline acetyltransferase and a twofold reduction

in nasal secretions.

Kikawada (2007) first described the posterior nasal neurectomy (PNN) as an alternative to

vidian neurectomy (Fig. 6). A vertical incision is made in the posterior middle meatus over the

perpendicular process of the palatine bone, a mucoperiosteal flap is elevated over the palatine

bone, and the sphenopalatine foramen (SPF) can be identified immediately posterior to the

crista ethmoidalis. The posterior nasal nerve can be identified emerging from the SPF, within

the neurovascular bundle containing the nerve and the sphenopalatine vessels. The entire

sphenopalatine bundle (nerve and artery) can be ligated together when performing the PNN, or

the nerve and its branches can be dissected free from the artery and transected separately (Fig.

7). Alternatively, a transturbinate approach has been described. From an anterior incision in

the inferior turbinate, a submucoperiosteal dissection is performed until the SPF is identified.

The neural bundle can be visualized exiting the SPF toward the inferior turbinate. After PNN

has been performed, a submucosal resection of the inferior turbinate soft tissue can be

performed through the same incision.

The efficacy of the PNN procedure has not been studied as thoroughly as that of vidian

neurectomy. There is currently a paucity of literature that evaluates the outcomes of PNN for

NAR specifically. Two recent systematic reviews performed found that most studies discussed

the effects of PNN on patients with AR. As the only outcomes study that included patients with

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NAR, Ikeda et al. (2008) performed 56 PNN procedures in patients with recalcitrant AR or

NAR and noted a 80% improvement in total symptomatic scores for 86% of the patients. In

patients with AR, Kobayashi et al. (2012) reported significant improvement in sneezing,

rhinorrhea, and nasal obstruction after transturbinate neurectomy of peripheral branches of the

posterior nasal nerve; the addition of a concurrently performed transection of the main posterior

nasal nerve did not result in further improvement. In human histologic studies, the post-PNN

nasal cavity demonstrates decreases in the density of nasal gland cells and inflammatory cells.

Cassano and colleagues noted improved mucociliary transport time in patients with VMR who

underwent sphenopalatine artery ligation and PNN with ITR compared with those who

underwent ITR alone.

Despite the symptomatic improvements and low complication rate associated with PNN,

some patients may not have a complete response after PNN. This may be because of gradual

postoperative reinnervation, or to the presence of persistent accessory secretomotor fibers to

the posterolateral mucosa that do not transverse the sphenopalatine foramen. In 90% of cadaver

models studied, additional rami were found traversing the perpendicular process of the palatine

bone that were separate from the contributions found in the sphenopalatine foramen. Histologic

studies confirmed the presence of these autonomic fibers. Thus, to perform a complete

postganglionic pterygopalatine parasympathectomy, one must meticulously trace and transect

the array of these accessory fibers in addition to the primary posterior nasal nerve to fully

denervate the nasal mucosa.

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 Figure 6. Endoscopic posterior nerve neurectomy (A). Vertical incision made in posterior
middle meatus (B). Sphenopalatine palatine bundle identified at sphenopalatine notch (C, D).
Posterior superior nasal nerves separated from sphenopalatine artery and ligated. IT, inferior
turbinate; MT, middle turbinate; PB, palatine bone; PSNN, posterior superior nasal nerve;
SPA, sphenopalatine artery; SPN, sphenopalatine notch.

Figure 7. (A) Depiction of the right posterior superior nasal nerve (PSNN) and vidian
nerve (VN) and their relationship to the sphenopalatine artery (SPA). (B) Isolation of the
SPA as it passes through the sphenopalatine foramen. LN, lacrimal nerve; PPG,
pterygopalatine ganglion.

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 5. Cryoablation of the Posterior Nasal Nerve

Cryotherapy has been safely used in the head and neck region for soft tissue ablation for

several indications. Cryotherapy offers unique advantages to other forms of tissue ablation in

that the zone of injury is predictably superficial, allowing for the ablation of nerve while

preserving the patency of the associated vasculature. The use of cryosurgical therapy for

rhinitis was first proposed in 1970 with the placement of a cryoprobe in the nasal cavity against

the posterior end of the inferior turbinate. The procedure showed promising efficacy; however,

the investigators reported complications of serous otitis media and septal perforations. These

complications were likely related to imprecise application of cryogen, perhaps exacerbated by

poor visualization of the posterior nasal cavity without the benefit of endoscopic visualization.

The requirement for very large cryogen reservoirs and nonergonomic cryoprobes also

contributed to the limited adoption of cryotherapy technology at the time. Recently,

cryotherapy has reemerged as a modality for ablating the posterior nasal nerve in an office-

based setting, obviating the need for general anesthesia. Interest in cryoablative technology

was revived with the introduction of an in-office cryosurgical ablation device developed to

deliver cryogen to the posterior middle meatus and freeze the posterior nasal nerve under

endoscopic visualization (Arrinex Inc, Redwood City, CA) (Fig. 8). A study of office-based

cryotherapy in patients with VMR and AR demonstrated that patients’ Total Nasal Symptom

Score decreased significantly up to 365 days after treatment, particularly in the symptoms of

rhinorrhea and congestion. There were no postoperative instances of dry eyes or palate

numbness. (Yan & Hwang, 2018)

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 Figure 8. Cryoablation of the right posterior nasal nerve (A). ClariFix cryodevice
(Arrinex, Inc) placed endoscopically in posterior middle meatus (B). Activation of cryogen
(C, D). Evidence of cryoablation with tissue blanching on withdrawal of the cryodevice. IT,
inferior turbinate; MT, middle turbinate. (Courtesy of Arrinex, Inc, Redwood City, CA).

