Transcript ACUTE AND CHRONIC RHINITIS

By-Dr. Sudeep K.C.
1) VIRAL RHINITIS
1)COMMON
COLD(CORYZA)
Aetiology: it is caused by
virus usually through
airborne droplets.
 Adeno virus , picorna
virus, rhino and coxsackie
virus.
 Incubation period is 1-4
days and illness last for 23 weeks.
CLINICAL FEATURES:
 Burning sensation of nose followed by nasal stuffiness ,
rhinorrhoea and sneezing.
 Low grade fever.
 Nasal discharge is initially watery and profuse but may
become mucopurulent due to sec. bacterial invasion.
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TREATMENT:
Bed rest
Plenty of fluids.
Antihistamine and nasal decongestant.
Analgesics to relieve headache and antibiotics if secondary
infection.
COMPLICATIONS:
 Disease is usually self limiting and resolves
spontaneously after 2to 3 weeks.
 Occasionally sinusitis, bronchitis, pharyngitis may
occur.
INFLUENZAL RHINITIS:
 Caused by influenza viruses A , B or C .
RHINITIS ASSOCIATED WITH EXANTHEMAS:
 Measles, rubella, chickenpox, are often associated with
rhinitis which precedes exanthemas by 2-3 days.
2) BACTERIAL RHINITIS
A)Non-specific infections:
 It may be primary or secondary.
 Primary bacterial rhinitis is seen in child usually
infected by pneumococcus , streptococcus or
staphylococcus.
 A greyish white membrane may form in the nose ,
which with attempted removal, cause bleeding.
B)Secondary bacterial rhinitis is result of bacterial
infection supervening acute viral rhinitis.
3) IRRITATIVE RHINITIS
 Caused by exposure to dust, smoke and irritating gases
like ammonia, formalin etc.
 May result from trauma on nasal mucosa during
intranasal manipulation.
CLINICAL FEATURES:
 Immediate catarrhal reaction with sneezing,
rhinorrhoea and nasal congestion.
 Symptoms may pass off rapidly with removal of
offending agent .
CHRONIC SIMPLE RHINITIS
Aetiology:
 Recurrent attacks of acute rhinitis in presence of
predisposing factors leads to chronicity.
Predisposing factors:
 Persistence of nasal infection due to sinusitis ,
tonsillitis and adenoids.
 Chronic irritation from dust, smoke etc
 Nasal obstruction due to DNS, synechia leading to
persistence of discharge.
PATHOLOGY:
 There is hyperaemia and edema of mucous membrane
with hypertrophy of seromucinous glands and increase
in goblet cells.
 Blood sinusoids over turbinates are distended.
CLINICAL FEATURES:
 Nasal obstruction
 Nasal discharge
 Headache
 Swollen turbinates- pit on pressure ,shrink with
decongestant.
 Post nasal discharge.
TREATMENT:
Treatment of causative agent.
Nasal irrigation with alkaline solution .
Nasal decongestant help to relieve nasal
obstruction and improves sinus ventilation.
A short course of systemic steroids helps to
wean patient already addicted to excessive use of
decongestant drops or sprays.
Antibiotics.
HYPERTROPHIC RHINITIS:
 It is characterised by thickening of mucosa, submucosa,
seromucinous glands, periosteum, and bone. Changes are
more marked on the turbinates.
AETIOLOGY:
 Recurrent nasal infections.
 Chronic sinusitis , chronic irritation of nasal mucosa due
to smoking and other irritants
 Prolonged use of nasal drops and vasomotor and allergic
rhinitis.
SYMPTOMS:
 Nasal obstruction is main symptom.
 Nasal discharge is thick and sticky.
 Headache and transient anosmia.
EXAMINATION:
 Hypertrophy of turbinates.
 Turbinate mucosa is thick and does not pit on
pressure. Little shrinkage with vasoconstrictor due to
underlying fibrosis.
TREATMENT:
 First is to discover the cause and remove it.
 Nasal obstruction can releived by reduction in size of
turbinates by various methods.
ATROPHIC RHINITIS(OZAENA)
 It is the chronic inflammation of nose characterised by
atrophy of nasal mucosa and turbinate bones . The
nasal cavities are roomy and full of foul-smelling
crusts.
 Two types
 Primary atrophic rhinitis
 Secondary atrophic rhinitis.
PRIMARY ATROPHIC RHINITIS
AETIOLOGY: (HERNIA)
 Hereditary factors.
 Endocrinal disturbance.
 Racial factors .
 Nutritional deficiency.
 Infective.
 Autoimmune process.
PATHOLOGY:
 Ciliated columnar epithelium is lost and is replaced by
stratified squamous type.
 Atrophy of seromucinous glands, venous blood
sinusoids and nerve element.
 Turbinate undergoes resorption causing widening of
nasal chambers.
CLINICAL FEATURES
SIGN & SYMPTOMS
 Common in females during puberty.
 Foul smell from nose , but patient remains unware.
 Marked anosmia(merciful anosmia)
 Nasal obstruction inspite of wide nasal chambers due
to large crust formation.
 Epistaxis.
 EXAMINATION shows nasal cavity to be full of greenish
or greyish black dry crusts covering the turbinates &
septum.
 Attempt to remove my cause bleeding. If removed , nasal
cavities appear roomy with atrophy of turbinates so much
so that the posterior wall of nasopharynx can be easily
seen .
 Nasal turbinates may be reduced to mere ridges.
 Nasal mucosa appears pale .
 Nasal vestibule may be present shows saddle defromity
 Atrophic changes may be seen in pharyngeal mucosa
larynx with cough and hoarseness of voice.
