turbinate hypertrophy

5/21/2018 Turbinate Hypertrophy

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Turbinate Hypertrophy

The turbinates are structures on the side wall of the inside of the nose. They project into the

nasal passages as ridges of tissue. The inferior turbinates can block nasal airflow when they

are enlarged. The pictures below demonstrate how the inferior turbinates can block airflowwhen they are enlarged and touch the nasal septum.

The turbinates are made of bone and soft tissue. Either the bone or the soft tissue can become

enlarged. In most patients, enlargement of the soft tissue part of the turbinate is the major

problem when the turbinates become swollen. When the turbinates are large, they are called

hypertrophic turbinates.

http://www.miamientdoctors.com/condition-turbinate-hypertrophy.html


Diagnosis

The diagnosis of enlarged inferior turbinates can be made by your doctor with a thorough

evaluation of your symptoms and nasal examination. Your doctor may perform a procedure

in the office called a nasal endoscopy to diagnose the cause of your nasal obstruction. After

making the diagnosis, your doctor can discuss treatment options for you. If the turbinates areswollen, your doctor may recommend medications for you. For many patients, medications

can help reduce the size of the turbinates and can help improve their nasal obstruction. If you

have troublesome symptoms even after using medications, you may be a candidate for

surgery to shrink the size of your turbinates.

Turbinate Reduction

There are many ways to shrink the size of the turbinates. Surgery is typically called turbinate

reduction or turbinate resection. In many instances, turbinate surgery is performed in

conjunction withseptoplasty.It is important that the turbinate not be removed completely

because its removal can result in a very dry and crusty nose. In the absence of a turbinate, the

air that is breathed may not be to adequately humidified and warmed.
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You may hear of many different terms being used when it comes to surgery for the turbinates.

Examples of these terms are cauterization, coblation, radiofrequency reduction,

microdebrider resection, and partial resection. These all refer to different methods of reducing

the size of the turbinates.Some methods rely on shrinking the turbinates without removing

any of the turbinate bone or tissue. These methods include cauterization, coblation, and

radiofrequency reduction. In each of these methods, a portion of the turbinate is heated upwith a special device. Over time, scar tissue forms in the heated portion of turbinate, causing

the turbinate to shrink in size.

If a portion of the turbinate is removed, a procedure called a submucosal resection is typically

performed. This means that the lining of the turbinate is left intact, but the stuffing from the

inside of the turbinate is removed. As the turbinate heals, it will be much smaller than before

surgery. Sometimes, this resection can be performed with a device called a microdebrider.

This device allows the surgeon to remove the stuffing through a small opening in the

turbinate.

Although rare, turbinate tissue can re-grow after turbinate surgery and the procedure mayneed to be repeated. In more severe cases, a larger portion of the turbinate, such as the bony

framework, can be removed if needed.


Nasal Obstruction

Nasal obstruction is basically due to problems

with one of two areas, the nasal septum or the

inferior turbinates (or both).A deviated septumis a fixed obstruction that can only be

corrected with surgery. Inferior turbinate

hypertrophy, often related to allergens or other

irritants in the air, can sometimes be

dramatically improved with medications or

allergy treatment alone.

The nasal septum and the turbinates are normal

structures inside the nose. The nasal septum is

the structure that divides your nasal passages

into the right and left sides. A deviated septum

refers to a septum that is crooked. The

turbinates are near the septum, but there is usually space between the septum and turbinates

to allow air to pass through the nose. The turbinates can contribute to nasal obstruction if they

are too large. There are several different types of turbinates in the nose. The ones that most

commonly affect airflow are called the inferior turbinates. The picture below shows the nasal

septum and the inferior turbinate on the left side of the nose.

http://www.miamientdoctors.com/condition-nasal-obstruction.html

http://www.miamientdoctors.com/condition-nasal-obstruction.html
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History of the Procedure

Inferior turbinate surgery dates to the 1890s when Jones first described it. In 1900, Holmes

described the stages of inferior turbinate hypertrophy and his surgical experience with 1500

turbinectomies. Turbinectomy later fell out of favor because of rising concern over

complications such as rhinitis sicca, atrophic rhinitis, and ozena. The enlarged nasal cavity

resulting from turbinate resection was believed to increase nasal airflow and reduce the

humidifying capabilities of the nasal mucosa, resulting in drying, crusting, and mucosal

atrophy. However, several studies have reported large series of turbinectomies without these

complications. This aspect of turbinate surgery remains controversial.

