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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4416_Библиотеки_им_академика_М_И_Перельмана
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■ Deformities in median nasal clefts may range from a simple median scar
at the cephalic end of the nasal dorsum to a completely bid nose with
two dierent halves with separate median nasal walls.
■ Lateral nasal clefts range from alar scar like lines to triangular defects
from medial canthus up to ala and aecting the nasolacrimal apparatus.
■ Multidisciplinary surgical correction is indicated.
Developmental Errors of the Nasobuccal Membrane
■ Persistence of the embryonic nasobuccal membrane, which separates
the nasal cavity from the buccal space, gives rise to choanal atresia.
Choanal Atresia
■ Unilateral atresia is twice more common than bilateral and when
unilateral, right-sided atresia is more frequent.
■ Unilateral atresia may be missed during early childhood and present
with persistent unilateral nasal discharge.
■ Bilateral choanal atresia is an emergency.
■ Complete physical examination is done to assess for other congenital
anomalies.
■ Apart from diagnosis, radiology in the form of CT helps in dierentiating
it from deviated nasal septum, septal hematoma, turbinate hypertrophy,
mid nasal stenosis, encephalocele, dermoid, hamartoma, chordoma,
and teratomas.
■ After initial maintenance of airway (by a simple nipple or endotracheal
intubation), endoscopic surgical correction is warranted.
295Chapter 21 Pediatric Sinonasal Disorders: Surgical Perspective
RHINOSINUSITIS
■ Rhinosinusitis is an inammatory condition of the nose and paranasal
sinuses.
■ Common cold caused by viruses is the most common form of
rhinosinusitis.
■ Following viral respiratory infection, mucosal edema, and obstructed
sinus ostia along with hypofunctioning of the sinus ciliary function leads
to stasis of secretions in the sinuses.
■ Symptoms and signs of sinusitis appear when these sinuses become
secondarily infected by bacteria from the nose and nasopharynx.
■ In pediatric population, approximately 0.5–10% of upper respiratory
infections may evolve into bacterial sinusitis.
■ Other underlying factors associated with sinusitis are deviated nasal
septum, adenoid hypertrophy, allergy, gastroesophageal reux disease
(GERD), passive smoking, and systemic illnesses like immune deciency,
primary ciliary dyskinesia, and cystic brosis and should be looked for in
recurrent rhinosinusitis.
■ Based on the duration of symptoms, pediatric rhinosinusitis is categorized
as acute (between 1 weeks and 4 weeks), subacute (4–12 weeks), and
chronic (more than 12 weeks).
1,2
Section 5 Congenital/Pediatric Diseases296
Acute Bacterial Rhinosinusitis
■ Presentation—fever, facial fullness or pain, nasal stuness, purulent
nasal discharge, dental pain, cough, and ear pain or fullness persisting
beyond 10 days.
■ Severe headache, vomiting, seizures, focal neurological decits,
periorbital edema, proptosis, and diplopia due to restricted extraocular
muscle movement mandates CT to evaluate the complications.
3
■ Orbital complications constitute approximately 90% of the complications
of acute rhinosinusitis (ARS).
■ Medical management is the mainstay of treatment of uncomplicated
ARS, which includes antibiotic therapy for at least 10 days along with
antihistamines, oral, and nasal decongestants, topical steroid, and nasal
irrigation.
■ Patients with orbital complications are managed with parenteral
antibiotics and functional endoscopic sinus surgery (FESS) with abscess
drainage.
Chronic Bacterial Rhinosinusitis
■ Presentation—persistence of the above-mentioned symptomatology
beyond 12 weeks.
■ Young patients may be irritable and may show behavioral changes.
■ Chronic rhinosinusitis (CRS) is treated with broad-spectrum antibiotics
for 3–6 weeks and oral decongestants, topical steroids along with saline
irrigation.
■ Surgery is planned after failed medical management.
■ Preoperative CT scan is performed to know about the disease extent for
complete disease clearance and anatomical abnormalities to reduce the
risk of surgical complications.
■ Surgery consists of adenoidectomy ± FESS.
■ In pediatric patients, FESS does not have clinically signicant impact on
facial growth.
4
CHRONIC ADENOID HYPERTROPHY
■ Adenoids are favorably situated in the nasopharynx to mediate
immunological protection of the upper aerodigestive system against
inhaled antigens. ey are small at birth, grow till 5 years of age and
gradually get atrophied by adolescence.
■ Chronic bacterial infection, passive smoking, and gastroesophageal
reux may lead to adenoid hypertrophy, which may obstruct the
nasopharynx to variable extent.
■ Patients present with snoring, mouth breathing, sleep disturbances like
restless sleep, night terrors, sleep walking, etc. hearing impairment,
enuresis, and recurrent rhinosinusitis.
■ When associated with tonsillar hypertrophy, patients might have features
of obstructive sleep apnea.
