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Fisiologi & histologi hidung &
sinus paranasal
LO 1
Atlas of Ear, Nose and Throat Pathology
Volume 16 of the series Current Histopathology pp 40-48
AIRFLOW:
• Flow is turbulent but
considered laminar at
rest
• Gases flow faster
through the choana
• Pressures vary during
respiratory cycle & rate
~8-10 cycles a minute in
adults at rest
INSPIRATION
• Upwards & backwards
from nasal valve 
turbinates (mainly
inferior)  splits into 2,
below & over middle
turbinate  rejoin in
poster choana
• Velocity at anterior
valve: 12-18 m/sec
during quiet respiration
EXPIRATION
• Lasts longer than
inspiration & is more
turbulent
• Extrapulmonary airflow is
turbulent bcs direction
changes
• Walls are not smooth
• Surface area is enlarged by
turbinates &
microanatomy of
epithelium
 NASAL RESISTANCE
• Nose accounts for up to ½ total airway resistance
(produced by 2 resistors in parallel)
• Made up of 2 elements:
– Fixed comprising bone, cartilage, attached muscles
– Mucosa
• High in infants (initially obligatory nose breathers)
• Expiration: +ve pressure is transmitted to alveoli
• Tracheostomy  reduces dead space  removal of
resistance  degree of alveolar collapse

Nasal resistance is the resistance offered by the nasal cavity to inspired air. This resistance plays
a vital role in preventing collapse of lung. It goes without saying a collapsed lung will hamper
normal respiration. In adults nasal resistance constitutes about 2/3 of total airway resistance.
Current respiratory physiologists consider this to be one of the functions of nose inaddition to
olfaction and airconditioning.
 Anterior nasal valve
• Narrowest part of the nose
• Less well defined physiologically than
anatomically
• Greatest resistor  most turbulent airflow
• Formed by lower edge of the upper lateral
cartilages, anterior end of inferior turbinate &
adjacent nasal septum + surrounding soft tissue
• Electromyography shows contraction of dilator
naris alone during inspiration
– Increases during exercise & can be mimicked by
voluntary dilatation
 Nasal Cycle
• Consist of alternate nasal blockage b/w passages
• Changes are produced by vascular activity (vol.of blood on venous
sinusoids (capacitance vessels))
• Cyclical changes occur b/w 4-12 hrs
• Constant for each person
• Factors modifying nasal cycle:
– Allergy, infection
– Exercise
– Hormones, pregnancy, sexual activity
– Autonomic nervous system
• Vagal overactivity  nasal congestion
– High lvl of CO2 in inspired air by rebreathing  nasal resistance 
hyperventilation
– Drugs  block NE  nasal congestion

Saving energy and moisture by high airway resistance and low turbulance
Important to consider when making clinical assessment of obstruction complains
 Protection of lower airway
(mechanical)
• Nose protects by removing particle down to
~30 μm
– Shape & roughness of smaller particle cause them
to deposit in nose
• Inspired air travels through 1800 & velocity
markedly after nasal valve
• Turbulence deposition of particles
• Vibrissae only stops the largest particles
Nasal secretion
• 2 elements:
– Mucus
– Water
• 2 secretory cells: mucus & serous cells
– Glycoprots produced by mucus glands
• Goblet cells w/in epithelium
• Glandular mucus cells
Both contain acidic glycoprots, large electron-lucent
secretory granules
– Water and ions mainly from serous glands & indirectly
from transudation from capillary network
• Discrete electron dense granules
• Granules w/ core of greater density
• Neutral glycoprot enzymes (lysozymes, lactoferin, IgA2)
• Submucosal glands are mixed & arranged around
ducts
• Anterior part of nose: SEROUS GLANDS only in
VESTIBULAR region
– Produce copious watery secretion when stimulated
• Sinuses have fewer goblet cells & mixed glands
Glycoproteins give mucus its two most commonly measured properties,
viscosity and elasticity.
Viscosity is lowered by reducing the ionic content.
Movement of the cilia produce shearing e ects that the elasticity counteracts and if it
is the right consistency, viscosity and elasticity complement each other and mucus
moves.
 Cilia
• Cilia are found on the surface of cells in the respiratory tract
• propel mucus backwards in the nose towards the nasopharynx
• Nine paired outer microtubules surround a single inner pair of
microtubules.
• Outer-paired microtubules are linked together by nexins and to the inner
pair by central spokes.
• Outer dynein arms, consist of an ATPase
– lost in Kartagener's syndrome
• Nasal mucus film is in two layers
– one upper more viscous layer
– a lower more watery layer in which cilia can move freely.
– Tips of the cilia on which there are small hooks enter the viscous layer
to move it.
mucus produced in the sinuses to reach the throat, the cilia throughout the sinonasal cavity are
“programmed” to beat in a very specific direction. Each sinus has an ostium (opening) that the cilia carry the
mucus towards and through into defined anatomical areas within the sinonasal cavity
http://care.american-rhinologic.org/nasal_physiology?print
 Ciliary action
• Beat frequency is between 7 and 16Hz at body
temperature
• Beat frequency remains constant between 32 and
40°C.
• beat consists of a rapid propulsive stroke and a
slow recovery phase
– propulsive phase  the cilium is straight and the tip
points into the viscous layer of the mucus blanket
– recovery phase  the cilium is bent over in the
aqueous layer.
• Energy is produced by conversion of ATP to
ADP by the ATPase of the dynein arms and the
reaction is dependent of Mg2+ ions.
• Motion is produced by the pair of outer
microtubule slidding with respect to each
other.
• ATP is generated by mitochondria near the cell
surface next to the basal bodies of the cilia.
• Mucus flows from the front of the nose
posteriorly.
• Mucus from the sinuses joins that owing on
the lateral wall, with most mucus going
through the middle meatus.
• Most passes around the Eustachian orifice and
it is then swallowed
 Factors affecting ciliary action
• Drying stops the cilia
• Movement will cease below 10 degree C and above
45°C.
• Isotonic saline preserve activity,
– but solutions above 5% and below 0.2% will cause
paralysis.
• Cilia beat above pH 6.4 & will function in slightly
alkaline fluids of pH 8.5 for long periods.
• Upper respiratory tract infection may damage the
epithelium so that it sloughs away.
• Ciliary function may deteriorate with age
 THE PARANASAL SINUSES
• The physiological role of the paranasal sinuses is uncertain.
• Continuation of the respiratory cavity
• lined by a respiratory mucosa
• main interest relates to disease.
• Development of sinuses continues up to 25 years of age.
– ethmoids and maxillary sinuses are present rudimentarily at
birth
– the frontal sinuses develop after six but may be completely
absent (10 percent).
– The sphenoid sinus differs considerably in the degree of
development.
Whatever their physiological role is, it is of only minor importance.
T. Metin Önerci. Diagnosis in Otorhinolaryngology. Springer-Verlag: Berlin Heidelberg. 2009
• MUCOSA
– Continuity from nose
– Goblet cells & cilia (less #, but more frequent near
ostia & blood supply is less well dev w/ no cavernous
plexuses  pale color mucosa)
– Nerve supply less well dev  only basic vasomotor
response & mucus production w/ parasympathetic
stimulation

• DRAINAGE
– Mucociliary clearance in maxillary sinus is spiral &
towards natural ostium
– Frontal & sphenoid sinuses downwards, aided by
gravity, blood supply is better dev in frontal sinuses &
ostium is relatively large in sphenoid
– Secretion join the nasal mucus in middle meatus
• OXYGEN TENSION
– PO2 in maxillary sinuses than in nose & in frontal sinuses
– Ostium blocked  O2 tension further
– Ciliary motion normal if blood supply is adequate
• Blood supply impaired  ciliary activity   stasis of secretion
– NO lvl  in sinuses than nasal cavity

• OSTIUM SIZE
– Blockage of natural sinus ostium  of ventilation & stasis of
secretions
– Ostium <2.5mm predisposes to disease

• PRESSURE CHANGES
– Pressure in maxillary sinus vary w/ respiration but lag behind by 0.2s
– Little fluctuation when nose is patent & variation of pressure during
quite respi is +/- 4 pascals, 17-20m pascals on exercise
– Nose blocked  pressure fluctuation 
– Barotrauma is 5x << common than in ear & most freq seen in maxillary
sinuses in divers
 Physiological function of sinuses
• Vocal resonance
• Diminution of auditory feedback
• Air conditioning
• Pressure damper
• of skull weight
• Flotation of skull in water
• Mechanical rigidity
• Heat insulation