Problem

Nasal obstruction after rhinoplasty can result from alteration of the nasal valve or nasal vault

narrowing as a result of osteotomies. Beekhuis concluded that nasal obstruction

postrhinoplasty resulted primarily from inferior turbinate hypertrophy.[1] Changes in nasalairflow as a result of rhinoplasty may unmask inferior turbinate hypertrophy and obstruction

that were not clinically significant or evident preoperatively. See the image below.

(A) Endoscopic view of left nares showing caudal septal deflection to the left.

(B) Endoscopic view of right nares showing compensatory right inferior turbinate hypertrophy.

Etiology

Mink described the nasal valve in 1903. The nasal valve is formed medially by the septum

and laterally by the caudal edge of the upper lateral cartilage and it accounts forapproximately 50% of total upper airway resistance. The anterior tip of the inferior turbinate

is found in the nasal valve region, and hypertrophy of this structure can cause exponential

increases in airway resistance.

Inferior turbinate hypertrophy can result from mucosal hypertrophy, bony hypertrophy, or

both. Bony hypertrophy causes a fixed structural obstruction and is best treated with surgery.

More commonly, the problem is mucosal hypertrophy causing impingement on the nasal

valve, increased nasal resistance, and nasal obstruction. This can be managed medically or

surgically depending on the degree of hypertrophy and responsiveness to medical

management.

Pathophysiology
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The nose is a complex and highly specialized organ that plays a role in olfaction, heat

exchange, speech production, respiration, humidification, filtration, and antimicrobial

defense.

Mucus production is provided by goblet cells and submucosal and seromucous glands. Mucus

production is primarily controlled by parasympathetic innervation. The mucous blanketserves to humidify and clean the inspired air and eliminate debris from the nasal airway.

Nasal obstruction may be produced by overactivity of the parasympathetic innervation or

underactivity of the sympathetic innervation. Resistance is important in nasal function and

turbulence optimizes inspiratory air contact with the mucous membrane. Resistance must

remain within certain limits for the perception of normal breathing. If it is too high or too

low, a sensation of obstruction may occur. A cyclic alteration of constriction and dilation of

the inferior turbinates, known as the nasal cycle, occurs approximately every 2-7 hours.

The nasal valve provides approximately 50% of total airway resistance. The nasal valve is the

region of the nasal airway extending from the caudal end of the upper lateral cartilages andincluding the anterior end of the inferior turbinate. As airflow enters this constricted segment,

it accelerates and the pressure drops (per Bernoulli principle), which can result in nasal valve

collapse if the upper lateral cartilages are anatomically weak. The erectile tissue of the nasal

septum and inferior turbinate can impinge on the nasal valve and increase resistance. Because

the cross-sectional area of the nasal valve is small, minor changes in inferior turbinate

congestion can have marked effects on resistance. A major determinant of resistance to

airflow is the radius of the nasal vault. However, even in the presence of a normal radius, a

sensation of obstruction can occur from turbulent airflow.

Presentation

History

Nasal obstruction is a common complaint. Discerning the etiology is important so that

appropriate treatment can be initiated. History should address any alteration or unilaterality of

the obstruction, which may indicate a dynamic versus structural problem.

Address symptoms of rhinitis. Obstruction, rhinorrhea, and sneezing may occur withallergic

andnonallergic rhinitis.Elicit systemic symptoms of allergy such as watery itchy eyes,

asthma, and seasonal variation. Initial general examination should note "allergic shiners" or a

facial appearance that may indicate signs of chronic nasal obstruction. Vasomotor rhinitis is

typically exacerbated by irritants, temperature or humidity changes, or psychological factors.

Nonallergic eosinophilic rhinitis is generally perennial without allergen-induced symptoms.

Atrophic rhinitis is characterized by nasal dryness and crusting, frequently with a foul odor.

Rhinitis can also be associated with pregnancy and with systemic disorders such as

hypothyroidism.

