1) Paediatric rhinosinusitis and its complications discusses the anatomy, development, and types of sinusitis in children. It can cause orbital or intracranial complications if not properly treated. 2) Acute bacterial rhinosinusitis is diagnosed clinically based on symptoms and confirmed with imaging or culture if severe. Treatment involves antibiotics, intranasal steroids, and surgery if abscesses form. 3) Orbital complications range from preseptal cellulitis to orbital cellulitis, subperiosteal abscess, orbital abscess, and cavernous sinus thrombosis. IV antibiotics and surgical drainage may be needed for abscesses. Intracranial complications can also occur.

1. PAEDIATRIC RHINOSINUSITIS
AND ITS COMPLICATIONS
DR LATHIKA IIYR MS PG (ENT)
MODERATOR:PROF.DR ARUL SUNDARESH KUMAR MS(ENT)
CHAPTER:24
VOLUME:2 PEDIATRICS
PAGE NO-261-278

2. ANATOMY
• The paranasal sinuses are air-containing spaces which are
positioned around the nasal cavities, communicating with
these via natural ostia.
• They are lined by type II pseudostratified columnar
ciliated epithelium (respiratory mucosal epithelium),
• cilial function - facilitate mucus drainage & preserve a sterile
environment
Sinus development is progressive throughout childhood.
At birth, the maxillary sinuses measure 7 (d)* 3 (w)*(h) in mm.
The sphenoidal (sphenoid) sinuses and two or three ethmoidal
(ethmoid) cells are found on each side at this stage.
The ethmoid labyrinth is complete by 4 years of age.

3. Frontal sinuses
• The frontal sinuses not present at birth,
develop from cranial extension of the ethmoid
cells.
• Once the roof of these frontal cells-the level
of the upper orbit-around the age of 5 years,
they are termed ‘frontal sinuses’.
• These are demonstrable radiographically in
20–30% of children by 6 years and more than
85% by 12 years of age.

4. The maxillary sinuses
• Expand in parallel, reaching –level of nasal floor by 7–8 years
of age,
• 4–5 mm below this by adulthood.
• Sinus expansion causs dimensional changes of the midface
during adolescence and towards adulthood.
The maxillary and ethmoid sinuses-reach full size by the age of
15 or 16.
The frontal sinuses by 19 years of age.

5. Sphenoid sinuses
• The sphenoid sinuses
extend posteriorly over
the first 7 years, and are
radiologically distinct.
• completing growth by
15 years, although
some posterior
extension can be seen
into adulthood.

6. ‘Inflammation of the nose and paranasal sinuses characterized
by two or more symptoms, one of which should be either nasal blockage/
obstruction/ congestion or nasal discharge (anterior/posterior nasal drip):
• +/– facial pain/pressure
• +/– cough (as opposed to reduction or loss of smell in
the adult definition).
and either:
• endoscopic signs of:
❍ nasal polyps, and/or
❍ mucopurulent discharge primarily from the middle meatus, and/or
❍ oedema/mucosal obstruction primarily in the middle meatus
and/or:
• CT changes:
❍ mucosal changes within the osteomeatal complex
and/or sinuses’.
DEFINITIONS

7. SEVERITY OF DISEASE
• According to EPOS,visual analogue scale (VAS).
• A score of 0–3 is classed as mild,
• >3–7 moderate and
• >7–10 is severe.
• A score of greater than 5 indicates symptoms
which affect patient quality of life.
• Using a 10 cm scale, between 0 (not
troublesome) and (worst thinkable), the patient
(or parent) is asked to mark the severity.

8. Acute rhinosinusitis
(ARS) in children is defined by EPOS as:
‘Sudden onset of two or more of the symptoms:
• nasal blockage/ obstruction/ congestion
• or coloured nasal discharge
• or cough (daytime and night-time) for <12 weeks (with
symptom-free intervals if the problem is recurrent).’
The symptom profile defined by ICAR:RS4 is similar, but with
ARS defined by a duration of less than 4 weeks.
Both stress the inclusion of questions regarding allergic
symptoms (sneezing, watery rhinorrhoea, itching of the nose
and eyes), to help differentiate allergic from viral and bacterial
RS.

