Tuesday, November 14, 2006

Sleep-Disordered Breathing, Mouth Breathing and Quality of Life

Baby asleep; mouth slightly open, poster titled Perfect Moment
I'm british, so please overlook my frequent use of the word interesting. I have a strong interest in children with sleep-disordered breathing (SDB) so I've just looked through the abstract of an interesting paper on Factors affecting quality of life of pediatric outpatients with symptoms suggestive of sleep-disordered breathing.

The authors examined several factors in SDB and children's quality of life. They report the following:
The most common clinical findings was mouth breathing (41.2%). Tonsillar hypertrophy (>/=3+) was found in 62.7 and 52.9% had adenoid-nasopharyngeal ratio greater than 70%. Overweight/obesity were found in 35.3% of the patients. OSA-18 scores ranged from 22 to 85. Tonsillar hypertrophy was significantly related to QOL (p<0.05). Adenoid hypertrophy had trends towards impact on QOL (p=0.094). Mouth breathing correlated well with QOL (p<0.01).
We know from previous research that habits such as habitual mouth-breathing during the day may be clinically relevant in conjunction with other symptoms for severe obstructive sleep apnoea. The prevalence of mouth-breathing strongly supports my own anecdata working with children with SDB so I was pleased to see this.

Swollen tonsils and adenoids are common in children with SDB so I was intrigued to that the authors found that tonsillar hypertrophy was significant but not adenoidal hypertrophy in the population that they looked at. It was a contentious review in places but Gross and Harrison gave a common description of the consequences of mouth breathing in their discussion of tonsils and adenoids:
Mouth breathing presumably causes changes in facial growth patterns as the tongue is placed in an abnormally low position to expand the oropharyngeal cavity. Over time, due to altered vectors of force on facial development, the child develops a long and narrow face, a narrow upper jaw, steep palate, and open bite deformities. This classically is referred to as "adenoid facies".
Adenoid facies are further reviewed and discussed in Adenoid Facies and Nasal Airway Obstruction.

I'm going to be a little persnickety and say that although the authors declared that their objective is:
[t]o determine the relationship between causative factors of sleep-disordered breathing (SDB) and quality of life (QOL) of children who presented with SDB
they should not claim that they are looking at causative factors. Previous studies have reported strong correlations for some of the factors but I can not accept that they are established as causative. Kotagal and Pianosi published an excellent review of Sleep disorders in children and adolescents earlier this year and it is clear that there is much uncertainty about what may be considered as causative. As for the discussion on adenoid facies and nasal airway obstruction, the sequence of events is not clear.

Wherever possible, encourage children to breathe through the nose. Nose-breathing is a useful part of re-training the breathing of children. Maddeningly, I have colleagues in other countries who report that they have worked with children with adenotonsillar hypertrophy that has been documented in scans. They have worked with the children to re-train their breathing and when those children have returned for scans, their hypertrophy has been significantly reduced. Anecdotes are useless however; at the bare minimum, we need to see these examples published in a case series.

For more information about the image used in the illustration click on it or visit the detail on Flickr.

16 Comments:

Blogger Flea said...

Shinga,

It may be the lateness of the hour, but I'm having trouble understanding the mechanism to explain how nose breathing may reduce adenotonsillar hypertrophy!

Can you point to any sources?

best,

Flea

1:45 am  
Blogger Shinga said...

Hi Flea,

It's certainly not the lateness of the hour. I am frustrated with my colleagues who have reported the reduction in the size of adenoids and tonsils precisely because they have not documented the cases. At present, this is no better than anecdote. Even if individual case-studies or case-series were published, it would need an appropriate clinical trial before it could be validated as a useful intervention.

