This document discusses the evaluation and treatment of mouth breathing and snoring in children. It outlines the main causes of mouth breathing as allergic rhinitis, enlarged adenoids, enlarged tonsils, and deviated nasal septum. Clinical signs of mouth breathing include sleeping with an open mouth, snoring, nasal obstruction, and irritability. Evaluation involves taking a thorough history and performing physical exams to check for signs of enlarged adenoids or tonsils. Treatment options depend on the underlying cause, and may include removing enlarged adenoids or tonsils, treating allergies, or correcting structural issues.

1. APPROACH TO A CHILD WITH MOUTH
BREATHING AND SNORING
Dr. RAJENDRA SINGH LAKHAWAT
DEPARTMENT OF OTORHINOLARYNGOLOY
SMS MEDICAL COLLEGE, JAIPUR, INDIA

2. The main causes of mouth-breathing
• allergic rhinitis (81.4%)
• enlarged adenoids (79.2%)
• enlarged tonsils (12.6%)
• obstructive deviation of the nasal septum
(1.0%)

3. main clinical manifestations of mouth
breathers
• sleeping with mouth open (86%),
• snoring (79%),
• itchy nose (77%),
• drooling on the pillow (62%),
• nocturnal sleep problems or agitated sleep (62%),
• nasal obstruction (49%),
• irritability during the day (43%).

4. Patient history protocol with clinical criteria for
identifying mouth-breathing children
MAJOR SYMPTOMS
• Snores
• Sleeps with mouth open
• Drools on pillow
• Complains of a blocked nose every day

5. MINOR SYMPTOMS
• Itchy nose
• Complains of a blocked nose sporadically
• Nighttime breathing difficulties or agitated sleep
• Sleepy during the day
• Irritable during the day
• Difficulty or slow swallowing food
• More than three episodes of ear nose or throat infection
(confirmed by a doctor) during previous 12 months
• Problems at school or failed years
(Children were considered mouth breathers if they had two major signs or one
major sign associated with two or more minor signs at the time of the pediatric
consultation)

6. Physical examination protocol for
identification of mouth-breathing children
MAJOR SIGNS
• Craniofacial abnormalities (adenoid facies)
• High arched palate
• Open bite (with no history of thumb sucking or
pacifier use)
• Hypertrophy of nasal conchae
• Deviated nasal septum
• Tonsils increased in size to grade III or IV
• Cleft lip (protruding lower lip)

7. MINOR SIGNS
• Abnormal chest
• Abnormal posture
• Involvement of tympanic membranes (opaque
appearance, hyperemia, perforation and/or thickening)
• Nasal voice
• Speech disorders (tongue thrust, mixing up letters )
• Children were considered mouth breathers if they had
two major signs or one major sign associated with two
or more minor signs at the time of the pediatric
consultation.

8. Clinical Differences in Sleep-disordered Breathing
between Children and Adults

9. NASAL OBSTRUCTION
• SYMPTOMS – stertor , mouth breathing ,
feeding problems, sleep disturbances and
rhinorrhoea, failure to thrive, significant
nocturnal obstruction, intermittant cyanosis
or apnea.
• Nasal Blockage – may be U/L or B/L , complete
or partial, intermittant or constant, acute or
chronic, by birth or acquired later, gradual in
onset or sudden

10. Congenital causes of nasal obstruction
in children

11. ACQUIRED CAUSES OF NASAL
OBSTRUCTION
• STRUCTURAL - Osseocartilagenous nasal Deformity ,
Foreign body
• INFLAMMATORY
-Infective
-Allergic - Rhinosinusitis/polyposis
-Neonatal rhinitis , pubertal rhinitis
• TUMOURS – Angiofibroma , Olfactory neuroblastoma,
Rhabdomyosarcoma
Nasopharyngeal carcinoma
Haemangioma - vasoformative disorder
Fibro-osseous disease

12. Systemic diseases causing nasal
obstruction In children .
• Cystic fibrosis
• Ciliary dyskinesia
• Immune deficiency
• Sarcoidosis
• Wegener's granulomatosis

13. CHOANAL ATRESIA
• rare condition (incidence 1 in 7000 live births),
there is complete obstruction of the posterior
nasal openings on one or both sides.
• It is believed to be secondary to persistence of
the nasobuccal membrane.
• Bilateral choanal atresia will present as an acute
respiratory emergency at birth as newborns are
obligate nasal breathers.
• The classical picture of cyclical cyanosis (blue
spells relieved by crying) is seen

14. Unilateral choanal atresia as viewed from the nasopharynx with a 120
degree endoscope. A sound is perforating the membrane.