9. PAEDIATRIC ACUTE
RHINOSINUSITIS
Epidemiology and pathophysiology
• Sinuses are also involved in decreasing order of frequency:
1. Maxillary and ethmoid (60%),
2. Sphenoid (35%) and
3. Frontal (18%),
 RS is commonest in younger children, and the prevalence decreases
sharply after 6–8 years of age- immune system immaturity at an
early age.
 Seasonal variations in the prevalence of RS -viral URTI, with an
increase in occurrence in autumn and winter.
 Young children looked after in day care with other children have
markedly higher rates of RS than those managed at home.

10. Infections are often polymicrobial
• The commonest bacteria isolated
from maxillary sinus aspirates (ABRS)
are
1. Streptococcus pneumoniae,
2. Untyped Haemophilus influenza,
3. Moraxella catarrhalis, and
4. Staphylococcus aureus,
5. Streptococcus pyogenes
6. Streptococcus viridans
• Pseudomonas aeruginosa
1. Nosocomial infection,
2. Immunocompromised (including
HIV cases),
3. Patients- nasal catheters and other
devices,
4. cystic fibrosis.
• Anaerobes:
1. Peptostreptococcus
2. Fusobacterium,
odontogenic origin, oral pathogens
• Staphylococcus aureus is commonly
isolated from sphenoid sinusitis.
• methicillin-resistant S. aureus (MRSA)
are increasing in cases of ABRS.

11. Acute bacterial rhinosinusitis
(ABRS) is diagnosed clinically, according to EPOS,2 by the presence of
at least three of:
• discoloured discharge (with unilateral predominance)and purulent
secretion
• severe local pain (with unilateral predominance)
• ‘double sickening’ - deterioration after an initial milder
phase of illness
• elevated erythrocyte sedimentation rate (ESR)/C-reactive
protein (CRP)
• fever (>38 °C).
• In children, the cough often worsens at night (in 80% of cases),
with nasal symptoms (anterior/posterior discharge) in 76%, and
associated fever for more than 3 days in 63%.
• Halitosis is commonly seen in addition, but associated facial pain
and swelling, headache and sore throats are unusual in children

12. Differential diagnoses
IN CHILDREN WITH NASAL DISCHARGE:
A. Nasal foreign body or
B. Choanal stenosis or atresia.
C. Dental disease may also give rise to sinonasal and
facial symptoms.
D. Hypertrophy and inflammation of the adenoids
(adenoiditis) may also present with nasal obstruction
and mucus.
E. Parental history may suggest allergic rhinitis
These can usually be excluded with careful examination,
including nasal endoscopy

13. CLINICAL EXAMINATION
• General observations:
1. temperature
2. Neurological status
• Complete ENT and head and
neck examination
1. Pharynx,
2. Oral cavity and teeth,
3. Orbits, ocular motility, vision,
pupillary response,
4. Facial palpation and
5. Percussion over the
paranasal sinuses,
6. Cranial nerves.
ANTERIOR RHINOSCOPY
(oedema, inflammation,
mucus/pus, foreign body)

14. Nasal endoscopy
• (rigid or flexible), including middle meatal swabs for
culture and sensitivity.
• The nasal and pharyngeal mucosa is typically
erythematous, with yellow/green nasal discharge of
varying consistency.
• ASSOCIATED FEATURES:
1. post-nasal drip of mucus into the pharynx in 60%,
2. middle meatal pus in 50%
3. oedema of the inferior turbinates in 29%.
4. Adenotonsillar enlargement
5. tender cervical lymphadenopathy

16. MICROBIOLOGY
• Antral aspiration-the gold standard- although it is impractical in
everyday practice. This is reserved for particularly severe or
resistant cases
• An alternative method -take a swab from the maxillary sinus under
endoscopic guidance.
• Isolates are considered positive when they contain >10,000CFU/ml
INDICATIONS FOR CULTURE ARE:
• severe symptoms and toxic patient
• illness not improving after 48–72 hours of medical treatment
• immunocompromised patient
• suppurative complications (orbital, intracranial) or systemic
sepsis.

