2-rhinosinusitis-141101070456-conversion-gate01.pdf

Rhinosinusitis

1. Rhinosinusitis
by : SameerS. Sawaed-MD

2. •Inflammation of the mucous membrane of
nose and paranasalsinuses
•since the nasal cavity & sinuses have the same
MM, so any pathological changes affecting the
nasal mucosa can spread to the paranasal
sinuses.

3. •The paranasalsinuses are a group of air containing
spacesthat 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
ethmoidsinuses, near the middle of the skull)

4. •The ethmoidand
maxillarysinuses are
present at birth.
•The frontal & sphenoid
sinuses are not … they will
develop later

6. Ethmoidsinuses
As u go posteriorlybecome:
•Larger
•Less in no.

7. Sinuses have small orifices (ostia) which open into recesses
(meati) of the nasal cavities.
•Meatiare covered by turbinates(conchae).
•Turbinatesconsist of bony shelves surrounded by erectile soft
tissue.
•There are 3 turbinatesand 3 meatiin each nasal cavity
(superior, middle, and inferior).
The drainage of the sinuses
•Frontal, maxillary, anterior ethmiodmiddle meatus
•Posterior ethmoidsuperior meatus
•Sphenoidsphenoethmoidalrecess

11. •Solid facial skeletal elements surrounding the nose are invaded
by respiratory mucosa and subsequently pneumatized.
•Begins in 3
rd
-4
th
month of fetal life and further development
takes place after birth
•TheEthmoidsinuses are present at birth, reach adult size by
age 12.
•The Maxillarypresent at birth.
•Frontalsinus rarely present at birth; usually not visible until
age 2, great variability in size; congenitally absent in 5%
•Sphenoidsinuses are rarely present at birth, usually seen
around age 4.

12. 1.Sinuses are normally sterile, but their proximityto
nasopharyngeal floraallows bacterial and viral
inoculation following rhinitis.
2.Diseases that obstructdrainage can result in a
reduced ability of the paranasalsinuses to function
normally. The sinus ostiabecome occluded, leading to
mucosal congestion.
3.The mucociliarytransport system becomes
impaired,leading to stagnation of secretions and
epithelial damage, followed by decreased oxygen
tension and subsequent bacterial growth.

13. Why pain??
Air trapped within a blocked sinus, along with pus or
other secretionsmay cause pressure on the sinuswall that
can cause theintense pain of a sinus attack.

14. •AcuteRhinosinusitis… up to 4 weeks
•Sub acute Rhinosinusitis… 4 to 12 weeks
•ChronicRhinosinusitis.. > 12 weeks
•Recurrentacute Rhinosinusitis

15. oIt is an inflammatory condition of one or more
of the para-nasal cavities
oLasts up to 4 weeks
oCan range from acute viralrhinitis (common
cold) to acute bacterialrhino-sinusitis

16. •lasts 4-12 weeks
•Sub-acute rhino-sinusitis usually involves one
or twopairsof the paranasalcavities.

17. •It is the inflammatory and infection that
concurrently affects the nose and para-nasal
sinuses
•Lasts for longer than 12 weeks

18. •4 or more recurrences of acute disease within a 12-
month period,
•With resolutionof symptoms between each episode
lasts greater than 2 months .
•In most cases, each episode lasts for at least 7 days

19. •URTI
•Cold weather
•Day care attendance
•Smoking in the home
•Anatomic abnormalities (nasal polyps, ciliarydisorder, septaldeviation,
conchabullosa, turbinate hypertrophy, tumors, congenital abnormalities i.e.
cleft palate)
•Immunesupressed
•Direct extension: dental infection, facial fractures
•Inflammatorydisorder:
–Wegener's Granulomatosis
–Sarcoidosis
•Mucosaldisorder
–CF
–Allergic Rhinitis and other hyperreactivity
–Samtersyndrome
•Asthma
•Nasal Polyps
•Aspirin intolerance .

20. •Viral(10-15%) -Rhinovirus(most common viral sinusitis cause),
Influenza, Parainfluenza, Adenovirus
•Bacterial
–AcuteSinusitis: S.Pneumoniae, H.Influenzae, Moraxella,
Streptococcus Pyogenes
–ChronicSinusitis:
•Anaerobes(>50%)
–Bacteroides, Anaerobic Gram Positive Cocci, Fusobacterium
species
•Other less common causes
–Staphylococcus aureus, HemophilusInfluenzae, Pseudomonas
aeruginosa, Escherichia coli, Beta-hemolytic Streptococcus,
Neisseriacauses
•Fungal(Immunocompromisedor DM)
Aspergillus, Mucormycosis…

21. Allergic Rhinitis

22. •Hypersensitivityof the nasal mucosa due to
exposure to allergens
•Acute & seasonalor
•chronic & perennial
Definition

23. What happens in allergic rhinitis?
1.Exposureto allergen
2.IgEproduction by the body
3.Formation of allergenIgEcomplex
4.Binding of the complex to mast cells
5.Degranulationof the mast cells and release of
inflamatorymediators including histamine.
6.Vasodilation
7.Increase in capillary permability.