We don't just ask people to shut their mouths and breathe through the nose - there is a fair amount more than that. I ask people to start doing this as a first step because it is easy to implement and doesn't need elaborate instructions. Unless people have nasal anomalies that they already know about - then there are few contraindications to be concerned about when recommending that people should breathe through the nose rather than mouth, wherever practical. Similarly, during the breathing re-training we emphasise diaphragmatic breathing rather than obvious effort in the upper-thoracic region. We be-labour the importance of posture. I don't find those easy to communicate in writing because so much depends on direct observation of the child's breathing pattern and posture.

However, with some children who are obvious and noisy mouth-breathers, once we have worked with them to clear the nose (if that is a problem) they derive a surprising amount of benefit just from something as simple as nose-breathing.

There are several putative mechanisms for why the method as a whole rather than just nose-breathing is helpful, but I will comfine myself to nose-breathing here for reasons of simplicity. Some of the support for this is patchy and garnered from sources that were not researching this area. I'm going to mention them here and will make a note to write them up in a post.

In Nose Breathing: The Why (If Not Yet The Dao) I mentioned the following.

Nose-breathing (in and out):
*filters
*warms
*humidifies
the air before it reaches the lungs: on exhalation, it contributes to an efficient heat and moisture exchange. So, the nose not only contributes to our sense of smell, it is involved in respiration, speech production, heat exchange, humidification, filtration and antimicrobial defence.

The nose has a very rich blood supply, so when we breathe in through the nose, the airstream is exposed to the protective mucus and serous defence mechanisms. An adult produces around 30 gloriously gloopy fluid ounces of mucus per day.

In a recent experiment, the volunteers took their shoes and socks off and half had their feet chilled in ice cold water for 20 minutes while the others sat with their feet in an empty bowl. 29% of the chilled volunteers developed cold symptoms over the next 4-5 days compared to only 9% in the control group.

One of the research authors, Professor Ron Eccles said: "When colds are circulating in the community many people are mildly infected but show no symptoms. If they become chilled this causes a pronounced constriction of the blood vessels in the nose and shuts off the warm blood that supplies the white cells that fight infection. The reduced defences in the nose allow the virus to get stronger and common cold symptoms develop. Although the chilled subject believes they have "caught a cold" what has in fact happened is that the dormant infection has taken hold."

Now, Professor Eccles does not explicitly recommend breathing through the nose but I believe that it is implicit in his comments. Eccles speculates that the research indicates the importance of keeping the nose warm, and the blood supply circulating freely: "A cold nose may be one of the major factors that causes common colds to be seasonal. When the cold weather comes, we wrap ourselves up in winter coats to keep warm, but our nose is directly exposed to the cold air. Cooling of the nose slows down clearance of viruses from the nose and slows down the white cells that fight infection."

Would you find it too much of a stretch from that to argue that if we are able to use the nose as a first line of defence against particle, bacteria and viruses then it is plausible that it is practical to reduce some of the defensive burden on adenoids and tonsils that can lead to them becoming swollen or even reservoirs of infectious bacteria?

I'm going to put some additional material in another comment because this is too long.

Regards - Shinga

4:18 pm  
Blogger Shinga said...

Crudely speaking (because this is a blog comment), nose-breathing also exposes the air to nitric oxide. Nitric oxide is a potent vasodilator and anti-microbial that also improves the free movement of the fine hairs that allow the efficient removal of detritus and mucus. So nose-breathing offer a number of benefits, including the efficient killing of harmful organisms and better gas-exchange in the lungs and increased PaO2 of the blood (estimated at 10%). There is speculation that nitric oxide is an important defence mechanism even when the nose and sinuses are blocked.

You will be more familiar than I am with the speculation about the origin of NO in nasal air and the relative contributions of the sinuses and other parts of the airway. There are, however, some plausible indications that indicate that the paranasal sinuses rather than the mucosa of the nasal cavity is a major source of nasal NO in adult healthy humans.

NO is a powerful vasodilator and will itself enhance blood flow and increase the exposure of viruses and bacteria to those useful white cells. I consider that it is plausible that NO contributes to better sinus ostia patency which improves drainage and lessens the risk of stagnancy and sinus infection that would place a defensive burden on the adenoids and tonsils.