17. IMAGING
• Plain sinus radiographs-in
common use
• Computerized tomography
(CT) is the modality of choice.
• MRI offers greater soft-tissue
resolution and does not
involve any radiation exposure
• However, the bony resolution
of CT is essential if surgery is
considered, particularly-the
size of the developing sinuses
in children -differs significantly
on the two sides.

18. Treatment of acute
rhinosinusitis
ANTIBIOTICS
• Antibiotics are the mainstay of management of children with ARS.
• The choice of antibiotics -activity against the likely organisms, and include
amoxicillin,amoxicillin-clav and cephalosporins (covering beta-lactamase-
producing organisms).
• patients with allergies to these agents include macrolides (azithromycin,
clarithromycin) or trimethoprim/sulfamethoxazole. for dose and duration
of antibiotic use, which may be adjusted according to severity of symptoms
and other factors.
• INTRANASAL STEROIDS
• There is evidence to support the use of intranasal steroids in conjunction
with antibiotics in the management of children with ARS

19. Complications of paediatric
acute rhinosinusitis
• ORBITAL COMPLICATIONS
Orbital complications can occur as a result of direct spread of infection across
the lamina papyracea, or via a haematogenous route through
small veins .This is most likely from the ethmoid sinuses, and less often the
maxillary, frontal and sphenoid sinuses in decreasing frequency.
• The Chandler classification -orbital complications of ARS -identifies five
stages of orbital sepsis:
1. Inflammatory oedema (preseptal cellulitis)
2. Orbital cellulitis
3. Subperiosteal abscess
4. Orbital abscess
5. Cavernous sinus thrombosis.

20. Preseptal cellulitis
• Preseptal cellulitis describes
inflammation of the eyelid and
conjunctiva, anterior to the
orbital septum).
• As a complication of
1. Urti
2. Dacryocystitis
3. Skin infection
4. Sinusitis.
• but may spread beyond the
orbital septum, with
intraorbital complications.
• As imaging is sometimes
considered.

21. • Presenting features include
eyelid oedema and
• erythema,
• orbital pain,
• with or without fever.
• There is typically no
proptosis or restriction of
Eye movements.
• Preseptal cellulitis usually
responds to an oral
antibiotic.

22. Orbital cellulitis
ORBITAL CELLULITIS AND
SUBPERIOSTEAL ABSCESS are
seen more commonly than
preseptal cellulitis.
• Inflammation behind the orbital
septum, within the tight confines
of the orbit itself, will reduce the
range of eye movements and
produce pain on movement,
diplopia, chemosis (conjunctival
oedema) and proptosis.
• This requires a proactive
management regime, including
treatment with intravenous
antibiotics and cross-sectional
imaging to exclude orbital or
intracranial abscess and other
complications.
.
Low-attenuation adjacent to
lamina papyracea on CT

23. SUBPERIOSTEAL AND ORBITAL ABSCESS
• A subperiosteal abscess
forms between the
periorbitaL (soft tissue
orbital contents) and the
sinuses, and is ‘extraconal’,
lying outside the cone of
ocular muscles.
• The clinical features of a
subperiosteal abscess are
similar to those of orbital
cellulitis: oedema,
erythema, chemosis and
proptosis with painful,
limited eye movements
• Rim-enhancing hypodensity
with mass effect

24. ORBITAL ABSCESS
• Symptomatology
• – Pus formation within orbital tissues
• – Severe exophthalmos and chemosis
• – Ophthalmoplegia
• – Visual impairment
• – Risk for irreversible blindness
• – Can spontaneously drain through
eyelid
• • Drain abscess and sinuses
• • Similar approaches as with
• subperiosteal abscess
• – Lynch incision
• – Endoscopic