15. Dermoid Cyst
• Dermoid cysts derive from ectoderm and
mesoderm and can contain all the structures
of normal skin. Nasal lesions account for
between 1 and 3 percent of all dermoids and
are the most common midline nasal mass.

16. • Septal haematoma/abscess -Persistent nasal
obstruction following injury should raise
concern regarding the possibility of a septal
haematoma.
• Foreign bodies- In a small child with unilateral
foul discharge, a nasal foreign body must be
excluded. If the object has been present for
some time, calcareous deposits can form
around it resulting in a rhinolith

17. Allergic rhinitis
• It is defined as an inflammatory process of the
nasal mucosa sufficient to provoke unilateral or
bilateral nasal obstruction with intermittent or
persistent obstruction resulting from hypertrophy
of the inferior, middle or superior nasal Conchae.
• It is nowadays a global public health problem in
the general population with a major impact on
children's quality of life.

18. Symptoms of AR
• Paroxysmal sneezing , 10 20 sneezes at a time
• Nasal obstruction
• Watery nasal discharge and itching in the nose
• Loss of sense of smell
• Frequent colds
• Hearing impairement due to ET tube blockade

19. SIGNS OF AR
• Nasal signs – transverse nasal crease, pale and
edematous nasal mucosa, turbinates are
swollen
• Ocular signs – retracted TM or serous OM
• Pharyngeal signs- granular pharyngitis d/t
hyperplasia of submucosal lymohoid tissue
• Laryngeal signs- hoarsness of voice and edema
of vc

20. • Treatment of AR
1. Avoidance of allergen
2. Antihistaminics
3. Sympathomimetic drugs
4. Corticosteroids
5. immunotherapy

21. ADENOIDS
• All immunologically healthy children have
adenoids from birth, which reach peak growth
between four and 5 years of age and then
undergo a process of atrophy, which is
complete at around 10 years of age

24. ADENOIDECTOMY
• Adenoidectomy with or without tonsillectomy
and/or insertion of ventilation tubes is one of
the most frequently performed surgical
procedures in children.
• Techniques employing direct vision have the
advantage of reduced blood loss <4 mL versus
> 50 mL) and the ability to remove adenoid
tissue from the choanae, while avoiding
trauma to the Eustachian cushions

25. • suction coagulator and the micro debrider has
the largest clinical experience
• microdebrider was 20 percent faster than the
curettage technique
• but the suction coagulator is significantly
cheaper than the microdebrider
• majority of children may be safely discharged
home within six hours of adenoidectomy.

26. COMPLICATIONS Of
ADENOIDECTOMY
• bleeding;
• dental trauma;
• airway obstruction, due to: - retained swab; -
nasopharyngeal blood clot;
• infection;
• cervical spine injury (particularly in Down
syndrome);
• velopharyngeal dysfunction;
• regrowth of the adenoid.

27. BLEEDING
• The reactionary haemorrhage rate, that is,
bleeding following adenoidectomy, within 6-
20 hours of operation is less than 0.7 percent
• if severe enough to require a return to
theatre, postnasal packing is the preferred
management
• postnasal packing left in situ for four hours
post -haemorrhage is as effective as packs left
for 24 hours

28. RETAINED SWAB
• A swab may be retained either in the
nasopharynx or in the laryngopharynx, hidden
from the operator's view

29. Nasopharyngeal blood clot
• Blood may pool and clot in the nasopharynx
during the procedure. The nasopharynx
should be gently suctioned to clear any clot
before removing the gag.
• Failure to do so may lead to the clot falling
onto the larynx during recovery and causing
potentially fatal acute airway obstruction (the
'coroner's clot')

30. Cervical spine
• Nontraumatic atlantoaxial subluxation (Grisel
syndrome) is rare, but associated with overuse
of diathermy either for removal of the
adenoid or following curettage when used for
haemostasis.
• Minimum power settings for diathermy should
always be used.
• Children with Down syndrome may have
atlantoaxial instability.

31. Typical adenoid facies
Note the long face, open mouth posture, short upper lip, larger lower lip,
small nose, and dull facial expression.