■ Diagnosis is made by endoscopic visualization of enlarged adenoids in
older children and by lateral neck X-ray in young patients.
■ Medical management consists of aqueous nasal steroid spray.
■ Surgical removal of the adenoids is considered for signicantly enlarged
adenoids causing obstructive symptoms as well as for recurrent or
chronic sinusitis.
SPECIFIC LESIONS
Antrochoanal Polyps
■ Mostly seen in pediatric patients.
• ese are unilateral and arise from the maxillary sinus. Large polyp
extents up to posterior choana through the maxillary ostium and nasal
cavity.
• Patients present with unilateral nasal stuness, nasal discharge, and
hearing loss due to middle ear eusion. When the polyp extends to the
nasopharynx, patients might have bilateral nasal obstruction, mouth
breathing, and mued voice.
• e CT scan helps in diagnosis and is performed prior to endoscopic
excision.
Allergic Fungal Sinusitis (AFS)
■ Less frequently seen in pediatric patients than adults. e details of the
symptomatology and management are like the adult patients.
297Chapter 21 Pediatric Sinonasal Disorders: Surgical Perspective
REFERENCES
1. Aitken M, Taylor JA. Prevalence of clinical sinusitis in young children followed up
by primary care pediatricians. Arch Pediatr Adolesc Med. 1998;152:244-8.
2. Revai K, Dobbs LA, Nair S, et al. Incidence of acute otitis media and sinusitis
complicating upper respiratory tract infection: the eect of age. Pediatrics.
2007;119:e1408-12.
3. DeMuri GP, Wald ER. Clinical Practice. Acute bacterial sinusitis in children. N
Eng J Med. 2012;367:1128-34.
4. Bothwell MR, Piccirillo JF, Lusk RP, et al. Long term outcome of facial growth
after functional endoscopic sinus surgery. Otlaryngol Head Neck Surg. 2002;126;
628-34.
Section
6
Systemic Disorders/Surrounding
Structures Involving PNS
22. Systemic Disorders Affecting Sinonasal Cavity
23. Anterior Skull Base Lesions: Imaging
24. Imaging of Dental Lesions and Sinonasal Cavity
25. Imaging of Disorders Involving Sinonasal Cavity and Orbit
22
CHAPTER
Systemic Disorders Aecting
Sinonasal Cavity
Surabhi Vyas, Ashu Seith Bhalla
• Introduction
• Infections
– Tuberculosis
– Leprosy
– Invasive Fungal Infections
– Syphilis (Treponema Pallidum)
Infection
• Chronic Inammatory Disorders
– Granulomatosis with Polyangiitis
– Sarcoidosis
– Relapsing Polychondritis
– Others
• Immunodeciency
– Primary Immunodeciency
▪ Structural Defects
▪ Cystic Fibrosis
▪ Primary Ciliary Dyskinesia
– Acquired Immune Disorders
▪ Acquired Immunodeciency
Syndrome
▪ Bone Marrow Transplant
Recipients
▪ Solid Organ Transplant
Recipient
• Disorders with Sinopulmonary
Involvement
– Allergic Bronchopulmonary
Aspergillosis
– Asthma
– Samter’s Triad
– Inammatory Bowel Disease
– Amyloidosis
• Granulomatous Disorders
– Immunoglobulin-4-Related
Disease
– Rhinoscleroma
– Rhinosporidiosis
• Illustrative Case
INTRODUCTION
Although involvement of the sinonasal cavity by systemic disorders is
uncommon, a gamut of inammatory disorders may involve the sinonasal
cavity (Flowchart 22.1).
Section 6 Systemic Disorders/Surrounding Structures Involving PNS302
Flowchart 22.1: Classication of systemic disorders affecting the sinonasal cavity.
(AIDS: Acquired immunodeciency syndrome; CVID: Common variable immunodeciency;
GPA: Granulomatosis with polyangiitis; IgA: Immunoglobulin A; SCID: Severe combined
immunodeciency; SLE: Systemic lupus erythematosus).
INFECTIONS
Tuberculosis
■ Sinonasal cavity is an uncommon site of involvement.
■ Clinical presentation is nonspecic with nasal obstruction or catarrh.
■ Imaging ndings include enlarged adenoids with enlarged nodes.
■ Inammatory polyps mainly in the region of inferior turbinate or septal
perforation may also be seen.
Leprosy
■ Nose may be involved in the lepromatous leprosy variant of the disease.
■ Mucosal thickening and septal perforation are seen, later causing saddle
nose (Fig. 22.1).
■ Mucosal thickening in other sinuses has also been described.
Invasive Fungal Infections
■ Invasive fungal infections in the immune-compromised host can involve
multiple sites especially lungs and sinonasal cavity (Figs. 22.2A and B)
and are covered elsewhere in the book.