25. Chandler Criteria
PRESEPTAL CELLULITIS ORBITAL CELLULITIS
ORBITAL ABSCESS
SUBPERIOSTEAL ABSCESS
CAVERNOUS SINUS THROMBOSIS

26. MANAGEMENT OF ORBITAL
COMPLICATIONS
• Orbital complications and their management are
considered together, -can coexist with intracranial
and osseous complications.
• The child’s vision is at risk, and there is also the
possibility of life-threatening intracranial
complications.
• This mandates a multispeciality approach, with
input from otolaryngology, paediatrics,
ophthalmology, neurosurgery and microbiology
personnel.

27. Investigation
The first-line is CT with contrast- including
• orbital detail,
• the paranasal sinuses and
• brain, with a view to assessing
orbital and intracranial
complications adequately.
This is usually quick to perform and
normally possible in an awake child.
CT may allow distinction between cellulitis
and orbital/subperiosteal abscess.
• In subperiosteal abscess,
findings include
• Oedema of the medial rectus
muscle,
• Lateralization of the periorbital,
• Displacement of the globe
downward and laterally.
1. Orbital abscess is associated
with obliteration of the detail of
the extraocular muscle and the
optic nerve by a confluent mass,
2. sometimes with gas bubbles
from anaerobic bacteria.
• The predictive accuracy of CT
91%.
• MRI may be useful in cases of
diagnostic uncertainty or when
intracranial complications are
suspected.

28. Treatment
Initial medical treatment consists of
1.High-dose intravenous antibiotics-
covering aerobic and anaerobic
organisms,
2.Analgesia/antipyretics,
3. Intravenous fluids and
4.Adjuncts-intranasal steroids
5.Saline douching
Antibiotics can be converted to an
oral preparation when the patient
has been afebrile for 48 hours
Where there is evidence of an abscess on
CT and/ or absence of clinical
improvement after 24–48 hours:
• i/v antibiotics, orbital exploration
and drainage
Preseptal and orbital cellulitis should be
treated with antibiotics.
While subperiosteal and intraorbital
abscesses require surgical exploration.
In adults, drainage may be attempted
endoscopically by opening the lamina
papyracea and draining the abscess after
completing an endoscopic
ethmoidectomy.

29. • However, in children with small noses and paranasal sinuses and
marked nasal congestion, access and the quality of the endoscopic
surgical field may be extremely unfavourable,
• such that external approaches (via a modified Lynch Howarth
incision in the case of medial subperiosteal abscess or eyelid
approaches for superior/lateral orbital abscess) are often used.
• However, good outcomes -seen with non-surgical management,
with i/v antibiotics - subperiosteal abscess, provided the following
apply:
1. There is clinical improvement within 24–48 hours.
2. There is no decrease in colour vision or visual acuity.
3. The abscess is subperiosteal and small (<0.5–1 mL volume) and
medially located.
4. There is no significant systemic involvement.
5. The patient age is less than 2–4 years.

30. Sequelae of orbital complications
• Patients will usually recover very well with minimal
problems.
• Some cases vision may be permanently compromised
or lost as a result of
Retinal artery occlusion and/or prolonged venous
congestion,
Optic neuritis and corneal ulceration,
Risk of diplopia.
• Sepsis may also spread intracranially.
• Careful follow-up is therefore required to identify these
Issues.

31. INTRACRANIAL COMPLICATIONS
• Intracranial complications include abscess formation (extradural,
subdural or intracerebral), meningitis, cerebritis and dural
venous thrombosis (including superior sagittal and cavernous sinus
thrombosis).
• These are most often associated with frontoethmoidal or sphenoidal
ARS,via direct extension or haematogenously via diploic veins.
• Flora is often mixed aerobic/anaerobic, so the antibiotic cover-
corroborated with culture of pus samples.
• Common pathogens -Streptococcus and Staphylococcus species and
anaerobes.
• The clinical presentation of intracranial sepsis is often non-specific,
including high fever with severe, intractable headache.