D. Surgical Technique of Posterior Nasal Neurectomy

Ahilasamy & Rajendran (2019) described the steps of surgical technique of posterior nasal

neurectomy as below:

1. Anaesthesia

This procedure can be conducted either under general anaesthesia or local anaesthesia.

Local anaesthesia is preferred at our centre, for a clear bloodless field, which enables better

visualisation of the slender nerve fibres.

2. Positioning

The patient is placed in a supine posture in a reverse Trendelenburg position. The head end

is elevated to 30 degrees, to decrease venous return. A 0-degree 4 mm rigid endoscope with a

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high-definition camera is used. Pre-medication with fentanyl and dexmedetomidine is

administered intravenously as per body weight.

3. Infiltration and nerve block

A dose of 1–2 ml ropivacaine (0.5 per cent) or lignocaine with adrenaline (1 per cent) at a

dilution of 1:40,000 solution is administered as a sphenopalatine block. The solution is injected

inferior to the posterior attachment of the middle turbinate, just behind the posterior fontanelle,

or through the greater palatine foramen (transoral) if there is a gross septal deviation. A 23

gauge spinal needle is used, with about 1.5 cm of the tip of the needle bent to 45 degrees.

4. Incision

A vertical incision is made (Figure 9) behind the posterior fontanelle. The posterior end of

the posterior fontanelle is identified by palpation with an elevator. Just behind this, a vertical

incision is made on the lateral nasal wall, starting opposite to the posterior end of the middle

turbinate and running all the way down until it reaches the attachment of the inferior turbinate.

The incision is made with an angled Cottle elevator. However, one could instead use a

needletipped electrocautery device or a Colorado needle, to prevent bleeding from the incision

site, if the procedure is performed under general anaesthesia.

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 Figure 9. Right side nasal cavity incision site.

Figure 10. A curved incision about 1.5 cm long is made with a laser in the middle meatus
(MT, middle turbinate; IT, inferior turbinate).

5. Posterior nasal nerve identification

The mucoperiosteum is raised gently using a Cottle elevator or a suction freer elevator,

after making the initial incision. Alternatively, if middle meatal antrostomy has been

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performed, the mucoperiosteum is elevated from the posterior edge of the MMA. Care must be

taken not to injure the sphenopalatine vessel during flap elevation.

The peripheral part of the posterior nasal nerve can usually be identified just behind the

incision, about 4–5 mm inferior to the sphenopalatine artery or crista ethmoidalis (Figure 11).

It is always better to identify the main trunk or the proximal part of the posterior nasal nerve

below the sphenopalatine foramen area, where the nerve lies inferior to the vessel.

The nerve may divide into several branches at its exit into the nasal cavity, each through

its foramen. The surgeon may miss a branch if the peripheral part of the nerve is targeted instead

of the proximal one near the foramen.

After identifying the nerve fibres, it is cauterised using monopolar suction cautery

(Figure 15) or cut using microscissors. It is essential to carry out this procedure on both sides

for effective results.

Figure 11. Right side nasal cavity: flap elevated, with posterior nasal nerve identified.

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 Figure 12. The dissected membrane is separated from the perpendicular plate of the palatine
bone, and the mucoperiosteal flap (*) is folded back until the sphenopalatine notch (SPN) and
the superior margin of the perpendicular plate of the palatine bone (PB) are exposed.

Figure 13. The periosteum of the sphenopalatine foramen is dissected with a right-angle ball
probe (*) until the sphenopalatine artery (SPA) is exposed.

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Figure 14. After careful dissection of the periosteum surrounding the sphenopalatine artery
(SPA), the posterior superior nasal nerve (PSNN) is identified.

Figure 15. Right side nasal cavity: suction cautery of posterior nasal nerve.

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Figure 16. The posterior superior nasal nerve (PSNN) is removed with a small forceps (*).

Figure 17. Subperiosteal tissue, including small branches of the sphenopalatine artery, is
cauterized with a bipolar coagulator (*).

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Figure 18. Submucosal tissue around the sphenopalatine artery is resected with a laser (*),
preserving the artery (SPA).

Figure 19. The intact sphenopalatine artery (SPA) after resection of the posterior superior
nasal nerve.

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 6. Closure

The mucoperiosteal flaps are repositioned (Figure 4). No nasal packing is required. Patients

are discharged on the same day. CSMT

Figure 20. Right side nasal cavity: repositioning of mucoperiosteal flap.

Figure 21. The mucosal flap (*) is returned to its original position.

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 CHAPTER III

CONCLUSION

NAR, including vasomotor rhinitis, is a common disease that impairs the quality of life

of many patients. Medical therapy is first-line treatment, but when treatments do not provide

adequate relief, there is a role for surgical management. Turbinate reduction surgery yields

well-studied benefits.

More directed targeting of the underlying autonomic dysfunction in NAR through

endoscopic vidian neurectomy and PNN have been shown to be effective in reducing symptoms

of chronic rhinitis, particularly congestion and rhinorrhea. The PNN has far lower rates of dry

eye complications although its efficacy is not as well established. The desire for in-office

treatment options makes botulinum toxin injection and cryotherapy of the posterior nasal nerve

potentially attractive options, but larger studies are required to characterize their long-term

treatment effects.

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