Nasal obstruction, Nasal Polyps,  Snoring and Sleep Apnoea

Darren Pinder, Specialist Registrar at St Michael’s Hospital, Bristol.
 
 
 
 

Introduction	Nasal Polyps
Congenital - choanal atresia	Nasal Polyps: Aetiology
Anatomical problems	Nasal Polyps: Treatment
Rhinitis
Allergic rhinitis	Snoring and obstructive sleep apnoea
Infective rhinitis	Pathophysiology of snoring
Non-allergic non-infective rhinitis	Investigations for snoring / OSA
Atrophic rhinitis	Treatment of snoring / OSA

 
 
 
 
 

Introduction

The patient complaining of a blocked nose is an extremely common presentation in the ENT clinic. There are a lot of potential causes; an easy way to sort them out is to think in terms of congenital vs acquired problems. Congenital causes are considered below. The acquired problems can be subdivided as follows:

• anatomical    e.g. a deviated septum. These patients usually complain of unilateral nasal obstruction, which has little variation with the season, time of day or environmental factors.
• variable        e.g. due to rhinitis. These patients will often have bilateral obstruction or obstruction which varies from side to side, with the season or time of day.
• remember that the nasal cycle also influences the sense of airflow through the nose. Put simply, the nasal cycle refers to the effect of the parasympathetic and hormone induced changes in blood flow through the nose. As blood flow increases the mucosa swells, increasing resistance to airflow. The side of maximal flow alters roughly every four hours. Thus it is not unusual for one side of the nose to feel more blocked than the other, and if the side varies through the day this is normal.

Congenital

    Choanal atresia

• This is a rare congenital abnormality in which there is a failure of canalization of the bucconasal membrane. Choanal atresia may be unilateral or bilateral, and structurally it is either bony or membranous. The neonate is an obligate nasal breather so bilateral atresia presents at birth as severe respiratory difficulties. An oral airway or immediate endotracheal intubation are required to safeguard the airway. Unilateral obstruction may be more difficult to diagnose, and can present later in childhood as unilateral nasal obstruction with a mucoid discharge from the affected side. A useful bed(cot)side test is to place a cold spoon under the infants nose; the side of the patent nasal airway mists when the child breathes out, whereas the affected side doesn't as there is no airflow. Another useful test is to try and pass a soft nasal catheter or infant feeding tube down the nose. Confirmation of the diagnosis can be made on endoscopy, and a CT scan helps to plan corrective surgery.
• Treatment is usually surgical. The approach to the atretic area may be through the nose or transpalatal.

Acquired Nasal Obstruction

Anatomical

    Septal deviation

• The nasal septum consists of cartilage anteriorly and bone posteriorly. It is rare to find a septum that is completely central, but only those deviations that cause symptoms are clinically significant. Septal deviations may be developmental in origin or acquired through trauma. The patient complains of long-standing unilateral nasal blockage or blockage which clearly began after trauma. There may be an obvious deformity of the external nose as well. It is thought that the most important point in the nose determining the sensation of blockage is at the nasal valve. This is at the level of the front end of the inferior turbinate. A narrowing here is far more likely to cause symptoms of nasal obstruction than elsewhere.

• Asymptomatic septal deviation does not require treatment. For symptomatic patients, a submucous resection (SMR) or septoplasty may be appropriate. An SMR aims to remove the bent piece of septal cartilage or bone. Whilst this is technically usually straightforward, removal of too much cartilage can leave the dorsum of the nose without enough support such that it sags, giving an ugly saddle deformity. Another well-recognised complication of SMR is a septal perforation, which arises if tears are made in the mucoperichondrial flaps and there is no cartilage between them. A septal perforation may be asymptomatic, but can give rise to bleeding as the edges become crusted, or a whistling sound when the patient breathes, as the perforation acts like the reed of a wind instrument. The septoplasty operation aims to reposition cartilage and preserve as much tissue as possible, thereby avoiding these complications. In reality, most septal operations involve a bit of both techniques.

    Alar collapse

• This can be more difficult to recognise than a septal deformity. The entrance to the nasal cavity is called the vestibule, and it is held open by the springy fibrocartilage of the lower lateral (alar) cartilage. Weakness or deformity of the the lower lateral cartilage can lead to alar collapse on inspiration. Correction of this type of problem is difficult, and may require complex surgery to the tip of the nose.