32. TONSIL SIZE GRADING
Grade 0: Tonsils absent
Grade 1: hidden behind tonsillar
pillars
Grade 2: Extend to pillars
Grade 3: Visible beyond pillars
Grade 4: Enarged to midlin

34. SNORING AND SLEEP APNEA
• SNORING – it is an undesirable disturbing sound
that occurs during sleep.
• MECHANISM – muscles of pharynx are relaxed
during sleep and cause partial obstruction.
Breathing against obstruction causes vibrations of
soft palate, tonsillar pillars and base of tongue
producing sound.
• Snoring may be primary, i.e. without association
with OSA , OR complicated i.e. associated with
OSA

35. • Simple snoring is defined as snoring without
obstructive apnoeas, frequent arousals or gas exchange
abnormalities.
• Upper airways resistance syndrome is a more subtle
form of sleep-disordered breathing than OSA.
• It is characterized by partial upper airway obstruction.
The frequency and severity of apnoeas is insufficient to
warrant a diagnosis of OSA.
• UARS can lead to significant clinical symptoms as a
result of night-time arousals and pulmonary
hypoventilation.

36. OSA
• Obstructive sleep apnea (OSA) is characterized
by episodic partial or complete obstruction of
the upper airway during sleep.
• An 'apnea' is defined in adults as cessation of
breathing for ten seconds or more. Six
seconds or less may be pathological in
children.

37. • OSA causes loud persistent snoring interrupted
by gasping or choking episodes and silent periods
which are apnoeas.
• It causes significant sleep disruption. This can
lead to daytime neurobehavioural problems such
as an increase in total sleep time, hyperactivity,
irritability, bed-wetting and morning headaches.
• Untreated OSA can result in significant morbidity
such as failure to thrive, pulmonary hypertension
and right heart failure.

38. • prevalence of sleep-disordered breathing in
children is unknown but may be as high as 11
percent.
• OSA has a prevalence of approximately 2 percent
in the paediatric population.
• Peak incidence is between the ages of three and
seven, when the adenoid and tonsillar lymphoid
tissue is disproportionately large relative to the
pharyngeal airway.
• There is an equal incidence in boys and girls but it
presents earlier in boys.

39. Children with increased risk of OSA

40. CLINICAL SIGNS OF SDB
• loud snoring
• increased respiratory effort with flaring of the
nostrils
• suprasternal and intercostal recession.
• Complete obstruction of the pharyngeal airway,
as in OSA, leads to silent periods followed by
choking or gasping as the child rouses from sleep
to reestablish their airway.
• Partial (hypopnoea) or complete upper airway
obstruction (apnoea) during sleep can lead to
hypoxia and hypercarbia.

41. • Full polysomnography is the 'gold standard'
investigation for sleep disorders.

42. SYMPTOMS
• Snoring
• Children with significant obstruction sweat
during sleep particularly in the nuchal area.
• tracheal tug and intercostal recession with
loud stertorous breathing.
• restlessness at night, often adopting unusual
sleeping positions in an attempt to relieve
their upper airway obstruction

43. • regurgitation or vomiting during sleep
(because of high intrathorasic pressure)
• Choking episodes.
• This is best enquired about by imitating a
guttural noise, as parents are often not aware
of why the noise is being created.
• Parents often describe witnessed apnoeas as
momentary breath holding.

44. • True daytime somnolence as described in
adults is unusual in children. Hyperactivity is
more common and affected children are often
irritable on waking.

45. CLINICAL EXAMINATION
• SDB is more common in the obese child
• Conversely, SDB in a child can cause failure to
thrive or a decrease in growth rate.
• Children with a triangular chin, steep mandibular
angle, retrognathia, narrow high -arched palate
and long soft palate are likely to have SDB
• Examination within the nose should look at the
structure of the septum and the quality of the
nasal lining for the presence of rhinosinusitis

46. • Daytime mouth breathers
• Hyporesonant voice points to enlarged
adenoids
• Nasendoscopy with a fibreoptic endoscope to
ascertain the size of the adenoid pad and
extent of choanal obstruction
• Examination within the oral cavity should
exclude a submucous cleft and be used to
document the size of the tonsils

47. A nasendoscopic view of the adenoids in a child showing > 50 percent choanal
obstruction

48. An endoscopic view of the same adenoids using a 90° rigid fibreoptic telescope introduced
through the mouth

49. An intraoral photograph of a seven-year-old child showing large obstructive tonsils

50. • Although most children with OSA have large
tonsils.
• But there is little correlation between the size
of the tonsils and the severity of SDB.
• SDB in which tonsils are smaller in size are
cerebral palsy, previous cleft palate repair,
very large adenoid pad, syndromic children
• Other