• Vol of the largest sinus is < 50 mL  contributes little to air

conditioning
• Apart from mucus production & some strengthening facial bones,
paranasal sinuses have little physiological function
 Olfaction & sinus development
• Dev of sinuses may be important in
olfactory area
• Most mammals have an ethmoturbinal system
– Complex convoluted arrangement  surface
area & doesn’t contain true sinuses
• Man & other animals use scent soon after
birth well before sinuses dev to recognize
parents & initiate behaviour
• Olfaction is fully dev at birth
• Two in vitro techniques are used to measure
the rheology:
– Microspherometry
– controlled stress technique
Mucus viscosity can be measured most easily by
drawing up mucus into a capillary tube under
negative pressure  measuring the flow relative to
the pressure.
Recoil may be measured when the pressure is
released.
Sistem Imun pada hidung & sinus
paranasal
LO 2
Protection of lower airway:
Immunological
 The Waldeyer’s Ring
• The palatine tonsils, nasopharyngeal tonsil
(adenoid) and lingual tonsil constitute the
major part of Waldeyer's ring or nasal-
associated lymphoid tissue (NALT)
• tubal tonsils and lateral pharyngeal bands as
less prominent components.
• The lymphoid tissue of Waldeyer's ring is
located at the gateway of the respiratory and
alimentary tract and belongs to the mucosa-
associated lymphoid tissue (MALT).
• As tonsils are the first site of encounter with
inhaled and ingested micro-organisms, they are
considered the first line of defense against
exogenous aggressors.
• The generation of B cells in the germinal https://www.uvm.edu/medicine/surgery/documents/Tonsillect
ectomy1.pdf
centers of the tonsil is one of the most
essential tonsillar functions.
Hellings P, Jorissen M, Ceuppens JL. The Waldeyer’s ring. Acta Otorhinolaryngol Belg. 2000;54(3):237-41.
Kelainan hidung luar

LO 3
• The nose occupies central feature of the face
• Concern of the patient with regard to causation &
apprehension as to aesthetic consequence
• Exterior of nose:
– Nasal vestibule composed of skin
Cutaneous disease
Dermatological term:
• Macule  flat lesion w/in the skin
• Papule  circumscribed raised lesion in dermis or
epidermis
• Nodule  comparable to a papule but >1 cm
• Plaque  irregular, superficial lesion, marginally
raised & has large surface area relative to its height
 Acute Nasal Infection
• Bacterial infection
Recognized by:
– Acute erythema
– Oedema
– Tenderness
– May be accompanied by indicators of systemic injury:
pyrexia & malaise
– Commensal bacteria residing in URT are the main
pathogen (30% S.aureus in nose & 10% S.pyogenes in
nasopharynx)
– Persisting, extreme, recurrent disease indicate an
underlying pathology (e.g. DM, immunocompromised)
 Vestibulitis
• Inflammation of the nasal vestibular skin
• Infective agents, trauma, or excoriation from
rhinitis
• Crusting  evident & mild to moderate
discomfort reported
• Topical agents: steroids or antibiotics are
prescribed according to aetiology T. Metin Önerci. Diagnosis in Otorhinolaryngology.

• Specific presentation of vestibulitis: Springer-Verlag: Berlin Heidelberg. 2009

FURUNCLE or COMMON BOIL arises in hair-

bearing region of nasal vestibule, result from
Staph.aureus infection of the follicle
• Tender nodule w/ surrounding inflammation
& induration  swells  discharges to
anterior nares
– Several boils coalesce  form carbuncle
• Responds quickly to local antiseptics and oral
antibiotics
Excoriation: abrading or wearing off the skin, raw irritated lesion (lecet)
 Erysipelas
• Bright red, flat, shiny, well defined lesion in the middle 3rd of the
face (outward extension from the nose is typical)
• Midface butterfly or malar distribution
– centring on the nose & spreading symmetrically across cheeks
• Provoking organism:
– Streptococcus  enters broken skin  infect dermis
– Less common: other streptococci (pneumonia), Staph.aureus or
H.influenzae produce identical clinical picture
• Appearance of bullae or vesicles may be seen
• Antistreptolysin titres show increasing level over a period of weeks
• Cellulitis: similar to erysipelas but surface lesion is well defined as
inflammatory changes involve deeper connective tissue layers
• Oral or IV AB are required
 Rhinophyma
• Overgrowth of the nasal tip, alar rim and columella tissue
• Progressive increase in connective tissue, sebaceous gland
hyperplasia & chronic deep inflammation
• Phymas may also involve chin, glabella, eyelid
• Glandular  massive increase in sebaceous glands 
pitted, dented, distorted, asymmetrical surface
• Fibrous rhinophyma  diffuse enlarged, more symmetrical
• May be removed and nose contour re-established w/
paring techniques
– scalpel or silver’s knife or electrocoagulation
– CO2, argon & pulsed dye lasers
 Granulomatous conditions
• SARCOIDOSIS
– Noncaseating (caseation: forming necrosis resembling cheese)
epitheloid granulomas
– Found in association w/ LOWER RESPI involvement
– Sympt: obstruction, mucopurulent blook stained disharge, crusting
– Associated sinus infection,septal perforation w/ saddling (depressed)
of nasal bridge, violaceous (violet color) lesions
– Mucosa inflamed w/ crust & old blood  STRAWBERRY SKIN effect
(yellowish granulomas against reddened lining)
– ESR rate, calcium, ACE
– Kveim test most accurate (has been withdrawn)
– Radiology of chest is MANDATORY
– Treatment w/ saline douche and topical corticosteroid, systemic
treatment
– Surgery should be avoided  exacerbate collapse of nose
• Wegener Granulomatosis
– Systemic condition
– Granulomas & vasculitis
– Autoimmune basis
– Affecting upper and lower respi tract + focal glomerulonephritis
 renal failure  death
– History of progressive malaise, pyrexia, weight loss,
disporportionate feeling of unwellness
– Nose swollen inflamed mucosa  blockage & blood stained
crusting
– Destruction of nasal septum  implosion of nasal bridge
– Nasopharynx, ear, mouth, trachea, cranial nerve, orbits involved
– High ESR, CRP, evidence of pulmo & renal damage
– CT of sinuses show midline destruction, opacification of sinuses
due to granulomatous infiltration
– Fibrotic discharge or secondary infection
– Treatment: systemic cortico & cytotoxic drugs
• Amyloidosis (amyloid: proteins)
– Deposits in skin of vestibule
– Histologically: congo red reactivity & green birefringence in polarized
light
– Colchicine has been used in treatment

• Nasal gliomas & encephalocele (ocele: protrisuion)

– Protrusion of brain through congenital defect in skull (failure of
foramen caecum to close)
– No defect  GLIOMAS
– Cerebrospinal fluid leaks & meningitis
– External lesions on dorsum or to one side
– May be compressible, fluctuant, pulsatile
– Intranasal encephalocoele mistaken as polyps. Swelling increase when
crying and straining
– Gliomas don’t change w/ crying or straining
– Imaging: MANDATORY in pts w/ swelling in frontonasal region or
unilateral polyps
 MECHANICAL NASAL OBSTRUCTION
• Septal deviation
– Congenital or acquired
– Prenatal or perinatal factors in utero or during delivery
– True dislocation is rare, more often fracture
• Small microfracture  exacerbation by falls during toddler stage
• Adolescence or young adults, sports injuries, assault, traffic accidents
– Effects:
• Internal external nasal structure maybe damaged
• Deflections & deformities of cartilage and bones
• With age loss  loss of tensile strength in collagen  collapse of nasal valve region
• Disordered airflow  crusting & epistaxis on deflected area
– Associated w/ cosmetic deformity of bridge and columella
– Assessment: anterior rhinoscopy & rigid endoscopu asses septal
position & spurs, turbinates, exclude other abnrs
– Topical decong  determine degree of mucosal swelling
– Treatment: septal manipulation (neonates), septoplasty or submucous
resection
• Complications
– Septal hematoma
• Formed b/w cartilage and perichondrium or
• b/w perichondrium & septal mucosa
• Blood supply to cartilage will be damaged
• Not drained  cartilage death
• Exacerbated by infection  septal abscess  absrb of cartilage &
saddling of nose
• Draining + broad spectrum AB
– Septal perforation
• Most common form of trauma, iatrogenic of self inflicted
• Most common site: chondro-vomerine suture
• Asymptomatic
• Small diameter: whistling sound
• Larger diameter: crusting, blood spotting, obstruction sensation due
to turbulence airflow
• More anterior  more likely causing sympt
• Never heal spontaneously
• Nasal douching + / - topical corticosteroid given
 • Infection/TSS
– After nasal surgery uncommon but very painful  elevation of
body temp
– Toxic Shock Syndrome  result of nasal packing
– Toxin of staphylococcus absorbed  headache, myalgia, nausea,
vomitting secondary to pyrexia
– Tachycardia, HT  hypotension, erythema of skin 
desquamation of skin of the hands
– Beta lactamase resistant antistaphylococcal AB given
systematically, all packs & stitches removed
• Turbinate enlargement
– Inferior turbinate, adjacent to nasal septum & middle turbinates
• Composed of complex submucosal structure & vascular sinusoids)
• Overdriven by exercise, posture, emotion, environmental tempt,
humidity
• Decong spray

