Rhinosinusitis by : Sameer S. Sawaed - MD
Rhinosinusitis
by : Sameer S. Sawaed - MD
• Inflammation of the mucous membrane of
nose and paranasal sinuses
• since the nasal cavity & sinuses have the same
MM, so any pathological changes affecting the
nasal mucosa can spread to the paranasal
sinuses.
• The paranasal sinuses are a group of air containing spaces that surround the nasal cavity
• Each sinus is name for the bone in which it is located:
Maxillary (one sinus located in each cheek)
Ethmoid (approximately 6-12 small sinuses per side, located between the eyes)
Frontal (one sinus per side, located in the forehead)
Sphenoid (one sinus per side, located behind the ethmoid sinuses, near the middle of the skull)
• The ethmoid and maxillary sinuses are present at birth.
• The frontal & sphenoid sinuses are not … they will develop later
Ethmoid sinuses
As u go posteriorly become:
• Larger
• Less in no.
Sinuses have small orifices (ostia) which open into recesses
(meati) of the nasal cavities.
• Meati are covered by turbinates (conchae).
• Turbinates consist of bony shelves surrounded by erectile soft
tissue.
• There are 3 turbinates and 3 meati in each nasal cavity
(superior, middle, and inferior).
The drainage of the sinuses
• Frontal, maxillary, anterior ethmiod middle meatus
• Posterior ethmoid superior meatus
• Sphenoid sphenoethmoidal recess
• Solid facial skeletal elements surrounding the nose are invaded
by respiratory mucosa and subsequently pneumatized.
• Begins in 3rd- 4th month of fetal life and further development
takes place after birth
• The Ethmoid sinuses are present at birth, reach adult size by
age 12.
• The Maxillary present at birth.
• Frontal sinus rarely present at birth; usually not visible until
age 2, great variability in size; congenitally absent in 5%
• Sphenoid sinuses are rarely present at birth, usually seen
around age 4.
1. Sinuses are normally sterile, but their proximity to
nasopharyngeal flora allows bacterial and viral
inoculation following rhinitis.
2. Diseases that obstruct drainage can result in a
reduced ability of the paranasal sinuses to function
normally. The sinus ostia become occluded, leading to
mucosal congestion.
3. The mucociliary transport system becomes
impaired, leading to stagnation of secretions and
epithelial damage, followed by decreased oxygen
tension and subsequent bacterial growth.
Why pain ??
Air trapped within a blocked sinus, along with pus or
other secretions may cause pressure on the sinus wall that
can cause the intense pain of a sinus attack.
• Acute Rhinosinusitis … up to 4 weeks
• Sub acute Rhinosinusitis … 4 to 12 weeks
• Chronic Rhinosinusitis .. > 12 weeks
• Recurrent acute Rhinosinusitis
o It is an inflammatory condition of one or more
of the para-nasal cavities
o Lasts up to 4 weeks
o Can range from acute viral rhinitis (common
cold) to acute bacterial rhino-sinusitis
• lasts 4-12 weeks
• Sub-acute rhino-sinusitis usually involves one
or two pairs of the paranasal cavities.
• It is the inflammatory and infection that
concurrently affects the nose and para-nasal
sinuses
• Lasts for longer than 12 weeks
• 4 or more recurrences of acute disease within a 12-
month period,
• With resolution of symptoms between each episode
lasts greater than 2 months .
• In most cases, each episode lasts for at least 7 days
• URTI
• Cold weather
• Day care attendance
• Smoking in the home
• Anatomic abnormalities (nasal polyps, ciliary disorder, septal deviation, concha bullosa, turbinate hypertrophy, tumors, congenital abnormalities i.e. cleft palate)
• Immunesupressed
• Direct extension: dental infection, facial fractures
• Inflammatory disorder:
– Wegener's Granulomatosis
– Sarcoidosis
• Mucosal disorder
– CF
– Allergic Rhinitis and other hyperreactivity
– Samter syndrome
• Asthma
• Nasal Polyps
• Aspirin intolerance .