    Alar stenosis

• stenosis of the alar rim may be congenital, but usually it is acquired through trauma or infection. Injuries to this part of the nose are surprisingly common, and if not dealt with carefully can result in scarring leading to stenosis. Infection or inflammation of the skin around the vestibule (vestibulitis), if long-standing, can give rise to the same problem.

Rhinitis is incredibly common - remember the common cold! It can be sub-divided into different types:

• allergic rhinitis
• infective rhinitis
• non-allergic, non-infective rhinitis (NANI)
• atrophic rhinitis

• allergic rhinitis (AR) is very common, affecting up to 30% of the Western population. It is due to an IgE-mediated type 1 hypersensitivity reaction in the mucosa of the nose. AR may be seasonal (hayfever) or perennial (all year round).
• the allergens responsible are highly soluble proteins or glycoproteins like pollens, moulds or house dust mite droppings.
• in allergic individuals there appears to be either over-production of IgE promoted by T-helper cells, or poor T-suppressor cell function. The Fab portion of IgE binds to the allergen molecule, and the complex then binds to mast cells and basophils, stimulating the release of arachidonic acid metabolites and histamine. The net result is vascular congestion, oedema, rhinorrhea and irritation.

• Seasonal rhinitis occurs at any time from the spring to early autumn, depending on the causal allergen. The typical features are profuse watery rhinorrhea, sneezing and watery, itchy eyes. Some patients will also have a strong family history of atopy or a history of asthma and eczema.
• Perennial rhinitis patients generally have these features too, but the predominant feature is nasal obstruction due to inferior turbinate hypertrophy. There may be a poor sense of smell (hyposmia). These patients are usually allergic to house dust mite, but don't forget to ask about occupational exposure to allergens too. Polyps may be seen, but they are more usually a feature of non-allergic, non-infective rhinitis.

• skin tests - a battery of allergen solutions are injected intradermally in the forearm skin. If there is an                        intense wheal, it is likely that the patient is allergic to that specific allergen. Histamine and carrier controls                         are also injected to ensure that the patient produces a response to histamine and is not allergic to the carrier                  substance. There is a theoretical risk of a severe anaphylactic response, so testing should be done by trained                 individuals with access to resuscitation equipment.

• blood tests - IgE to specific allergens can be measured with RAST (radioallergosorbant test) and total IgE with PRIST (plasma radioimmunosorbant tests). However blood tests are more expensive than skin tests and do not have any greater diagnostic value.

Treatment of allergic rhinitis

• allergen avoidance   helpful but not always possible. The value of house dust mite eradication measures is controversial.
• topical nasal steroid sprays the mainstay of treatment, and highly effective if used properly. Drugs such as fluticasone, beclomethasone and mometazone have minimal uptake from the nasal mucosa into the systemic circulation. The most common side effects are bleeding and crusting in the nose. Both will usually settle with prolonged use. They must be used for at least 6 weeks, probably 3 months, every day before they are deemed ineffective. It is extremely common to see patients who use them for just a few days before deciding they don't work. Not all of them are licensed for very young children, check first!
• topical antihistamines and sodium cromoglycate    not as effective in the nose as topical steroid sprays, but may be of some benefit in children. However, cromoglycate has to be used 5 to 6 times a day, so compliance is a big problem. Antihistamine eye drops seem to be beneficial for the control of local eye symptoms.
• oral antihistamines   e.g. cetirizine, loratidine, astemizole. These new generation anti-histamines are said to cause less drowsiness than older drugs such as chlorpheniramine, as they do not readily cross the blood brain barrier. Nevertheless some patients do experience drowsiness and it may be necessary to swap between drugs to find one suitable for that individual. They are usually well tolerated and many are available in once daily doses, improving compliance.
• depot or oral steroids  due to the systemic effects these are really only indicated to provide relief for special events such as exams.
• desensitization   much more popular in Europe than the UK, desensitization involves a series of injections of purified allergen in the hope that blocking antibodies will be produced. Really only suitable for patients in which one or two causal allergens have been identified.
• leukotriene inhibitors    very new, and of unproven benefit in rhinitis so far.