Nasal packing is the application of sterile tampons to the nasal chambers. The most common
purpose of nasal packing is to control bleeding and provide support to the septum following
surgery and nasal reconstruction. It is also used to treat chronic nosebleeds (Stool et al 1996).
• Foreign bodies
– Objects including: metals, plastic, organic
substances, live insects  to nose  unilateral
chronic purulent nasal discharge
– Foreign material present for sometime  nidus
for deposition of calcium and magnesium salt 
rhinolith (batu hidung) radioopaque
– Imagine  remove foreign body under short
general anesthetic
Gangguan rongga hidung (cavum
nasi)
LO 4
 EPISTAXIS
• Bleeding from the nose
• Hippocratic technique
– Simplest treatment for nose bleed: pinching ala nasi
• VASCULAR ANATOMY
Anastomoses of arterial plexus in anterior
of septum  Kiesselbach area/little’s area
frequently bleed

Posterior area the vessels are larger, easily

traced to the external or internal carotid
origin

http://www.aafp.org/afp/2005/0115/afp20050115p305-f1.jpg

essential-clinical-anatomy-keith-moore-4th/chapter-7/nose
Springer: Anatomic Considerations
Brian S. Jewett and Shan R. Baker
T. Metin Önerci. Diagnosis in Otorhinolaryngology. Springer-Verlag: Berlin Heidelberg. 2009
 Woodruff’s Plexus
• Plexus of prominent blood vessels lying just
inferior to posterior end of inferior turbinate
(conchae)
• Frequent site of adult epistaxis
• So called “posterior” epistaxis
• Endoscopic photography & anatomical
microdissection confirms the existence and it
is a venous plexus
 Classification of Epistaxis
CLASSIFICATION
Primary No proven causal factor (70-80%
idiopathic)
Secondary Proven causal factor (trauma,
surgery, anticoagulant overdose)
Childhood <16 yrs (common in childhood)
Adult >16yrs (less common in early adult
life, peaks in 6th decade)
Anterior Bleeding point anterior to piriform
aperture (from anterior septum &
rare bleeds from vestibular skin &
mucocutaneous junction)
Posterior Bleeding point posterior to piriform
aperture
Further division: Internal Valve Stenosis Rhinoplasty. Available from:

• Lateral wall http://emedicine.medscape.com/article/877468-overview

• Septal
• Nasal floor
• Further classification based on severity and
frequency can also be used:
Recurrent (usually minor & nonlife threatening) vs Acute, severe
Severity of epistaxis is inversely proportionate to is
frequency in adult
– Recurrent primary epistaxis  minor, easily
managed
– Acute, severe  one-time event 
hospitalization, high morbidity
 Adult Primary Epistaxis
• Demography:
– Peak presentation: 6th decade
– Slight male predominance (55 male, 45 female)
– Most cases are minor, self-limiting, easily
managed anterior bleeds
• Aetiology
– Unknown, but clear suggestion that systemic
factors may be important  table
Factors Proven association Pinching ala nasi

Weather ✓
NSAID ✓
Alcohol ✓
Hypertension ✗
Septal Deviation ✗
CHRONOBIOLOGY
• Greatest freq in autumn & winter Bleeding point
specific th/
• Biphasic pattern with peaks in morning
& late evening
NSAIDS
• Antiplatelet aggregation effect
ALCOHOL
• Associated w/ prolongation of bleeding
time
HYPERTENSION
• Elevated blood pressure
SEPTAL ABNR
• 1-80% population have significant
deviation
• Coincidental
 Direct management
• Anterior epistaxis
– Controlled w/ silver nitrate cautery
• Posterior epistaxis
– Bipolar diathermy
– Chemical cautery
– Electrocautery
– Direct pressure from miniature targeted packs
• Fail to locate bleed point on initial exam  use rod lens
endoscope (identify source of posterior epistaxis >80%
cases)
– Hot wire autery or modern single fibre bipolar electrodes
– Monopolar diathermy SHOULDNOT be used  blindness
 Indirect th/
• Nasal packing
– Ribbon gauze impregnated w/ petroleum jelly/bismuth iodoform paraffin
paste (BIPP) inserted the entire length of nasal cavity in attempt to tamponade
bleed  inserted  left in situ ~24-72 hrs
• Complication: sinusitis, septal perforation, alar necrosis, hypoxia, MI
• Indication for AB cover
– Anterior packing: tampons (merocel & Kaltostat) & Balloon catheters (Brighton
or Epistat)
• Favoured as 1st LINE TH/ for nonspecialists
Persistent bleeding or Rebleeding  further exam of caity
• Hot water irrigation
– Water at 500C
– Involve reflex vasodilation & reduction in nasal lumen dimensions
• Systemic medical th/
– Tranexamic acid & epsilon aminocaproid acid  Inh fibrinolysis, reduce risk
of bleeding 1.5g 3x/d. CI: preexisting thromboembolic disease
 Surgical management
• Endoscopic diathermy of bleeding
• Posterior nasal packs
– Under anasthetic (general preferrable)
• Ligation techniques
• Septal surgery techniques
• Embolization techniques
 Adult recurrent epistaxis
• More common in children
• Recurrent in adults  secondary epistaxis more likely
• Full & detailed history & examination:
– Aspirin use, liver disease, bleeding from margins of septal
perforation, nasal tumor should be distinguished
– Usage of topical nasal meds (steroid sprays)  minor
recurrent bleeds
• Bleeding point identified  cautery
• Topical antiseptic creams available from paediatric
studies (unproven in adults): chlorhexidine & neomycin
creams reduce freq of bleeds
 Secondary Epistaxis
• Commonly observed in:
– Liver disease
– Leukemia
– Myelosupression
Demand close liaision w/ haematologist &
physicians
• Trauma
– Persistent bleeding from
ethmoidal arteries +
frontoethmoidal fracture
– Catastrophic bleeding reporter
after head injuries (delayed
rupture of internal carotid
artery pseudoaneurysm)
– Indication for angiography
• Post-surgery
– Almost any nasal surgery,
seldom difficult management
– Severe hemorrhage b/w 3-9%
following inferior
turbinectomies
– Iatrogenic damage to anterior
ethmoidal artery during
endoscopic sinus surgery
– Massive & fatal epistaxis 
damage to internal carotid
artery during posterior
ethmoid or sphenoid sinus
surgery (packing, angiography
and embolization may be tried)
• Warfarin
– 9-17% epistaxis
– Due to overdose or loss of
control
– Wide large areas of bleed or
ooze  use fibrin glue as
hemostatic dressing
• Hereditary haemorrhagic
telangiectasia
– Rendu-Osler-Weber disease,
autosomal dominant affecting
BV in skin, mucous membrane
and viscera
– Gene anomalie in chrom
9q(HHT1) & 12q(HHT2)
– Classical features:
telangiectasia, arteriovenous
malformation, aneurysm
– Recurrent epistaxis 93% cases
– Management: packing,
cautery, antifibrinolytics,
systemic or topical oestrogen,
coagulative lasers, septal
dermoplasty, ligation and
embolization, permanen
surgical closure of nostril
(YOUNG’s OPERATION)
• Tumours
– Juvenile nasopharyngeal
angiofibroma
– Haemangiopericytoma
– Rare vascular tumors that can
present w/ recurrent or sever
epistaxis (+ nasal obstruction)
– Mainly surgical treatment, may
include preoperative
embolisation
 RHINITIS
• Inflammation of lining of the nose
• With 1 or more symptoms:
– Nasal congestion
– Rhinorrhea
– Sneezing
– Itching
Rhinosinusitis (with inflammation of paranasal
sinuses): + hyposmia, anosmia, facial pain, headache
 Classification of Rhinitis
Allergic Infectious Others (vasomotor)
• Intermittent • Acute • Occupational
• Persistent • Chronic • NARES
• Specific • Hormonal
• Non-specific • Drug induced
• Irritants
• Foods
• Emotional
• Atrophic
• Gastroeosophageal
reflux
• idiopathic
 Differential Diagnoses of rhinitis
FEATURES
Polyps
Mechanical factors • Deviated septum
• Hypertrophic turbinates
• Adenoidal hypertrophy
• Obstruction of ostiomeatal complex
• Foreign bodies
• Choanal atresia
Tumors • Benign
• Malignan
Granulomas • Wegener’s granulomatosis
• Sarcoid
• Midline destructive granuloma
Cerebrospinal rhinorrhea
 Allergic Rhinitis
• Rhinitis: combination of 2 or more nasal
sympts
– Running
– Blocking
– Itching
– Sneezing
• Allergic: sympts are the result of IgE-mediated
inflammation following exposure to allergen
Classification of Rhinitis (ARIA
Guildeline)
 Risk Factors
• Genetics & family history
– Best established RF for allergic rhinitis: family history of allergy
– Several genes involved in atopy:
• 5q chromosome  for IL-4,13, w/ markers associated w/ presence of
high lvl of serum IgE
• 11q, 13, 12q
• Environment
– Pollution  sympts of rhinitis
– Ozone (secondary pollutant) formed from NO2 & O2
• The Hygiene hypothesis
– Early exposure to animales allergic sensitization
– Early nursery attendance subsequent atophy
 Comorbidities
• Asthma
• Sinusitis
• Otitis media
• Sleep disorders
• LRTI
• Dental Occlusion