There is a lot of speculation about the defensive properties of NO against the growth of pathogens that include bacteria, fungi and viruses. NO has been variously credited as a major player in the host defence of the upper airways.

I will put together a post on NO but (as mentioned above) some researchers have argued that it stimulates ciliary motility and has a protective role in defending the upper airways from irritation.

There are several papers that describe the impact of humming on NO on the paranasal sinuses - and I shall pop those into a post. One of my least favourite references is from a less than satisfactory source. Warning: I disagree with some of the material in this case report, but I have used this technique with people with chronic rhinsiusitis. Strong humming for one hour daily to terminate chronic rhinosinusitis in four days: A case report and hypothesis for action by stimulation of endogenous nasal nitric oxide production.

Indirectly, there is a literature that supports the Categorization of patients with allergic rhinitis: a comparative profile of "sneezers and runners" and "blockers". The 'blockers' were found to be predominantly mouth breathing (81%) and to have perennial rather than seasonal allergic rhinitis. The 'blocking' is indirect support for lack of drainage of infectious material that stresses the ENT area, adenoids and tonsils.

Now - I have been told several times that there is evidence that the nasal route of breathing reduces the carriage of respiratory and other pathogens in the nasopharynx: I have even been told that the reduction is 15%. But - despite my chasing, I have never been given the source for this. I shall pursue this again.

Slightly OT for this but within scope is the immunological consequences of sleep-disordered breathing. A recent paper indicates that, even in normal awake subjects, mouth-breathing promotes the occurrence of SDB even in non-apnoeic people because of the influences of the breathing route in upper-airway dynamics.

Using my phonetics hat - mouth-breathing depletes the sol layer and dries the vocal folds, increasing the phonation threshold pressure (Pth). Increased Pth and vocal effort can irritate and inflame the UA and make them more hospitable to various pathogens that nestle into the naso-pharyngeal area.


Regards - Shinga

6:33 pm  
Blogger Shinga said...

I don't follow but do keep an eye on the research about saliva in mouth-breathers. Authors of a recent paper reported that "Since a higher level of free sialic acid is indicative of an increase in the number of bacteria in saliva, our findings suggest that mouth-breathers retain more bacteria in oral tissues." There are other papers that identify some of these bacteria and suggest that they are pathogens rather than useful bacteria. If this can be validated then it might suggest a plausible mechanism for the hypertrophy of tonsils and exacerbations of ENT infections.

There is an interesting tangent about the literature in dentistry research that reports that mouth-breathing children tend to have cranio-facial changes that are implicated in poorer drainage and a greater number of ENT infections.

Anatomy of oral respiration: morphology of the oral cavity and pharynx asserts that: "The anatomical states of the oral cavity and pharynx during mouth breathing in children with adenoid hypertrophy and in adults confirmed the speculation that mouth breathing is disadvantageous compared with nose breathing". It is pretty much a given among otolaryngologists - and I'm sure that the ones who taught me must have mentioned immunological consequences as well as anatomical - but we were more concentrating on the implications for speech physics and acoustic phonetics - so, perhaps not.

Dentists seem to expend considerable research effort on irritatingly small studies of caries prevalence, levels of mutans streptococci, and gingival and plaque indices in young mouth-breathing children v. the nasal breathers. The various reports are 'yes it does', 'no it doesn't'. So, depending on the populations and the research sources, mouth-breathing may again contribute to higher-levels of oral and naso-pharyngeal bacteria/pathogens which may or may not be of clinical relevance.

Regards - Shinga

7:08 pm  
Blogger Shinga said...

Final tangent - I'm also going to say (but track down some references to support) that nasal breathing rather than mouth-breathing is better at filtering out some particulates from exposure to environmental tobacco smoke. The relationship between ENT infections and ETS is well documented.

Regards - Shinga

7:27 pm  
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