Infective rhinitis

• usually virally mediated e.g. common cold, influenza, and self limiting. The nasal and sinus linings are in continuity so there is often sinus involvement as well, and the illness is better termed acute infective rhinosinusitis. This is not usually a big problem unless bacterial infection (by H. influenzae, streptococcal or staphylococcal species) occurs. This leads to purulent nasal discharge, headache and facial pain. There may be complications of acute sinusitis. Treatment is usually supportive in uncomplicated cases (paracetamol, NSAIDs, topical nasal decongestants). Antibiotics are used if complications ensue.

Non-allergic non-infective rhinitis (NANI)

This is an inflammatory condition of the nasal mucosa. In practical terms, it is a diagnosis of exclusion. Previously it was divided into two types, eosinophilic and non-eosinophilic, based on the number of eosinophils in the nasal secretions. However it seems that there is probably a spectrum of disorders, with more than one pathological process going on:
 

• imbalance in the autonomic control of mucus production, such that some patients produce copious clear nasal secretions (formerly called vasomotor rhinitis).
• immunological abnormalities are thought to be common, with some patients exhibiting elevated nasal IgE levels or anti-IgE antibodies.
• there may be an intrinsic disorder of mucosal prostaglandin metabolism. These patients may have associated asthma, aspirin hypersensitivity and nasal polyps (Samter's Triad).
• whatever the underlying mechanism, these patients show glandular hyperplasia and submucosal vasodilation, so that the nasal mucosa looks red and swollen, especially over the inferior turbinates.

• familial tendency
• preceding infection
• endocrine (puberty, menstruation, pregnancy)
• drugs (beta-blockers, aspirin, oral contraceptives)
• pollution (atmospheric, fumes, dust, industrial detergents, cigarette smoke)
• alcohol
• smoking

Investigations are aimed at excluding other forms of rhinitis (see allergic rhinitis).

Treatment is largely medical, although there are surgical options for those that do not respond to drug therapy. Predisposing factors, especially smoking, need to be looked at carefully.

• intranasal steroids are the mainstay of treatment. Again, an adequate trial of therapy is required and the importance of compliance cannot be overemphasized.
• antihistamines may be useful in isolated cases.
• topical ipratropium bromide, an anticholinergic can give good results if the main symptom is rhinorrhea.
• topical decongestants have often been tried by the patient before they present to a clinician. They shrink the nasal mucosa and relieve obstruction. However the effect is short-lived and when they wear off there is a reflex vasodilation. Long-term the mucosa becomes unresponsive to decongestant and remains permanently engorged, leading to rhinitis medicamentosa. This is treated by carefully explaining the cause to the patient, stopping the decongestant and using topical steroid sprays instead.
• surgery is reserved for cases refractory to adequate medical treatment. Most techniques are aimed at reducing the bulk of the inferior turbinate, and range from simple diathermy of the mucosa to radical trimming. Diathermy techniques are attractive in that they are fairly safe (although 2 cases of blindness have been reported!!) but the effect is usually short-lived (up to 2 years). Trimming the inferior turbinate probably gives longer term relief but may be associated with severe post-operative haemorrhage, occasionally life threatening.

Atrophic Rhinitis

This is a really unpleasant condition which is fortunately rare in the UK. There is atrophy of the mucosa and bony turbinate leading to a loss of surface area. The humidification action of the nasal lining is lost and the nasal secretions become dry and crusted. Secondary infection is common such that the patient becomes aware of a foul smell all the time (ozaena), which is often apparent to others as well. Even worse, many of these patients lose their sense of smell and are unaware of the foul odour. Like some patients with cholesteatoma, this a diagnosis that can often be made from the odour of the patient when he or she walks into the room. The precise aetiology is not clear but syphilis, TB and nasal surgery have all been implicated. In this country it is most commonly seen after extensive resection of intranasal tissue in cancer surgery. It seems to be more common in hot climates.

Management consists of meticulous local toilet with douches and debridement of the crusts. Surgical management aims to increase the surface area inside the nose by interposition of bone or cartilage. As a last resort, surgical closure of the nostrils (Young's procedure) may allow the mucosa to regenerate.