Rhinitis = RF for dev of asthma

Patient w/ rhinitis should be evaluated for asthma
Pathophysiology (4 phases)
 Clinical presentation
• Immediate-type allergic symptoms
– Sneezing, rhinorrhea, itch
• Perennial allergic inflammation expressed
mainly as nasal obstruction, hyperreactivity,
poor sense of smell
• Sinus lining  picture 1 of a chronic
inflammatory rhinosinusitis
• Patient often not identified as allergic  may
undergo unnecessary operations for septal
deviation or turbinate hypertrophy before true
nature of the problem is revealed
 Diagnosis
• History + Examination + SPT (skin prick test) or RAST
(radioallergoabsorbant tests for specific IgE)
• History:
– Presenting symptoms
– Comorbidities
– Medication history
– family history
– Occupational and environmental exposure
– Dietary history
– Drug use
– Ask main symptoms
• Rhinorrhea and conjunctivitis  common in seasonal allergic rhinitis
• Nasal obstruction more common in perennial rhinitis
– Frequency, severity, duration, persistence, intermittence or seasonality
of symptoms
 T. Metin Önerci. Diagnosis in Otorhinolaryngology.
Springer-Verlag: Berlin Heidelberg. 2009

Examination
• Assess any obvious external features
– Allergic crease
• is a transverse line, common among patients who
suffer from allergic rhinitis
– Allergic salute
• habitual gesture of wiping and/or rubbing the
nose in an upwards or transverse manner with the
fingers, palm, or back of the hand
• Full ENT examination
• Allergic nasal mucosa  bilaterally
swollen, pale or bluish color, oedematous,
covered w/ watery secretions
• Exam the chest w/ measurement of
pulmonary function
– Persistent rhinitis
– Suspicion of asthma or other pulmo
disorders
 Allergy diagnosis
• SPT
– Standardized allergen  skin (volar) using lancet degranulation of
IgE-sensitized mast cells  release mediator  wheal & flare
– (+) control – histamine & (-) control – saline or diluent
– Read mean wheal d at 15 minutes (+)
– >2mm under fives
– >3mm in older subjects
+ result should be at least 2 mm > -ve control
RAST testing should be employed when:
• Test in which –ve control gives + rxn = invalid
• No + rxn to histamine

Exclusion:
SPT (x) performed if patient is on anti-histamines, has severe eczema,
had previous life-threatening anaphylaxis or has dermographism
Dermographism: exaggerated wealing tendency when the skin is stroked. It is the commonest
form of physical urticaria. It is also called dermatographism, dermatographia and
dermatographic urticaria.
Treatment
 Prevention
• Primary
– Early use of AB w/ alteration in gut flora &
vaccinations in early childhood  possible causal
factor in prevalence of allergic disease
– Restriction to allergenic exposure to inhalant allergens
& allergenic foods during early life
– Smoking during pregnancy & early life 
prevalence of atopic sensitization, rhinitis, asthma
– Obsessional house dust mite avoidance  lung
function at 3 years
• Secondary
– Allergen avoidance as complementary to usual
pharmacotherapy w/ antihistamines & topical intranasal
corticosteroid
– House dust mite avoidance/reduction:
• Encase mattress & pillows in plastic covers or special allergen-
proof fabric
• Hot wash bedding (55o) & damp wipe mite-proof covers every
1-2 wks
• Remove objects that accumulate dust or place in a cabinet
• Store clothing in drawers & remove unused clothing from
bedroom
• Remove upholstered furniture & replace w/ leather, plastic or
vinyl furniture
• Remove carpets, replace w/ washable rugs, install hardwood
floors
• Treat carpets w/ acaricide, 3% tannic acid, vacuum regulargly
(not patient)
• Use washable curtains or venetian blinds, clean every 2 weeks
• Replace or wash air filters on AC every month to remove debris
Other measures to reduce exposure to cat allergen are detailed below:

• remove cat, replace upholstered furniture and carpets, steam clean walls; if
refusal: keep cat out of bedroom and other commonly used rooms;
• wash the cat weekly using 1 L of water;

• replace upholstered furniture with leather, vinyl or plastic and wash weekly

• remove carpets, replace with washable rugs or hardwood doors, clean

regularly;
• vacuum rugs with HEPA-filter vacuum cleaner;

• increase ventilation with fans, air-conditioning or by opening windows;

• use HEPA-type air cleaner in rooms where patient spends majority of time;

• electrostatic filters may be considered but are likely to have limited value.
• Avoidance of pollen not possible. Keep windows in cars and buildings tight shut.
Car w/ pollen filter. Avoid grassy open spaces
• Food allergy almost never causes isolated nasal symptoms
Antihistamines:
• rapidly relieve running, itching,
sneezing
• Little or no effect on blockage (except
desloratadine & levocetirizine)
• st
1 gen histamines: chlorphenarimine,
diphenhydramine (AVOID! Sedation,
psychomotor retardation, learning
impairment)  CROSS BBB
• 2nd gen acts w/in 1 hrs, topical w/in
15 minutes
• Cetirizine & fexofenadine &
desloratadine  safer to cardiac pts
(don’t block K+
channels,✗arrythmias)
• More effective to use regularly than
intermittent
SODIUM CROMOGLICATE
• Spray weakly effective against all rhinitis
symptomes
• Needs to be use 3-4 x daily
• Useful for small children (<4 yrs) – topical
corticosteroid is not available
Topical glucocorticosteroids
• MOST EFFECTIVE TREATMENT FOR RHINITIS
• Regular treatment necessary
• SE: Minor & include EPISTAXIS & nasal irritation
• Reduce inflammation & hyperreactivity, nasal &
eye symps & sense of smell
• Max effects occuring after several days
• Risk of asthma exacerbation/hospitalization
DECONGESTANTS
• Topical, nasal obstruction but
rhinorrhea
• Regular use >> a few days  rhinitis
medicamentosa (α stimulation by
sympathetic nervous system)
• Very short term use (flying, otitis
media w/ effusion & rhinosinusitis
recommended)
• Systemic ✗hyperreactivity,
insomnia & HT in adults
IPRATROPIUM BROMIDE
• Atropine-like nasal spray against watery
rhinorrhea, regularly used  curative
• SE: worsening of glaucoma orprostatism
& dry mouth & eyes
SYSTEMIC CORTICOSTEROID
• Unblock nose at start of treatment or
for very severe symptoms
• Should be combined w/ topical
corticosteroid
• Injection into turbinates & polyps 
blindness & not recommended
ANTI-LEUKOTRIENES
• Effective against congestions & mucus
production
• Helpful in nasal polyposis
 NON ALLERGIC PERENNIAL RHINITIS
• Any nasal condition w/ identical sympts to those seen in
allergic rhinitis but allergic etiology has been excluded
• Classified broadly as:
– Idiopathic rhinitis / vasomotor or nonallergic noninfectious
perennial rhinitis (NANIPER)
– Nonallergic occupational rhinitis
– Hormonal rhinitis
– Drug-induced rhinitis
– Other forms
• nonallergic rhinitis w/ eosinophilia syndr (NARES)
• Physical and chemical factors induced rhinitis
• Food induced
• Emotion induced
• Atrophic rhinitis
 • No specific diagnostic test
– Diagnosis on basis of rhinitis symptoms in absence
of identifiable allergy (allergy testing), structural
abnormality, immune def, sinus disease, other
causes
• Five or more sneezes and /or nose blowing/day 
possible indicative of nasal disease
• Condition persist for >9 months/year & produces 2 or
more symptoms
– Hypersecretion, blockage, sneezing, post nasal drip