51. • Daytime stertorous breathing and growth
retardation are indicative of severe sleep
apnoea.
• broken veins on the face indicates raised
venous pressure in the face due to upper
airway obstruction.
• Pectus excavatum can result from long-
standing intercostal recession during sleep

52. INVESTIGATIONS
• Pulse oxymetry is a screening tool
• Visi-Lab includes pulse oxymetry , video
footage for movement detection and sound
recording.
• apnoea/hypopnoea index

53. • The gold standard investigation for sleep
disorders is full polysomnography.
• This monitors EEG activity, chest and abdominal
movement, oxygen saturation, nasal or oral
airflow, end tidal carbon dioxide and continuous
ECG recordings
• full polysomnography is detailed and expensive
and cannot be provided for every child suspected
of suffering with SDB

54. RECOMMEDATIONS FOR INVESTIGATIONS

55. SLEEP ENDOSCOPY
• In children, sleep nasendoscopy can be performed with
the child breathing spontaneously a mixture of
halothane and oxygen.
• The sites of upper airway obstruction can be
documented using a four-level classification system.
• level 1 or Adenoid pad and velopharyngeal obstruction
• level 2 or tonsillar obstruction;
• level 3 or tongue base obstruction;
• level 4 or supraglottic obstruction.

56. LEVEL 1 LEVEL 3
LEVEL 2
LEVEL 4

57. Rigid laryngobronchoscopy
• Performed in the assessment of syndromic
children with complex obstructive breathing and
in children who have a history of prematurity and
prolonged inhalation on a neonatal intensive care
unit.
• It is important to exclude the presence of
pathology distal to the glottis that may be
exacerbating the upper airway symptoms.
• E.g. subglottic stenosis, tracheomalacia,
innominate artery compression, bronchomalacia
or vascular rings

58. IMAGING
• Chest X-Ray is mandatory in all cases of
moderate to severe OSA to identify pulmonary
hypertension and RVH
• It also detects atelactasia due to chronic
hyperventilation
• A lateral x-ray of the post-nasal space is useful
in ascertaining adenoid size in children in
whom flexible nasendoscopy has not been
possible

59. A lateral soft tissue
x-ray of the head
and neck of a
three-year-old
child with
significant
obstruction of the
nasopharyngeal
airway by enlarged
adenoids.

60. MEDICAL TREATMENT OF OSA
• Children with OSA who present with
mucopurulent nasal discharge should have
this treated. It will improve their nocturnal
symptoms.
• Four to six-week course of systemic antibiotics
combined with topical intranasal steroids.
These children should be tested for sensitivity
to airborne allergens.

61. • CPAP provides continuous insufflation of the
nasopharyngeal airway during sleep, thereby
splinting the airway and maintaining its patency
• Obese child, syndromic children and children with
cerebral palsy may not be considered surgical
candidates and may benefit from long-term CPAP
• Nasopharyngeal Airway is of particular use in the
newborn and in the first few months of life

62. SURGICAL TREATMENT
• Adenotonsillectomy is the treatment of choice for
otherwise healthy children suffering with sleep-
disordered breathing.
• 10 percent of apparently healthy children
continue to have OSA after adenotonsillectomy
• This group consists of the clinically obese, those
with mild craniofacial disproportion, deviated
nasal septum, and those with small tonsils on
examination

63. • Other surgical treatments for OSA in Down
syndrome include tonsillar pillar plication after
tonsillectomy, midface advancement,
uvulopalatopharyngoplasty (UVPP) , anterior
tongue reduction and hyoid suspension.

64. TREATMENT OPTIONS ACCORDING TO THE
LEVEL OF OBSTRUCTION SEEN AT SLEEP
NASENDOSCOPY
• Level 1 obstruction (velopharyngeal obstruction) is relieved
by adenoidectomy or UVPP.
• Level 2 obstruction (tonsillar) is relieved by tonsillectomy.
• Level 3 obstruction (tongue base) can be relieved with the
use of nasopharyngeal airways, glossopexy, mandibular
advancement splints or CPAP.
• Level 4 obstruction (supraglottic) is due to collapse of the
supraglottic tissues and manifests in its commonest form as
laryngomalacia. It is a common finding in children with
cerebral palsy who have upper airwaY obstruction. The
treatment obstruction at this level can be site specific in
the form of laser supraglottoplasty or anterior
epiglottopexy

65. THANK YOU