33. Most cases, specific signs and symptoms are present, including nausea
and vomiting, neck stiffness and altered mental state.
• Intracranial abscesses are often heralded by signs of increased
intracranial pressure, meningeal irritation, and focal neurologic
deficits, including cranial nerve palsies (III, VI and VII), or more
generalized neurological deficit (altered consciousness, gait
disturbance, confusion).
• As with orbital complications, CT with contrast allows an accurate
delineation of bone involvement.
• MRI is an excellent adjunct, especially where neurosurgical
intervention is being considered. It is more sensitive than CT in
discriminating intracranial complications,with particular value in
venous sinus thrombosis, or where there is soft-tissue involvement.
• The same considerations apply in terms of availability of MRI and
likely requirement of general anaesthesia in young children.

34. • Options for culture include swabs from the nose (with
endoscopic guidance if practical),
• sampling of pus during formal sinus surgery or during
neurosurgical drainage,
• plus blood cultures and lumbar puncture (after first excluding
raised intracranial pressure).
• As for intraorbital abscesses, drainage of intracranial
abscesses is usually undertaken (neurosurgical burr hole
drainage, craniotomy or image-guided aspiration)
• Combined drainage of the paranasal sinuses can be
performed endoscopically or via an open approach.
• In some cases, where abscesses are small and/or
inaccessible,non-surgical management may be reasonable,
only after expert neurosurgical consideration.
• High-dose long-term antibiotic therapy is often needed.

35. Cavernous sinus thrombosis
• This potentially devastating
complication is seen where veins
around the paranasal sinuses are
congested during ARS, and
become phlebitic, with
propagation centrally.
• This can lead to cavernous sinus
thrombophlebitis causing
sepsis and multiple cranial nerve
involvement.
This accounts for around 9% of
intracranial complications:
• particularly after ethmoidal or
sphenoidal sinusitis.
• In adults, the mortality rate is
30%.

36. Clinical features
• Bilateral ptosis
• Proptosis and chemosis
• Ophthalmic nerve neuralgia
• Retro-ocular headache, which can be severe
• Complete ophthalmoplegia,
• Papilloedema
• Signs of meningeal irritation, associated with
spiking fevers
• Confusion and reduced level of consciousness.

37. • Similar investigations will be required as for other forms of
intracranial complications.
• MRI (in particular MR venography) is especially sensitive, with
absence of flow in the thrombosed sinus. As an alternative, CT with
contrast may show equivalent filling defects.
• Treatment is undertaken in a specialist neurosurgical centre.
• Anticoagulants may be considered, as long as imaging has excluded
intracerebral haemorrhage, in conjunction with intravenous
antibiotics and/or steroids.
• Drainage procedures will include attention to the involved
paranasal sinuses.

38. OSSEOUS COMPLICATIONS
• ARS may lead to infection spreading to the surrounding bone, producing
osteomyelitis and in some cases onward spread to the brain and central nervous
system.
• The frontal sinuses are most often implicated.
• Particularly in infancy, where the maxillae can be affected.
• Osteomyelitis produces avascular necrosis of bone and localized venous
congestion.
• In the case of the frontalsinus, erosion of the anterior table in this way causes
oedema of the overlying skin (Pott’s puffy tumour).
• Spread via the posterior table can give rise to meningitis and other intracranial
complications.
• The changes are well delineated by CT, with MRI as an adjunct if intracranial
complications are suspected.
• The incidence of these complications has been well documented in adults, but is
less certain in children.
• Management, as often requiring multimodality treatment.

39. Pott’s puffy tumor (osteomyelitis of the frontal
bone)
• Frontal sinusitis with acute osteomyelitis