Medications can also cause rhinitis and nasal obstruction. Rhinitis medicamentosa results

from rebound vasodilation after prolonged use of topical nasal decongestants. Typically the

patient begins using the topical agent to treat an underlying disorder causing the nasal

obstruction. Other medications causing increased nasal congestion include certainantihypertensives, antidepressants, antipsychotics, and oral contraceptives.
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Examination

Physical examination of the external nose is, of course, critical. In addition to assessing nasalaesthetics, note the patency of the nasal valve and any alar collapse since these may need to

be addressed to ensure functionality of the nose postrhinoplasty. The Cottle maneuver

involves pulling the patient's cheek laterally to open the nasal valve angle. If nasal airflowsymptomatically improves, this may indicate nasal valve pathology. A crooked nose may

indicate prior trauma and this history should be elicited. A saddle nose deformity may

indicate previous trauma, prior surgery, cocaine abuse, or an inflammatory process.

Additionally, the focus of the physical examination is anterior rhinoscopy, which reveals

caudal septal deformities or inferior turbinate hypertrophy that may account for the patient's

symptoms. If the patient has a significant caudal septal deflection, typically the inferior

turbinate on the side opposite the deviation is enlarged. Apply topical decongestant to

evaluate the response of the turbinate mucosa. This may assist in delineating mucosal versus

bony hypertrophy.

If indicated based on history, symptoms, or signs, a more extensive examination of the nose

can be performed via a rigid or flexible endoscope. This examination allows additional

assessment of the septum posteriorly, the nasopharynx, and the sinus ostia. Nasal masses or

polyps as a cause of obstruction can be evaluated. Purulent drainage may indicate sinusitis.

Evidence of a septal perforation may indicate prior surgery, cocaine or topical decongestant

abuse, or an inflammatory disease. Significant crusting or abnormality of the mucosal

appearance may indicate a systemic disorder.

History or symptoms and signs of other systemic disorders that may affect the nose and

turbinates warrant further investigation. Wegener granulomatosis and sarcoid can result innasal obstruction and crusting. Infectious rhinitis can result from a variety of organism-

caused conditions such as rhinoscleroma, tuberculosis, syphilis, rhinosporidiosis,

histoplasmosis, and aspergillosis. If suspected, address a history of exposure and travel and

perform further appropriate testing. A significant history of epistaxis may raise the concern of

an inflammatory or neoplastic process.

Indications

Nasal obstruction may result from mucosal hypertrophy of the inferior turbinate, structural

deformity of the nasal airway (septal deviation, bony inferior turbinate hypertrophy), or

dynamic airway collapse.

Typically, in the patient with significant nasal septal deviation, unilateral compensatory

turbinate hypertrophy may be present on the side opposite the deviation. However, if the

septal deviation is S shaped or deflections exist bilaterally, then bilateral inferior turbinate

enlargement may be present. If the hypertrophied turbinate is not addressed, nasal airway

obstruction may persist despite correction of septal deformities.

Similarly, relative inferior turbinate hypertrophy occurs in patients with a narrow nasal vault

either inherently or secondary to rhinoplasty maneuvers. Failure to perform reduction of the

inferior turbinates may result in nasal airway obstruction despite correction of any septaldeformities.


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Relevant Anatomy

Lateral nasal wall

The lateral nasal wall is composed of the nasal, frontal, occipital, lacrimal, ethmoid,maxillary, and palatine bones. The inferior turbinate constitutes a separate bone and

articulates with the maxilla, lacrimal, ethmoid, and palatine bones. The superior and middle

turbinates project off the ethmoid bone. The lacrimal process of the inferior turbinate forms

the medial wall of the nasolacrimal duct, which drains into the inferior meatus.

Nasal valve

The nasal valve is formed laterally by the caudal end of the upper lateral cartilages andmedially by the septum. The anterior tip of the inferior turbinate lies in the area of the nasal

valve.

Nasal mucosa

The nasal vestibule, constituting the first 1-2 cm of the nasal cavity, is lined with keratinized,

stratified squamous epithelium containing hair follicles and sebaceous and sweat glands. At

the mucocutaneous junction (limen nasi), the epithelium transitions to pseudostratified

ciliated columnar cells. This epithelium lines most of the sinonasal tract with the exception of

the olfactory mucosa.

Blood supply

The arterial blood supply to the nose originates from the maxillary and facial branches of the

external carotid artery and from the ophthalmic branch of the internal carotid artery. The

anterior facial vein, sphenopalatine vein, and ethmoid vein supply venous drainage. The nasal

vasculature is composed of arterioles, submucosal capillary beds, and venules. Specifically,

the nasal vasculature of the inferior turbinate is a sinusoidal network of large capacitance

vessels. These sinusoidal vessels are found primarily in the inferior turbinate and the anterior

septum. The result is that the inferior turbinate functions as erectile tissue.