Fig. 22.1: Leprosy—Patient of leprosy showing depressed and deformed nasal bridge.
303Chapter 22 Systemic Disorders Aecting Sinonasal Cavity
BA
Figs. 22.2A and B: Mucormycosis in a poorly controlled diabetic lady. (A) Extrasinus soft
tissue anterior to left maxillary sinus; and (B) Permeative bone destruction of left maxillary sinus
lateral wall.
Syphilis (Treponema pallidum) Infection
■ Nasal manifestations of syphilis are infrequently seen nowadays.
■ While primary syphilis may have chancre of nasal vestibule, secondary
form presents with copious nasal discharge, it is the tertiary form which
has the most severe manifestations.
■ Soft tissue thickening (gummata) seen resulting in septal perforation and
eventually the typical “saddle nose deformity”.
■ Congenital syphilis also presents nasal discharge and may cause septal
perforation.
CHRONIC INFLAMMATORY DISORDERS
Granulomatosis with Polyangiitis (GPA)
■ Previously called Wegener granulomatosis.
■ Multisystem auto-immune disease of unknown etiology, disorder
characterized by necrotizing granulomas with small and medium vessel
vasculitis.
Section 6 Systemic Disorders/Surrounding Structures Involving PNS304
■ Characteristically involve the kidneys, sinonasal cavity, and lungs.
■ Laboratory investigations: Elevated antineutrophil cytoplasmic antibodies (ANCAs), but these may not be elevated in a fourth of patients.
■ Two forms: (1) Limited, and (2) Severe.
1. Limited: Where no threat to life/vital organs function (earlier used
for renal sparing forms).
2. Severe: Severe forms need more aggressive management with
cyclophosphamide or rituximab in addition to glucocorticoids.
■ Head and neck region involvement includes the following sites: Nasal
cavity, sinuses, orbits, anterior skull base, upper airway, and temporal bone.
■ Sinonasal involvement:
• Imaging ndings in the sinonasal cavity primarily consist of nodular
and mucosal thickening with bone erosion and sclerosis due to neoosteogenesis.
• Maxillary sinus is the predominant site of mucosal thickening. It is
indistinguishable from chronic rhinosinusitis except that nodularity
is seen more often in GPA
• Bony erosions occur more frequently in the anterior ethmoid regions
but other sinuses may also be involved
• e destructive changes begin in the nasal septum, spreading laterally
to the turbinates and then to the maxillary antra and subsequently to
the other sinuses. Finally the sinonasal space appears as a single large
cavity
• e hard palate is usually spared, though it can be involved occasionally
• Avascular necrosis due to vascular occlusion is the mechanism for
bone destruction
• Anterior skull base erosions may occur due to contiguous spread from
the sinonasal disease process
• On computed tomography (CT), sclerosis gives a layered appearance
with less dense and more sclerotic bone seen parallel along the sinus
wall (Figs. 22.3A and B)
• On magnetic resonance imaging (MRI), while the more dense bone
appears hypointense on T1-weighted images, the less dense bone
may be hyperintense due to marrow in areas of neo-osteogenesis
(vs periostitis) (Figs. 22.4A and B). MRI may reveal thickening and
enhancement of the olfactory nerves in cases of olfactory nerve
neuropathy with the patient developing anosmia.
Sarcoidosis
■ Sinonasal cavity involvement is seen in less than 1% patients of
sarcoidosis.
■ Nodular mucosal thickening, or even polyposis may be seen, mainly
involving inferior turbinates and nasal septum.
305Chapter 22 Systemic Disorders Aecting Sinonasal Cavity
A
Figs. 22.3A and B: GPA , (A) Axial; and (B) Coronal CT images. Bony destruction, sclerosis
with typical layered appearance of maxillary walls, zygoma, and nasal septum (*). Hard palate
involvement (arrow) though seen in this patient is an unusual feature. (CT: Computed tomography;
GPA: Granulomatosis with polyangiitis).
A
Figs. 22.4A and B: GPA, (A) Axial T1W; and (B) Postcontrast MR images. (A) T1W MRI showing
hypointense sclerotic bone (*), and hyperintense marrow containing bone (arrow); and (B)
CEMRI showing areas of enhancement in the involved bones (arrow). (GPA: Granulomatosis
with polyangiitis; CEMRI: Contrast-enhanced magnetic resonance imaging; T1W: T1-weighted).
B
B
■ Septal perforations and hard/soft palate erosions are rare. Neo-osteogenesis may be seen.
Relapsing Polychondritis
■ Synonym: Relapsing perichondritis/chronic atrophic polychondritis.
■ Chronic inammatory disorders aecting cartilage of pinna, nose, airway
with arthritis, and hearing loss.
■ Nasal chondritis results in saddle nose deformity.
■ ere is no mucosal involvement hence no mucosal thickening/
hypertrophy seen (vs GPA).
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