Post nasal drip: swallowed unconsciously, the

feeling of it accumulating in the throat or
dripping from the back of your nose
 Pathophysiological considerations
• Nasal hyperreactivity to various stimuli
– Odors, position, tempt, histamine, etc
• Etiology & pathophysiology largely unknown
– Maybe associated w/ sympathetic & parasympth nervous systems 
imbalance neuronal control of end organs in nose
– Capcaisin  stimulates afferent nerve fibers  dose-dependent leukocyte
influx, albumin leakage, glandular secretion in allergic rhinitis & as
treatment of NANIPER
– Nonallergic rhinitis indicated several pathologic mechanisms:
• Non-IgE-mediated inflammatory responses
• C fiber stimulation
• Parasympth hyperreactivity and/or sympathetic hyporeactivity
• Glandular hyperreactivity
• Diagnostic tools:
– Skin reactivity to vasomotor agents (papaverine, methacholine, histamine,
compound 48/40)  pathological skin reactivity to PAPAVERINE ONLY
increased in perennial nonallergic rhinitis
– Methacholine tests  differentiate idiopathic rhinitis subjects from
control, only in those suffering from rhinorrhea as main symptoms
 Types of nonallergic rhinitis
• Idiopathic rhinitis
– Characterized primarily: nasal blockage, rhinorrhea, sneezing
– Etiology: thought to be triggered mainly by irritants & change in
atmospheric conditions
– Increase progressively with age reaches >60% beyond age of 50
yrs (functional abnr due to aging process of nasal mucosa)
• Nonallergic occupational rhinitis
– Exposure to airborne agents present in workplaces
– Via IgE mediated and nonimmunologic mechanisms
• Nonimmunologic trigers: irritant or toxic small molecular weight
compounds
– Aldehydes, isocyanates, aircraft fuel, jet stream exhaust, solvents, etc
• Physical exposure (cold air)
• Airborne exposure to nonallergenic microbial agents
– Endotoxin & beta 1,3 glucan in compost workers  total neutrophils, MPO,
IL8, NO, albumin >>
• Vanadium peroxide (fuel oil ash) = respiratory irritant  increase # of
PMN in nasal lavage
• Hormonal rhinitis
– Associated w/ pregnancy
– Women who smoke significantly increased incidence
– Asthma nor rhinitis  risk factors for pregnancy
rhinitis
– Due to hypothyroidism or acromegaly
– Oestrogen  vascular engorgement (swell)  nasal
obstruction or hypersecretion
– Beta-estradiol & progesterone  increase histamin
H1 receptors on human nasal epithelial cells &
mucosal microvascular endothelial cells  induce
eosinophil migration and/or degranulation
– Testosterone  decrease eosinophil activation &
viability
• Drug-induced rhinitis
Aspirin, NSAIDS, beta-blockers, ACE-I, methyldopa, oral
contraceptives, psychotropic agents, nasal topical
decongestants  induce symptoms of rhinitis (topical or
systemic)
– Hypersensitivity to drugs, particularly aspirin 
exacerbate rhinitis & asthma
– Intolerance to aspirin or/and NSAIDs  produces
rhinorrhea
– Intolerance to ACE-I, methyldopa, oral contraceptives
 predominantly nasal blockage
– Overuse of topical nasal decongestion  rebound
effect following withdrawal of the drugs
– Excessive use  nasal hyperreactivity & hypertrophy
of nasal mucosa (rhinitis medicamentosa)
• NARES
– >20% eosinophils in nasal smears of symptomatic patients
w/ perennial sneezing attacks, profuse watery rhinorrhea,
nasal pruritis, incomplete obstruction & loss of smell
– Lack of evidence of allergy (-ve SPT or absence of IgE Ab to
allergens)
– Specific etiology is not clear
– NARES patients frequently dev nasal polyps & asthma later
on
– May be an early expression of triads (nasal polyposis,
intrinsic asthma, intolerance to aspirin)
– ~50% NARES pts w/out history of respi symptoms,
bronchial responsiveness  increase # of eos in sputum,
not in nasal
– NARES is a variant of vasomotor rhinitis (perennial intrinsic
rhinitis)
• Due to physical & chemical factors
– Cold, dry air  SKIER’S NOSE
• Rhinorrhea features prominently
– Exposure to chemicals, particularly air pollutants from cigarrete
smoke, liquid petroleum fuels  directly exacerbate symptoms of
rhinitis in nonallergic individuals
• Food induced rhinitis
– Hot & spicy foods contains capcaisin (stimulate sensory nerves to
release neuropeptides & tachykinins)  watery rhinorrhea
(GUSTATORY RHINITIS)
– Alcoholic beverages  induce sympts as a result of vasodilation
– Dyes & preservatives & sulphites  contain histamine or other
biogenic amines
• Emotionally induced
– Stress & sex arousal  autonomic stimulation
• Atrophic rhinitis
– Primary  predominant in women, characterized by progressive
atrophy of nasal mucosa & underlying bone of turbinates  formation
of thick crusts  foul smell (OZAENA) in nose
– Nasal cavities enlarged, sensation of nasal congestion
– Develops directly as result of granulomatous nasal infections, chronic
rhinosinusitis, excessive nasal surgery, trauma, irradiation
 Diagnosis
• Based on thorough case history + step-wise
exclusion of possible DD
– Check possible stimuli, severity, duration of disease
– Check drug use, exposures, hormonal status,
involvement of other organs
– Exclude nasal diseases by rigid nasal endoscopy
– Exclude allergy
– Exclude chronic rhinosinusitis by CT scan
– Perform nasal cytology (eosinophilia), +  perform
oral aspirin challenge
 Therapy
• Specific avoidance: 1st line th/ for drug, food, occupational
rhinitis
• Idiopathic nonallergic rhinitis:
– Intranasal anticholinergics (ipratropium bromide) for nasal
secretion as predominant sympt
• Nasal decongestants should be avoided or limited to 10 days
– Topical steroids & antihistamines (2 main classes of drugs
employed)
• Fluticasone, propionate, bodesonide, beclomethasone, azelastine 
approved by FDA (Food Drug Administration)
• Topical nasal steroids used for more severe sympts whom an
inflammatory pathogenesis is a prominent feature
• Intranasal capcaisin once daily for 5 wks improve all symptoms
– Nasal obstruction is resistant to medical treatment & if inferior
turbinate is hyperplastic  surgical intervention to reduce size
 OCCUPATIONAL RHINITIS
• Episodic work-related symptoms of rhinitis
– Manifest sympts on weekdays, abate during weekends and holidays
– Prolonged exposure  irreversible  sympts persist
– Coexist w/ asthma & conjunctivitis
• Occupational asthma rarely occurs as an isolated disease w/out occupational
rhinitis
• Incidence is underestimated due to failure to diagnose & it is not
life threatening condition
• Men: highest incidence at 25-29 yrs  gradually declines
• Women: peaks b/w 40 – 44 yrs
• 200 chem & organic dusts as cause
• Allergic reaction or irritation of nasal mucosa
• Sympt dev after latency period of 2 moths to 18 years in case of
allergic occupational rhinitis (doesn’t apply to irritant occupational
rhinitis  dev on immediate exposure)
• Risk factors
– Exposure (intensity + duration)
– Atopy & specific sensitization
– Smoking
• Pathogenesis
– Nose: 1st portal of entry, exposed to constant steam of air
– Materials accompanying are steam impact on mucus
surface as function of their aerodynamic equivalent
diameter (AED)
– AED >9 micrometer  stick to nasal wall
– High soluble materials: ammonia, sulphur dioxide,
formaldehyde deposit in upper airway
– Smaller particles & less water-soluble gases  pass to
lower airways
– Occupational rhinitis may be allergic or irritant
 Allergic occupational rhinitis
• Particles may trigger IgE-mediated (type I) immune
response
• Late-phase response dev 4-6 hrs after initial rxn
• Causative agents
• IgE dependent mechanism: SPT, RAST to most
HMWCs
 Irritant occupational rhinitis
• Irritant chemicals trigger release of substance P &
inflammatory mediators from sensory C-fibers
after binding to chemoreceptors on their surface
– Neurogenic inflammation  vasodilatation 
oedema & manifestation of inflammation
• Patient complain of burning, stinging, painful
sensation in nasal passages + nasal congestion &
rhinorrhea
• Delayed response doesn’t occur
• Results from acute exposure to high [] of respi
irritant & persist after exposure
Substance P; pain information,
neuromodulator part of tachykinin
• Corrosive rxn may occur do to excessive [] of irritating &
soluble chem gases
– Ammonia
– Hypochloric acid
– Vinyl chloride
– Organic sulphur containing compound
– Acrylamide
– Cyanide
– Nitriles
– Organophosphoside compounds
• Disorders of olfaction  result of rhinitis or direct effect of
irritants on olfactory receptors
• Manifest nasal hyperreactivity to non specific
environmental agents
– Temperature & humidity
– Tobacco smoke and strong odours
• HIGH RISK OCCUPATIONS (highest & followings)
– Who are exposed to different kinds of animal
epithelium (highest)
– Livestock breeders
– Bakers
• Wheat, cereal flours, cereal amylases, fungal amylases,
storage mites, additives
– Farmers
• Agricultural exposures, grain farming, storage mites in hay
(cause of barn allergy)
– Food processing workers
• Food industry accounts for largest # of cases
– Detergent manufacturers
– Animal lab workers
– Healthcare workers
 • SBS (sick building syndrome)
– Eye, nose, throat irritation, fatigue, headache among office workers
temporally associated w/ time at work
– Characterized by absence of abnr physical findings & lab results
– >300 VOCs identified as indoor pollutants causing SBS
– Originates from building materials, combustion fumes, cleaning
compounds, paints, stains + tobacco smoke
– Type of ventilation is important in causation of SBS
• Examination
– Crusting & epistaxis common in irritant rhinitis
– Chest exam for signs of asthma & inspection of dermatitis (occurs in
latex allergy)