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Nasal Polyps
 

Key points

• most nasal polyps are inflammatory in origin
• inflammatory polyps are usually bilateral
• be suspicious of a unilateral polyp – it requires biopsy
• if asymptomatic, inflammatory polyps do not require treatment
• suspect cystic fibrosis in a child with polyps

Introduction

Nasal polyps represent the commonest space-occupying lesion in the nose. Although they were originally thought to be a true tumour, they are in fact fluid filled sacs originating from the prolapsed lining of the paranasal sinuses. They have been recognised for thousands of years; Ancient Egyptian skulls have been found bearing the gross features of nasal polyps. Hippocrates (460-370) even described a method for their removal, using a piece of string passed through the nose to the post-nasal space. A sponge was tied to this before pulling it back through the nose, dragging the polyps with it! Even today, the instruments used for surgical treatment of polyps originate from the Middle Ages.

Incidence

The true incidence is difficult to establish, as many people with polyps do not realise they have them, and do not seek medical help. However a rough estimate is 2%. They are much less common in children (0.1%), although 20% of children with cystic fibrosis have nasal polyps.

Age

Nasal polyps are most commonly seen between the ages of 30 and 60, with a peak incidence around the age of 50.

Aetiology

The underlying cause of nasal polyps has puzzled people for many years. Many theories have been proposed. Christopher Heath wrote in 1882: "the influence of the weather upon polypus nasi should be noted, damp causing them to increase largely in size." Many other theories have been added to this, but essentially polyps are a manifestation of inflammation in the nose.

• Allergy 3 factors make allergy an attractive potential cause. First, there is a high concentration of eosinophils, mast cells, histamine and IgE in nasal polyps. Second, they are often associated with asthma (20-40% of cases). This seems to be of late onset, as polyps are not seen to the same extent in children with asthma. Third, the symptoms and signs of polyps may mimic those of allergic rhinitis.

• Infection support for an infectious aetiology comes from the fact that intense antibiotic therapy against pseudomonas along with mucolytic therapy in these patients reduces polyp frequency to 2%-5%. Also, it may explain why polyps are more common in conditions where there is a build up stagnant mucus in the sinuses due to faulty ciliary function, such as Kartagener’s Syndrome and Young’s Syndrome.

Nasal polyps are twice as common in men, although there is no sex difference in patients with Samter’s Triad, suggesting perhaps a different aetiology.

Pathology

• Macroscopic The colour of nasal polyps varies, but they are usually a translucent white, similar to a lychee. With trauma, they may become red and haemorrhagic. They originate from the paranasal sinuses, usually the ethmoids but more rarely the maxillary sinus, which may give rise to the antro-choanal polyp. This fills the nose and extends to the posterior choana.
• Microscopic Nasal polyps have a respiratory epithelium with ciliated columnar cells, like that lining the paranasal sinuses. However the polyp stroma is grossly oedematous with numerous inflammatory cells and very few blood vessels

• Symptoms The commonest complaints are nasal obstruction and hyposmia (poor sense of smell) or anosmia (complete loss of smell). Other prominent symptoms include allergic complaints like watery rhinorrhea, sneezing, and itchy eyes. They may also complain of headache, asthma, or postnasal drip. Pain is usually present when an acute infection exists. Some may have middle ear pathology or rhinitis medicamentosa from chronic vasoconstrictor use. Many have had prior nasal surgery. Antor-choanal polyps may act like a ball valve in the posterior choana, allowing inspiration but blocking the nose on expiration.

• Signs On simple inspection the nose may be widened due to pressure from longstanding polyps. Gross polyps may prolapse from the nose or can be seen with a nasal speculum but less extreme cases may only be evident when the nasal cavity is inspected with an endoscope. Simple inflammatory polyps are usually bilateral, but any unilateral nasal polyp should be viewed as a potential neoplasm and requires biopsy. Polyps are painless on palpation and this can be useful when trying to distinguish them from the turbinates.

	Widened nose due to polyps
	Gross left nasal polyp
	Endoscopic view of polyp in left middle meatus

Differential diagnosis unlike simple inflammatory polyps, neoplasms are usually unilateral, firm, friable and bleed easily.

• inverted papilloma
• meningioma

• meningomyelocoele
• haemangioma
• angiofibroma
• dermoid cyst
• squamous cell carcinoma
• adenocarcinoma

Investigation

No investigation is required for bilateral polyps until surgery is contemplated. A coronal CT scan of the sinuses helps to outline the anatomy of the paranasal sinuses and extent of the disease.