• Viral (10-15%) - Rhinovirus (most common viral sinusitis cause), Influenza, Parainfluenza, Adenovirus
• Bacterial
– Acute Sinusitis: S.Pneumoniae, H.Influenzae, Moraxella, Streptococcus Pyogenes
– Chronic Sinusitis:
• Anaerobes (>50%)
– Bacteroides, Anaerobic Gram Positive Cocci, Fusobacteriumspecies
• Other less common causes
– Staphylococcus aureus, Hemophilus Influenzae, Pseudomonas aeruginosa, Escherichia coli, Beta-hemolytic Streptococcus, Neisseria causes
• Fungal (Immunocompromised or DM)
Aspergillus, Mucormycosis…
Allergic Rhinitis
• Hypersensitivity of the nasal mucosa due to
exposure to allergens
• Acute & seasonal or
• chronic & perennial
Definition
What happens in allergic rhinitis?
1. Exposure to allergen
2. IgE production by the body
3. Formation of allergen IgE complex
4. Binding of the complex to mast cells
5. Degranulation of the mast cells and release of
inflamatory mediators including histamine.
6. Vasodilation
7. Increase in capillary permability.
Symptoms:
Nasal obstruction with sneezing
Clear rhinorrhea (containing increased eosinophils)
Itching of eyes with tearing
Frontal headache and pressure
Signs:
Mucosa edematous, pale or violet in color
Allergic salute transverse nasal skin crease from rubbing the nose
Clinical features
Allergic salute
Allergic Rhinitis
Allergic Rhinitis
2 Types:• Seasonal (summer, spring, early autumn)
– Tree pollens, grass pollens, mold spores– Lasts several weeks– Disappears and recurs following year at the same time
• Perennial– Inhaled: house dust, wool, feathers, foods, tobacco, hair– Ingested: wheat, eggs, milk, nuts occurs intermittently for years with no pattern or may be constantly present
Types
• Chronic sinusitis
• Polyps (swollen edematous nasal mucosal
tissue, they can cause complete nasal
obstruction)
• Serous otitis media
Complications
Diagnosis
• History (atopy & family history)
• Physical examination:
1. Redness ,swelling of the mucosa (particularly
the turbinates) & mucoid discharge.
2. Check for structural anomalies (septal deviation
or nasl polyps).
• Sensitivity test for specific allergen (skin prick tests)
1. Identification and avoidance of allergen
2. During the acute attack:
1. Antihistamine (systemic or intranasal)
2. Local steroids
3. Decongestant (ephedrine)
3. Sodium cromoglycate (mast cell stabilizer used as prophyaxis)
4. Desensitization (we keep exposing the body to gradually increased amounts of allergen until the body fails to produce IgE as a result to exposure).
Treatment
Allergic Rhinitis
Vasomotor Rhinitis
• Very common
• Non-inflammatory, non-allergic rhinitis
• Characterized by a combination of symptoms that
includes nasal obstruction and rhinorrhea
• Vasomotor rhinitis is a diagnosis of exclusion reached
after taking a careful history, performing a physical
examination, and, in select cases, testing the patient with
known allergens
• 2 types ; eosinophilic & non-eosinophilic (according to
the number of eosinophils found in the nasal secretion)
Definition
• Temperature change
• Alcohol, dust, smoke
• Stress, anxiety, neurosis
• Endocrine – hypothyroidism, pregnancy,
menopause
• Parasympathomimetic drugs
Causes
Symptoms:
• Chronic intermittent nasal obstruction
• Rihinorhea (thin, watery)
Signs:
• Mucosa & turbinates : swollen, pale between
exposure
Clinical features
• Elimination of irritant factor
• Symptomatic relief with exercise
• Parasympathetic blocker
• Steroids
• Surgery
Treatment
Acute Suppurative Sinusitis
• Acute infection and inflammation of paranasal
sinuses
Defenition
Diagnosis
Major sx
Fever
Facial pain/ pressure
Facial fullness
Nasal obstruction
Nasal dicharge
Hyposmia/ anosmia
Minor sx
Headache
Fatigue
Ear pressure/ fullness
Halitosis
Dental pain
Cough
At least 2 major symptoms or 1 major and 2 minor symptoms
• Viral: Rhinovirus, Influenza, Parainfluenza
• Bacterial: Streptococcus Pneumoniae,
Haemophilus Influenzae, Moraxella catarhalis,
anaerobes
Etiology
Sudden onset of :
• Facial pain or pressure
• Nasal blockage & or nasal discharge/ posterior nasal drip
• Hyposmia
Signs more suggestive of a bacterial etiology:
• Erythematus nasal mucosa
• Mucopurulent discharge
• Pus originating from middle meatus
• Presence of nasal polyps of a deviated septum
Acute viral rhinsinusitis lasts < 10 days.