Volatile organic compounds (VOCs) are organic chemicals that have a high vapor pressure at ordinary room
temperature. Their high vapor pressure results from a low boiling point, which causes large numbers of
molecules to evaporate or sublimate from the liquid or solid form of the compound and enter the
surrounding air, a trait known as volatility. For example, formaldehyde, which evaporates from paint, has a
boiling point of only –19 °C (–2 °F).
 ATROPHIC RHINITIS
• Chronic nasal disease characterized by progressive atrophy of mucosa &
underlying bone of turbinates
• Viscid secretion  dry  crusting  foul odour (ozaena)
• Precise etiology unknown, no specific etiologic factor  PRIMARY
ATROPHIC RHINITIS
• Specific etiologic factor  SECONDARY ATROPHIC RHINITIS
– Chronic sinusitis
– Chronic granulomatous lesions (TB, syphillis, leprosy, excess destruction of
nasal tissue caused by surgery)
• Bacterial flora from nasal secretion:
– Coccobacillus foetidus ozaena
– Diptheroid bacilli
– Klebsiella ozaenae
– Bortedella bronchoseptica
– Pasteurella multocida
Inoculation of these organisms  changes similar to atrophic rhinitis
• Nasal aspirate  significant decrease in total
phospholipids, change in phospholipid profile
– Possible role for surfactant deficiency
• Primary atrophic rhinitis commences at
– puberty, common in females
• Endocrine imbalance
– Low socioeconomic background
• poor nutrition and iron deficiency
– Heredity
• Racial influence (yellow latin & american blacks)
– Autoimmune etiology
 Pathology
• Patches of metaplasia in epithelium
– Transition of ciliated columnar epithelium 
nonkeratinized or keratinized squamous epithelium
• Lamina propria: chronic cellular infiltration,
granulation tissue, fibrosis
• Mucous gland decrease in size & number
• Decreased vascularity, periarteritis, endarteritis
of terminal arterioles
• Vasodilatation of capillaries

Periarteritis: inflammation of the outer coat of an artery and of the tissues surrounding it
Endarteritis:inflammed inner lining of artery
 Clinical features
• Nasal crusting (brown black or dark green) + thick purulent
discharge + foul smell (due to anaerobic flora in nasal
cavity)
• Anosmia
• Headache, epistaxis, nasal obstruction
• Crust  mechanical obstruction  blunting sensory nerve
endings  diminished sensation of airflow
• Presence of fetor (foul smell) in all but the earliest cases
• Atrophy of turbinates  widening of cavity  green crust +
thick purulent discharge
• Complicated by maggot infestation in nose
 Treatment
• Medical
– Douche nose 2x daily (nasal irrigation/lavage) w/
hypertonic & alkaline solution
• Sodium bicarbonate + sodium chloride + warm water
(1:1:2)
– Rifampicin oral 600 mg 1x daily for 12 wks
• Surgical
 Rhinitis Sicca
• Similar to mild atrophic rhinitis w/out progressing to its full clinical
picture
• Widespread condition freq in dry, hot, dusty occupation
• Caused by variety factors: alcoholism, anemia, nutritional,
constitutional diseases
• Deficiency & inactivity of seromucinous glands
• Metaplasia of clumnar ciliated epithel  squamous or cuboidal
epithelium
• Deificiency of mucous blanket
• Complains discomfort, irritation, epistaxis, crusting (thin & dry,
don’t extends to posterior part of nasal cavity)
• Fetor absent
• Treatment: removal of all possible causes, supplementing iron &
vitamins, douching nose
Kelainan sinus paranasal

LO 5
 Rhinosinusitis
• Rhino: nose, sinusitis: inflammation of mucosa of paranasal
sinuses  inflammation of mucosa of nose & paranasal
sinuses
• 4 clinical forms of rhinosinusitis:
ACUTE rhinosinusitis 7 days – 4 weeks