24. Symptoms:
Nasal obstruction with sneezing
Clear rhinorrhea(containing increased eosinophils)
Itching of eyes with tearing
Frontal headacheand pressure
Signs:
Mucosa edematous, paleor violetin color
Allergic salute transverse nasal skin crease from
rubbing the nose
Clinical features

25. Allergic salute

26. Allergic Rhinitis

27. Allergic Rhinitis

28. 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

29. •Chronic sinusitis
•Polyps (swollen edematous nasal mucosal
tissue, they can cause complete nasal
obstruction)
•Serous otitismedia
Complications

30. Diagnosis
•History(atopy& family history)
•Physicalexamination:
1.Redness,swellingof the mucosa (particularly
the turbinates) & mucoiddischarge.
2.Check for structural anomalies(septaldeviation
or naslpolyps).
•Sensitivity testfor specific allergen (skin prick tests)

31. 1.Identification and avoidanceof 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
IgEas a result to exposure).
Treatment

32. Allergic Rhinitis

33. Vasomotor Rhinitis

34. •Very common
•Non-inflammatory, non-allergicrhinitis
•Characterizedby 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 eosinophilsfound in the nasal secretion)
Definition

35. •Temperature change
•Alcohol, dust, smoke
•Stress, anxiety, neurosis
•Endocrine–hypothyroidism, pregnancy,
menopause
•Parasympathomimeticdrugs
Causes

36. Symptoms:
•Chronic intermittent nasal obstruction
•Rihinorhea(thin, watery)
Signs:
•Mucosa & turbinates: swollen, palebetween
exposure
Clinical features

37. •Elimination of irritant factor
•Symptomatic relief with exercise
•Parasympatheticblocker
•Steroids
•Surgery
Treatment

38. Acute SuppurativeSinusitis

39. •Acute infection and inflammation of paranasal
sinuses
Defenition

40. 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

41. •Viral: Rhinovirus, Influenza, Parainfluenza
•Bacterial: Streptococcus Pneumoniae,
HaemophilusInfluenzae, Moraxellacatarhalis,
anaerobes
Etiology

42. Sudden onset of :
•Facial pain or pressure
•Nasal blockage & or nasal discharge/ posterior nasal drip
•Hyposmia
Signsmore suggestive of a bacterial etiology:
•Erythematusnasal mucosa
•Mucopurulentdischarge
•Pusoriginating from middle meatus
•Presence of nasal polyps of a deviated septum
Acute viral rhinsinusitislasts < 10 days.
Clinical features

43. •History & PE
•Anterior rhinoscopy
•X-ray/ CT scan not recomndedunless
complications are suspected
Diagnosis

44. •Symptoms relieved within 5 days symptomatic
reliefand expectant management
•Moderatesymptoms that worsen or persist
beyond 5 days intranasal corticosteroid spray
•Severesymptoms that worsen or persist beyond 5
days and refractory to intranasal corticosteroid 
Clarythromycin, INCS , referral to specialist
•Surgeryif medical treatment fails
Management

45. Chronic Sinusitis

46. •Inflammation of the paranasalsinuses lasting
>3months
Defintion

47. •Inadequate treatment of acute sinusitis
•Untreated nasal allergy
•Allergic fungalrhinosinusitis
•Anatomic abnormality e.g. deviated septum
•Underlying dentaldisease
•Cilliary disorder e.g. CF
•Chronic inflammatory disorder e.g. wegener’s
Etiology

48. •Bacterial: S. Pneumoniae, H. Influenzae, M.
catarhalis, S.pyogenes, S.auereus, anaerobes
•Fungal: Aspergillus
Organisms

49. •Chronic nasal obstruction
•Purulentnasal discharge
•Headache & Painover sinuses
•Halitosis
•Yellow-brownpost-nasal discharge
•Chronic cough
•Maxillary dental pain
Clinical features

50. •Antibioticsfor 3 to 6 weeks for infectious etiology
–Augmented penicillin (Clavulin™)
–Macrolide(clarithromycin)
–Fluoroquinolone(levofloxacin)
–Clindamycin, FlagyjTM
•Topical nasal steroid, saline spray
•Surgeryif 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

51. •Benign to potentially fatal
•The incidence of complications from both acute and
chronic rhinosinusitishas decreased as a result of the
use of antibiotics.
•Complications can be divided into 3 categories:
–Orbital
–Intracranial
–Bony
Complications

52. •Most commonly involved in complicated sinusitis.
•Orbital extension is usually the result of ethmoid
sinusitis.
•Childrenare more prone to orbital complications,
probably secondary to high incidence of URI and
sinusitis.
Orbital complications

53. •Uncommon but devastating.
•2 major mechanism:
–Direct extension.
–Retrograde thrombophlebitisvia valveless
diploeveins.
* Frontal sinus is rich in diploeveins
especially during adolescence
IC complications

54. •MeningitisSphenoid, ethmoid
•Epidural abscessFrontal
•Subdural abscess Frontal
•Intracerebralabscess Frontal
•Superior sagittalsinus thrombosisFrontal
•Cavernous sinus thrombosis Sphenoid, ethmoid
–Proptosis
–Chemosis
–Opthalmoplegia
Complications

55. X-ray