Clinical features
• History & PE
• Anterior rhinoscopy
• X-ray/ CT scan not recomnded unless
complications are suspected
Diagnosis
• Symptoms relieved within 5 days symptomatic
relief and expectant management
• Moderate symptoms that worsen or persist
beyond 5 days intranasal corticosteroid spray
• Severe symptoms that worsen or persist beyond 5
days and refractory to intranasal corticosteroid
Clarythromycin, INCS , referral to specialist
• Surgery if medical treatment fails
Management
Chronic Sinusitis
• Inflammation of the paranasal sinuses lasting
>3months
Defintion
• Inadequate treatment of acute sinusitis
• Untreated nasal allergy
• Allergic fungal rhinosinusitis
• Anatomic abnormality e.g. deviated septum
• Underlying dental disease
• Cilliary disorder e.g. CF
• Chronic inflammatory disorder e.g. wegener’s
Etiology
• Bacterial: S. Pneumoniae, H. Influenzae, M.
catarhalis, S.pyogenes, S.auereus, anaerobes
• Fungal: Aspergillus
Organisms
• Chronic nasal obstruction
• Purulent nasal discharge
• Headache & Pain over sinuses
• Halitosis
• Yellow-brown post-nasal discharge
• Chronic cough
• Maxillary dental pain
Clinical features
• Antibiotics for 3 to 6 weeks for infectious etiology
– Augmented penicillin (Clavulin™)
– Macrolide (clarithromycin)
– Fluoroquinolone (levofloxacin)
– Clindamycin, FlagyjTM
• Topical nasal steroid, saline spray
• Surgery if medical therapy fails or fungal sinusitis
• Surgical Treatment
– Removal of all diseased soft tissue and bone
– Post-op drainage
– Obliteration of pre-existing sinus cavity
• FESS: functional endoscopic sinus surgery
Treatment
• Benign to potentially fatal
• The incidence of complications from both acute and
chronic rhinosinusitis has decreased as a result of the
use of antibiotics.
• Complications can be divided into 3 categories:
– Orbital
– Intracranial
– Bony
Complications
• Most commonly involved in complicated sinusitis.
• Orbital extension is usually the result of ethmoid
sinusitis.
• Children are more prone to orbital complications,
probably secondary to high incidence of URI and
sinusitis.
Orbital complications
• Uncommon but devastating.
• 2 major mechanism:
–Direct extension.
–Retrograde thrombophlebitis via valveless
diploe veins.
* Frontal sinus is rich in diploe veins
especially during adolescence
IC complications
• Meningitis Sphenoid, ethmoid
• Epidural abscess Frontal
• Subdural abscess Frontal
• Intracerebral abscess Frontal
• Superior sagittal sinus thrombosis Frontal
• Cavernous sinus thrombosis Sphenoid, ethmoid
– Proptosis
– Chemosis
– Opthalmoplegia
Complications
X-ray