SUBACUTE 4 – 12 wks

RECCURENT ACUTE >= 4 episodes of ARS/year

CHRONIC >= 12 wks

ACUTE EXACERBATION OF CHRONIC RS Worsening of existing symptoms or

Appearance of new symptoms
Complete resolution of ACUTE (but not
chronic) symptoms b/w episodes
 RS Task force’s definition:
Symptoms for clinical diagnosis
2 MAJOR or 1 MAJOR+2MINOR
MAJOR MINOR
1. Nasal blockage/obstruction 1. Headache
2. Nasal 2. Fever (in ARS)
discharge/purulence/discoloured 3. Halitosis (bad breath)
posterior drainage 4. Fatigue
3. Hyposmia/anosmia 5. Dental pain
4. Purulence on nasal examination 6. Cough
5. Facial pain/pressure 7. Ear pain/pressure/fullness
6. Facial congestion/fullness
7. Fever (ACUTE RHINOSINUSITIS ONLY)
Since viral infection are self-limited, most interest: BACTERIAL DISEASES
Valuable for acute bacterial rhinosinusitis (ABRS)
Difficult to apply to SUBACUTE & CHRONIC RHINOSINUSITIS (difficult to establish
bacteria for chronic, except AECRS). Wide variety of conditions have been found to be
associated with CRS.
Thus, chronic rhinosinusitis is defined:
RS of AT LEAST 12 CONSECUTIVE weeks duration
 Pathophysiology
• Sinus ostia obstruction
• Predispose to development of an infection
• Factors related to dev of ABRS:
FACTORS
Genetics Immotile cilia syndrome
Cystic fibrosis
Anatomic abnormalities Concha bullosa
Septal Spur
Paradoxal turbinate
Systemic Diseases
Medical Treatment
neoplasms
Allergic or immune
response
Environmental Bacterial
Virus
Fungal
Trauma
Tobacco-exposure
Irritants or noxious chemicals Sinus ostium: opening that
Iatrogenic Surgery connects sinus to the nasal cavity.
Medications Tight area that have higher % of
Nasal packing
Nasogastric tube placement cilia than surrounding mucosa
 • Individuals with allergies tend to have higher incidence
of A/CRS
• ARS  in conjunction w/ acute viral upper
respiratory tract infection causing:
– Mucosal swelling (occlusion of sinus ostium)
– of O2 tension, mucociliary transport
– Transudation of fluid into sinuses
– Viscous mucus & alter Ciliary beat freq
– Mucostasis & bacterial colonization
• Other factors for dev or perpetuation of CRS
– Biofilms
– SuperAntigens
– Osteitis
Perpetuation: preserve
Biofilms: any group of microorganisms in which cells stick to each other & often adhere to surface
Assemblage of surface-associated microbe in EC polymeric substance matrix
SuperAg: class of Ag that cause non-specific activation of T-cells  massive cytokine release
Osteitis: inflammation of the bone substances
T. Metin Önerci. Diagnosis in Otorhinolaryngology. Springer-Verlag: Berlin Heidelberg. 2009
 Histopathology
• CRS:
– Proliferation process occur w/ lymphocytes. Plasma cells &
eosinophils
• Eosinophilic infiltration seen either in mucosa or sinus cavities
– ✓evidence of fibrosis of lamina propria
– ✓fungi & bacteria

• ARS: Predominance of
– neutrophils
– Hemorrhage
– Ulceration
– Necrosis
– Exudate
• Resistance of AB rate for both H influenzae & S pneumoniae are NOT UNCOMMON for both:
• MACROLIDES & BETA LACTAMS
• Resistance mech:
– AB deactivating enzymes
– Alter in target site of AB
– Changes in influx or eflux process
• CRS may or may NOT involve pathogenic microbes
• If pathogenic microbes ✓,
– 55% Staphylococcus species (aureus 20%)
– Enterobactericeae
– Anaerobs
– Gram negative & fungi

DIAGNOSIS
• Gold standard for ABRS: Maxillary Sinus tap with culture
– To identify ethmoid infections and sensitive
• Available: Endoscopic-guided middle meatal cultures
– Less traumatic and allow more frequent cultures
• Nasal endoscope
– Assess anatomy
– Confirm drainage
– Evaluate treatment responses
• Preferred radiologic test:
– Sinus CT scan for abnr in patients w/out sympt of RS, acute viral respi infection or viral RS
– Complication of ABRS (orbital/intracranial)
– Assess severity of diseases or respond to treatment in CRS
• RSDI (Rhinosinusitis disability index)
– Assess physical, emotional, functional impacts  QOL
 Complications of Rhinosinusitis
• Any adverse progression of chronic or acute
bacterial infection beyond paranasal sinuses
or compromised in function of any part of
body due to local or distant effects of the
condition
 Classification
• ACUTE & CHRONIC
ACUTE
• Local
– Via areas where surrounding bone
is thin (e.g lamina papyracea)
– Direct anatomical connection by
way of nerve or blood vessels (e.g.
infraorbital canal, diploeic vein of
frontal & sphenoid bones)
– Absence of valves in veins b/w orbit
& sinuses  retrograde venous
spread of infection
– 2nd Premolar & 1st molar dental root
canals  direct route of spread Textbook of pediatric care. Chapter 313: Preseptal and Orbital
Cellulitis Ellen R. Wald, MD

Progression in sinuses will give effects

that are specific for indiv.sinuses
FRONTAL
• Subperiosteal abscess through outer table of skull • Most important & freq acute complication of
 POTT’s PUFFY TUMOR
• Inward progression  acute intracranial
complication (abscess or meningitis)
Cavernous sinus: The cavernous
sinus is a small but complex
structure consisting of a venous
plexus, the carotid artery, cranial
nerves, and sympathetic fibers.
http://www.ajronline.org/doi/full/10.2214/ajr.181.2.18105
83
ETHMOID
ethmoid  ORBITAL CELLULITIS
• Clinical classification of 5 stages to determine
overall management of pts
• Preseptal cellulitis (inflammation ✗ beyond
orbital septum
• Postseptal cellulitis or orbital cellulitis
w/out abscess (extends into tissue of orbit)
• Subperiosteal abscess (abscess formation
deep to periosteum of orbital bones, lamina
papyracea)
• Cavernous sinus thrombosis/abscess
(extended through optic foramen into
cavernous sinus, thromboses & possibly
progresses to abscess formation)

MAXILLARY
• Isolated maxillary RS rarely give rise to acute local
complication
• Patient w/ acute swelling of cheek (primary
dental disease complication rather than sinus)
SPHENOID
• Acute local complication are rare
• Can result in cavernous sinus thrombosis by
direct spread
• Intracranial complications can occur as result of a
base of skull fracture through the sphenoid sinus
 DISTANT
• Brain abscess
– Hematogenous spread may occur (secondary to
maxillary RS associated w/ dental disease)
• Septicaemia
• Toxic shock syndrome
TSS: caused by toxins produced by bacteria
(staph)
flu-like symptoms including headache, muscle aches, sore throat and cough
nausea and vomiting
diarrhoea
fainting or feeling faint
dizziness or confusion
A widespread sunburn-like skin rash may also occur, with the whites of the eyes, lips and tongue becoming
more red than usual.
One or two weeks after the rash appears, it is common that the skin begins to shed in large sheets,
especially from the palms of the hands and soles of the feet.
 Chronic
• Mucoceles: chronic slow expanding lesions in any
of sinuses  bony erosion  extension beyond
sinus
– If become secondarily infected  purulent contents
 pyocele
• Maxillary sinus due to proximity of dental roots
 protrude to maxillary antrum  teeth may be
affected by maxillary RS (much more likely to be
due to malignant > inflammatory of sinus)
• Orbital cellulitis or intracranial complication ONLY
IF THERE IS AN ACUTE EXACERBATION
Cellulitis is a common skin infection caused by bacteria. It affects the middle layer of the skin
(dermis) and the tissues below.
mucocele is a benign, mucus-containing cystic lesion of the minor salivary gland.
 ORBITAL COMPLICATIONS
• History of mild upper respi tract infection + swelling around
the eye
• More common in children (50% <6yrs) & young adults (76-
85% <20 yrs)
• Visual problems if STAGE 3 (subperiosteal abscess) or beyond
– Visual acuity or color vision
• Stage 5 (cavernous sinus thrombosis), chemosis, periorbital
oedem, proptosis  progressive opthalmoplegia(paralysis of
muscles w/in or surrounding eye) (lateral gaze first) & visual
impairment (probably total blindness) due to direct cranial
nerve involvement + sympts (headache + trigeminal
parasthesia – tingling or pricking)
– Often bilateral
 Group II - Orbital cellulitis
• Infection of ORBITAL SOFT TISSUES POSTERIOR TO SEPTUM w/out
abscess formation
• Major cause: sinusitis
• Common in pts <9 yo
• + HIB vaccine change in average age
• Eyelid edema, erythema, conjunctival chemosis, axial proptosis,
limitation of occular movement, pain w/ eye movement,
increased ICP
• Imaged + IV AB th/ + nasal decongestant
• Failure to improve 48-72 hrs  surgical sinus drainange + culture

Proptosis: protusion of eyeball (menonjol)