Treatment

• Medical About 50% of patients will respond positively to medical treatment. The mainstay of medical treatment is a topical nasal steroid. On a cellular level, steroids bind to cytoplasmic glucocorticoid receptors and, within hours, they modify gene transcription inducing a change in cellular protein synthesis. There is evidence that the inflammatory reaction in asthma, allergic rhinitis, and nasal polyposis is in part driven by T lymphocytes and the cytokines products they produce. Cytokine production and activation is highly steroid sensitive. Initially we use betamethasone nose drops twice a day for one month to induce shrinkage of the polyps, often in conjunction with one week of ephedrine drops to reduce oedema and allow the steroid drop to get into the nose. Betamethasone is systemically absorbed, and this dose is equivalent to 1mg prednisolone per day, so can only be used for short-term treatment if systemic side effects are to be avoided. Maintenance treatment is given in the form of a non-absorbed topical steroid such as beclomethasone (Beconase). For more severe cases, good response can often be achieved with systemic steroids such as prednisolone 30-40mg daily for 7 days.
• Surgery Reserved for cases refractory to medical treatment, surgery for nasal polyps ranges from simple avulsion with a snare to complex endoscopic procedures aimed at removing all of the diseased sinus lining as well.

For both treatment modalities, there is often a good initial response in nasal airway patency. Improvement in anosmia is harder to predict and varies greatly from patient to patient.

Prognosis

Nasal polyps tend to recur despite treatment, presumably because the underlying causative factor is still present. Unfortunately, there are no good quality randomised trials comparing medical treatment with surgery. Patients with Samter’s Triad show a shorter symptom free interval after treatment.
 

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Snoring and Obstructive Sleep Apnoea

Pathophysiology
Investigations
Treatment
 
 

Introduction

Snoring and obstructive sleep apnoea (OSA) are part of the spectrum of sleep-disordered breathing. Snoring is defined as a noise generated as a result of partial upper airway obstruction during sleep. It should be thought of as one end of a spectrum, with OSA at the other. Not all snorers have OSA, but most patients with OSA snore. Snoring tends to be thought of as rather amusing, but it can cause huge social problems for the patient and his or her partner, and is often blamed for marital disharmony. Interestingly, correction of snoring does not always alleviate these problems!

Pathophysiology

Snoring is a form of "pharyngeal stridor" produced by vibration of  structures such as the tongue, soft palate and lateral pharyngeal wall. The noise is due to the generation of turbulent airflow over these structures. Attempts have been made to predict which of these structures is responsible for the snoring noise by analysing the sound characteristics of the snore.

Obstruction of the airway at any level from the anterior nares to the larynx increases the negative pressure within the oropharynx and nasopharynx during inspiration. The tone within the pharyngeal muscles during sleep is usually sufficient to hold the pharynx open, but if there is increased negative pressure the upper airway can collapse, leading to obstruction.

As the level of sleep deepens, partial relaxation of the pharyngeal muscles may lead to obstruction in susceptible patients. The effect of this may be hypoxia, leading to cardiac dysrhythmia, systemic and pulmonary hypertension and eventually cor pulmonale. There is increased negative intrathoracic pressure as the patient tries to breath against a closed airway, leading to increased cardiovascular strain. Strain receptors in the thoracic wall are activated and this in turn leads to partial arousal of the patient from sleep. The sleep level lightens to a point where pharyngeal tone is sufficient to open the airway. This can happen hundreds of times a night, so that the sleep pattern is severely disrupted. It is this disruption that is thought to be responsible for the characteristic daytime somnolence seen in patients with OSA.

Not all patients with apnoea have OSA. Rarely, apnoea is due to central pathology in the medulla resulting in a failure of respiratory drive, such as the Shy-Drager syndrome.

OSA is not confined to adults. In children, obstruction is usually due to enlarged tonsils and adenoid hypertrophy, but can occasionally be seen in patients with other anatomical problems, such as macroglossia (e.g. Down's syndrome) or a hypoplastic mandible (Treacher -Collins). Such children can have a combination of obstructive and central apnoea - mixed apnoea.
 