Constriction of postsinusoidal venules results in engorgement of the sinusoids and an

enlargement of the nasal turbinates. In addition, multiple direct arteriovenous anastomoses

bypass the capillary beds. This allows significant increases in blood flow and heat exchangewithout a great increase in nasal blood volume, which facilitates the temperature regulatory

function of the inferior turbinates. The nasal mucosal vasculature is intimately related to its

autonomic innervation.

Innervation

In general, the nose is innervated by the olfactory nerve, branches of the ophthalmic and

maxillary divisions of the trigeminal nerve, parasympathetic secretomotor fibers, and

sympathetic fibers. The autonomic nerve supply to the nose regulates vascular tone, turbinate

congestion, and nasal secretion. Parasympathetic fibers synapse in the sphenopalatine

ganglion before innervating nasal mucosa. These fibers travel with the facial nerve, exiting atthe geniculate ganglion as the greater superficial petrosal nerve. The vidian nerve is formed


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by the union of the greater superficial petrosal and deep petrosal nerves and carries the fibers

to the sphenopalatine ganglion, where they synapse.

Sympathetic fibers also pass through the sphenopalatine ganglion but do not synapse there.

The sympathetic fibers exit the spine and travel in the cervical sympathetic trunk, synapsing

in the superior cervical ganglion. Postsynaptic fibers contribute to the sympathetic plexus ofthe internal carotid artery from which the deep petrosal nerve originates. It then joins with the

greater superficial petrosal nerve to form the vidian nerve and its fibers pass through the

sphenopalatine ganglion and along branches of the trigeminal nerve and nasal blood vessels.

Thus, branches of the sphenopalatine ganglion carry sympathetic, parasympathetic, and

trigeminal fibers.

Contraindications

The inferior turbinates are very vascular structures and one of the risks of surgery is

hemorrhage. Patients with coagulopathies are clearly at increased risk of complications.Similarly, patients should not be taking any medications or herbs that affect their coagulation

cascade.

Take care when resecting turbinate tissue in patients who have preexisting reports of nasal

dryness and crusting secondary to the concern about atrophic rhinitis.

http://emedicine.medscape.com/article/1292809-overview#showall

Septal Deviations/Turbinate Hypertrophy

Nasal septal deviations are common, and it is rare for doctors to see a perfectly straight nasal septum-

-the dividing line of cartilage between your two nostrils.

Tubinate hypertrophy is due to an enlargement of the turbinates- the small structures within your

nose that cleanse and humidify air as it passes through your nostrils into your lungs. Seehow the

sinuses work.

Symptoms of septal deviations/turbinate hypertrophy

Congested or blocked nasal breathing

Breathing trouble at night and snoring

Chronic nosebleeds

Chronic sinus infections

Causes of septal deviations/turbinate hypertrophy

When septal deviations do cause problems, they are largely due to airway obstruction. It simply feels

as though you cannot breathe well through one or both sides of your nose. This tends to bother

people more at night. Nasal septal deviations can also cause sinus problems and may contribute to

chronic infections.

Patients may also suffer from enlargement of the inferior nasal turbinates. Seehow the sinuses work.

The enlargement of these turbinates can also contribute to nasal obstruction

Diagnosis of septal deviations/turbinate hypertrophy
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Diagnosing septal deviations/turbinate hypertrophy will include the following:

Your doctor will ask for a complete medical history and will perform a thorough physical

examination.

Imaging scans may be ordered including computed tomography (CT) scans.

Your doctor will use an endoscope, a small telescope rod with a lighted end, to examine theinsides of your nose. This will allow your doctor to determine the extent of the deviation or

turbinate hypertrophy.

Treatment

Nasal steroids sprays can be used for problems associated with nasal septal deviations and turbinate

hypertrophy. These medications help to reduce mucosal inflammation and therefore decongest the

nose improving nasal breathing.

However when the septum or turbinate bony structures are causing nasal obstruction or medications

fail to improve symptoms, surgery is often required. This surgery may involvestraightening the

septum(septoplasty) orturbinate reduction(turbinoplasty).

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