 Group III – Subperiosteal abscess
• Fluids collect in potential spcases b/w periorbita &
orbital wall
• Confirmed by CT scan as convex mass adjacent to sinus
involved
• Limited extraocular motility, pain on globe movement
towards abscess
• Most common location: along medial orbital wall
secondary to ethmoid rhinosinusitis
• Abscess  infection break through lamina papyracea
or foramina of anterior/post ethmoidal neurovascular
bundles
• Treatment: IV AB alone & surgical in refractory cases
 Intracranial complications
• Adolescent & young adult males are more
commonly affected (possibly due to
vascularity of diploic system in this age group)
• History:
– Mild confusion or mood change (w/ well-defined
intracranial abscess)  acute pain & possible loss
of conciousness (acute meningitis)
– Scanning all pts w/ acute frontal RS or orbital
cellulitis to exclude serious complications (initially
be clinically silent)
 Examination
• Endoscopic of nose
– Determine site & extent of disease
• Orbital cellulitis
– Range of eye movement
– Degree of proptosis
– Relative afferent pupillary defect
– Visual acuity (snellen chart)
– Color vision (Ishihara plates)
– Inspection of optic disc
Repeated daily. Increasing concern  6 hrs monitoring should be
undertaken + regular temperature & pulse measurements
• Intracranial complications
– Examination of cranial nerves & CNS
– Possibility of occult (hidden) intracranial complications should be
considered
 Investigation
RADIOLOGICAL
– Confirm diagnosis of complication
– Define the extent and site of
complication
– Help planning treatment
– Confirm no other covert
complication
• Orbital complication
– Investigation of choice is HD CT
scan taken in coronal & axial
planes  greatest chance of
picking up small abnr
– MRI has no evidence that it is
more accurate than CT
– US imaging do not demonstrate
important surgical anatomy
• Intracranial complication
– MRI scan >> CT scan
– If synchronous sinus surgery
needed  CT scan (define bony
anatomy) desirable
HEMATOLOGICAL
– Ensure no serious underlying
disease (e.g.leukemia)
– Act as assessment of fitness for
surgery
– Monitor respond to treatment
Full blood count should be performed
OTHERS
• Infective  blood cultures ASAP 
prior AB treatment or culture of
purulent material at time of
surgery in sinus or from abscess
• Urinalysis
– to detect DM  immunocompromised
• Ongoing monitoring of treatment
– Temperature measurement
– Persisting infection: spiking pyrexia 
indicate further radiological
investigation
 Treatment
• Abscess not demonstrated by investigation  nonsurgical management
Except: vision was affected by pressure on optic nerve due to surrounding inflammation w/out abscess
• Aim of medical treatment:
– Control & eliminate disease process (complications)
– Eliminate primary RS
• Nasal decongestion
– Intranasal ephedrine 0.5% drops 2 drops 6-hourly to affected side of nose
• Antibiotics
– Broad spectrum but reasonably selective (minimize resistance)
– IV cephalosporin + metronidazole (FIRST CHOICE)
– Systemic steroid recommended to acc resolution of inflammatory process
• Immunosuppressive action of steroids may mask other complications
No significant clinical improvement 1st 24 hrs,surgical intervention considered
• Orbital complications
– IV AB administration continue until improvement, then oral treatment (7-14 d)
• Absence of pyrexia for 24 hrs + general clinical improvements
• Intracranial complications
– Prolonged (4-8 wks) course of IV AB. Oral AB not sufficient to cross BBB
• Cavernous sinus thrombosis
– + anticoagulation to AB th/ + surgical drainage
 Surgical
• For Rhinosinusitis or Complications
• For RS:
– Contraindications for endoscopic
approach: intracranial complication,
osteomyelitis of frontal bone or orbital
complications + acute visual problem
• Orbital cellulitis
– Cellulitis alone  conservative
treatment
– +proptosis but normal eye movements
& visual acuity (sharpness)  surgery
• >15 yrs more likely to dev complications
require surgery
 POLYPOSIS
• A sinonasal disease
• Presents in nasal cavity w/ grape-like appearance (having a
body & stalk)
• Surface is smooth, more yellow than pink mucous
membrane
• Originate in upper part of nose around openings to
ethmoidal sinuses
• Protrude to nasal cavity from middle & superior meatus 
nasal blockage  abolishing airflow to olfactory region
• Nasal polyposis: multiple, bilateral polyps
– Part of inflammatory reaction involving mucous membrane of
nose, paranasal sinuses & lower airways
• Peak age: 50 or older Male : female  2:1
The polyp recurrence rate depends upon the the of disease.
Low in cytic fibrosis patient
High in patients with non-steroidal antiinflammatory drug (NSAID) intolerance and asthma.
 Aetiology & Associated diseases
• Aspirin Triad
– Triad: Nasal polyposis, asthma, aspirin intolerance
• Allergic fungal sinusitis
– Inflammation: eosinophil dominated (as in aspirin triad)
• Cystic fibrosis
• Primary ciliary dyskinesia (Kartagener’s syndrome)
– Absent mucociliary clearance & reccurent bacterial
infection
• Young’s syndrome
– Respi disease + chronic RS + nasal polyps + bronchiectasis
+ azoospermia
 Pathology & Pathogenesis
• Site of polyp formation
– Mainly situated in middle meatus
– Originates from mucous membrane of outlets (ostia,
clefts, recesses) from paranasal sinuses
• Ostiomeatal complex
– Touching mucous membranes in narrow ostiomeatal
complex  proinflammatory cytokines released from
epithelial cells
– Nerve endings near borderline b/w nose & paranasal
sinuses are thin  easily damaged by cytotoxic
proteins released by eosinophils
• Surface epithelium
– Major part of polyp surface covered by ciliated pseudostratified
epithelium
• Transitional & squamous epithelia are found esp in anterior polyps
• Innervation
– Denervation of nasal polyps  decrease in secretory activity of
glands & induces abnr vascular permeability  tissue oedema
• Vascularity of polyps is minimal, venules show unusual
organization
• Cell junctions  web of villous processes, incompletely
sealed, wide open  promote oedema
• Ultimate inflammation of upper airways
• Increased # of epithelial mast cells in nasal polyps, total
histamine lvl >> other tissues (100-1000x plasma)
– Highly characteristic of polyps: OEDEMA-FILLED SACKS
• High # of IL-5
 Clinical presentation
• Rhinosinusitis • Asthma & NSAID
– Perennial nonallergic
rhinitis (idiopathic)  intolerance
watery rhinorrhea for – Severe polyposis & blood
some years  nasal
blockage dev  persistent eosinophils  asthma
• Secretion become more 30% and/or NSAID
viscous  removed by noisy intolerance 15%
sniffing as postnasal drip
– Impaired airflow in upper – Most pts dev asthma
part of nose  reduced before polyps
sense of smell  taste 
unpleasure eating &
drinking
– Polyps dev in children 
widening of ethmoidal
cells, flattening,
broadening of nasal bridge
= FROG NOSE
 Diagnosis & staging
• Rhinoscopy, endoscopy
– Endoscopy w/ rigid scope 
diagnose small polyps in middle
meatus & superior assessment of
extent of disease & anatomical
abnr
• Imaging
– CT scan of nose & paranasal
sinuses  anatomy & pathology
demonstration
• Indicated when supsect of
malignancy or meningocoele or
before endoscopic surgery
• Use for staging disease
• Other
– Evaluation for cystic fibrosis
– DD/: malignant tumors, inverted
papillomata, meningocele(in child)
as simple polyps
 Treatment
• Medical
– Intranasal corticosteroids  FAR BEST DOCUMENTED type
of treatment for nasal polyposis
• Some pts respond after short course of systemic steroids
• Do not eliminate polyps but reduces their size
– Only small fraction reaches middle meatus
• Topical steroids  delay recurrence of polyps after surgery,
postpone need for new surgery
– Systemic corticosteroids
• Tablets (prednisolone) & injection
– 25 mg prednisolone daily for 10-14 days
• w/in few days  reduce all nasal symptoms including sense of
smell
• Short course  medical polypectomy
• Surgical
– Cannot be expected to cure disease
• Polypectomy have long lasting effects for first time w/
large polyps
– Severe cases w/ persistent symptoms  surgery +
medical treatment  reduce # of inflammatory
tissue  open up nasal airway  improve
ventilation of paranasal sinuses
Conclusion:
Medical treatment is sufficient to treat most cases
of nasal polyposis
If nasal obstruction remains main problem after
medical treatment  indicate surgical treatment