 

Clinical features

Snoring in adults is extremely common, in fact most people will snore at some point in their lives. The incidence is greater:

• in men
• with increasing age (10% of men under 30, 60% over 60)
• in obese patients
• in patients with a high alcohol intake

Symptoms

Simple snorers usually present to clinic saying "my wife says I snore". They may be vaguely aware at night of making excessive noise or even of waking themselves up. The patient often volunteers that his or her partner has taken to sleeping in another room and they have stopped going away or staying with friends due to the embarrassment of their snoring. It is well worth asking the patient to attend with his partner and find out what sort of noise they are describing, as there are sleep related noises which are not snoring! The partner may also volunteer the information that the patient "stops breathing" during sleep. Whilst his may be indicative of sleep apnoea it is not unfortunately a good predictor.

Patients may complain of excessive sleepiness during the day. This is a cardinal feature of OSA but may simply represent a manifestation of excessive workload, stress, ill health due to other causes or drug treatment. The Epworth questionnaire (see link) is designed to identify those at risk of sleep apnoea.

Signs

A thorough ENT examination is essential. The aim is to try and identify the cause of the obstruction but this can be extremely difficult. The following may be seen:

• nasal obstruction from a septal deflection or polyps
• adenotonsillar hypertrophy
• palatal oedema or enlargement of the uvula
• crowding of the oropharyngeal isthmus, particularly in obese individuals
• macroglossia or retrognathia
• tongue base enlargement (look for a tumour)
• a "bull" neck. Collar size of >16.5 is said to be the single most reliable predictor for sleep apnoea
• obesity. The body mass index (BMI) helps define the degree of obesity. It is calculated by dividing the mass in Kg by height in metres squared. Tables are available to make this easy. BMI of 19-25 is normal, 26-30 overweight, obese 31-40 and very obese >41. It is important because palatal surgery for snoring is less effective in obese individuals and the risk of OSA increases with BMI.
• flexible nasendoscopy. Essential to exclude laryngeal pathology and assess the airway. Some authors find the Muller manoeuvre useful. The nasendoscope is positioned via the nose at the level of the tongue base, and the patient is asked to breath in with the mouth shut and nose held closed. The degree of collapse is noted, and the manoeuvre is repeated with the 'scope just above the level of the soft palate to assess velopharyngeal closure.

• Overnight pulse oximetry - this is probably the simplest way to detect OSA. It will detect all those with severe OSA but miss some with mild or moderate disease. However it is cheap and simple to do, and may help to screen those who need full polysomnography.
• Polysomnography - the gold standard. Involves the recording of the electroencephalogram, electromyogram to detect limb movements, ECG, abdominal and chest movements, oxygen saturation, body position monitor and microphone to record snoring noise. Some units video the patient whilst asleep too.
• In children with OSA, airway endoscopy under general anaesthesia may be needed to rule out other airway pathology.

Treatment

There is no universal treatment for snoring as it is a multifactorial problem. In general, conservative measures should be exhausted before resorting to surgery.

• General - weight loss, avoidance of sedative medication and alcohol are all worth looking at.

• Nasal obstruction - treatment of nasal problems, whether by medical or surgical means may be helpful - but an improvement in snoring or OSA are not guaranteed. Nasal splints such as the Nozovent may help relieve obstruction.

• Mandibular advancement splint - this is rather like a gum shield but with a lower half as well. It is designed to hold the lower jaw forward to prevent tongue base obstruction. Although it is reported to give good results compliance can be a problem. Also, the splint may be uncomfortable to wear due to strain on the temporo-mandibular joint.

• Uvulopalatopharyngoplasty (UVPPP) - involves tonsillectomy, excision of the uvula and trimming of "excess" soft palate tissue. Short term results (at 6 months) appear to be good with about an 80% chance of abolition or improvement in snoring. However long-term results are less convincing, with up to 50% of patients snoring again at 2 years. It is an extremely painful operation with the potential for significant side effects. There may be nasal escape of fluids short-term due to trimming of the soft palate. This will usually settle but is occasionally permanent. A lot of patients report a change in the quality of voice, taste sensation and on-going throat discomfort.

• Laser-assisted uvulopalatoplasty (LAUP) - the uvula is vaporized by the laser and troughs are cut in the soft palate to form a neo-uvula. Again, the operation is painful and long-term results are lacking.

• Somnoplasty - radio-frequency energy is delivered to the soft palate via a needle to induce scarring and hence stiffening of the tissue. No long-term results yet but appears to be less painful than more traditional procedures.

• Adenotonsillectomy - usually deals with OSA in children if no other pathologies are present.

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