Radiographic Findings
1.
Mucoperiosteal thickening of the paranasal sinuses.
2.
Loss of definition of the OMC secondary to resorption of
the ethmoid bulla and uncinate process.
3.
Hypoplasia of the maxillary sinuses.
4.
Enlargement of the nasal cavities with erosion and
bowing of the lateral nasal wall.
5.
Bony resorption and mucosal
atrophy of the inferior and
middle turbinates.
PROGNOSIS
 The disease persists for years but there is a tendency to
recover spontaneously in middle age.
Current Therapies
 Goals of therapy
 Restore nasal hydration
 Minimize crusting and debris
 Therapy options
 Topical therapy
 Saline irrigations
 Antibiotic irrigations
 Systemic antibiotics
 Implants to fill nasal volume
 Closure of the nostrils
Local therapy
 Irrigations
Saline
 Mixtures
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Sodium bicarbonate
Shehata: Sodium Carbonate 25g, Sodium Biborate 25g, and Sodium Chloride
50g in 250ml water.
 Antibiotic solution
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Moore: Gentamycin solution 80mg/L
 Anti-drying agents
 Glycerine
 Mineral Oil
 Paraffin with 2% Menthol
 Other
 Acetylcholine
 Pilocarpine
Systemic therapy
 Oral antibiotics
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Tetracycline
Ciprofloxacin
Aminoglycosides
Streptomycin injections
 Medication avoidance
 Vasoconstrictors
 Topical steroids *
 Other
 Vitamin A (12,500 to 15,000
Units daily)
 Potassium Iodide (Increases
nasal secretions)
 Vasodilators
 Iron therapy
 Estrogen
 Corticosteroids *
 Vaccines
 Antibacterial (Pasturella,
Bordetella)
 Autogenous
SURGICAL:
A) Young’s operation:
 Both the nostrils are closed completely just within the nasal
vestibule by raising flaps. They are opened after 6 months or
later. In these cases, mucosa may revert to normal and
crusting reduced.
 Young’s procedure
 Circumferential flap elevation 1 cm cephalic to the alar rim.
 Sutures placed in center of elevated flap to close the nostril
 Advantages
 Often provided relief of symptoms
 Disadvantages
 Difficult to elevate circumferential flap
 Breakdown of central suture area common
 Does not allow for cleaning
 Did not allow for periodic examination
 Recurrence after flap takedown
Modified young’s operation:
 To avoid discomfort of B/L nasal obstruction , modified
young’s operation aims to partially close the nostrils. It is also
claimed to give the same benefit as young’s.
 Modified Young’s
 Elevation of extended perichondrial flap through contralateral
hemitransfixion incision.
 Short skin flap elevated from the intercartilaginous line on the ipsilateral
side.
 Suture lateral and medial flaps with vicryl.
 Staged second side with first side takedown in 6 mon.
 Advantages
 Technically easier than Young procedure
 No suture line breakdown
 No vestibular stenosis on takedown
 Disadvantages
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Not possible with large septal defects
Does not allow for cleaning
Does not allow for periodic examination
Recurrence after flap takedown
Modified Young
B) Narrowing of nasal cavities:
 Nasal chanbers are very wide in atrophic rhinitis and air
currents dry up secretion leading to crusting .
Narrowing the size of nasal helps relieve the symptoms.
i. submosal injection of teflon paste.
ii.insertion of fat, cartilage, bone or teflon strips under the
mucoperiosteumof the floor and lateral wall of nose and
mucoperichondrium of the septum
iii. Section and medial displacement lateral wall of nose.
SECONDARY ATROPHIC RHINITIS
 Complication of sinus surgery (89%)
 Complication of radiation (2.5%)
 Following nasal trauma (1%)
 Sequela of granulomatous diseases (1%)
 Sarcoid
 Leprosy
 Rhinoscleroma
 Sequlae of other infectious processes
 Tuberculosis
 Syphilis
RHINITIS SICCA
 It is also a crust- forming disease seen in patients who
work in hot,dry and dusty surrounding, e/g/ bakers, iron
and goldsmiths / condition is confined to the anterior
third of nose particularly of the nasal septum. Here, the
ciliated columnar epithelium undergoes squamous
metaplasia with atrophy of seromucinous glands. Crusts
form on the anterior part of septum and their removal
causes ulceration and epitaxis, and may lead to septal
perforation .
Treatment
 Correction of the occupation al surroundings and
application of bland ointment or one with an
antibiotic and sterioid, to the affected part. Nose
pricking and forcible removal of crusts should be
avoided.
 Nasal douche, like the one used in cases of atrophic
rhinitis , is use fulL.
RHINITIS CASEOSA
 It is an uncommon condition , usually unilateral and mostly
affecting males.
 Nose is filled with offensive purulent discharge and cheesy
material . The disease possibly arises from chronic sinusitis
with collection of inspissated cheesy material . Sinus mucosa
becomes granulomatous.
 Bony walls of sinus may be destroyed, requiring
differentiation from malignancy .
TRETMENT
Removal of debris and granulation tissue and free drainage of
the affected sinus .
Prognosis is good
PNEUMONICS
 THEORIES FOR ORIGIN OF CHOLESTEATOMA:-
CRUSHCongenital theory
Ruedi's theory
Wittmaacks's theory(use W instead of U)
Saade's theory
Habermann's theory
 contraindications of stapedectomy-(I POD)
Quote:
I-Infections in ext/middle ear
P-perforation should be closed first
O-only hearing ear is a contraindication
D-deafness (sensorineural)
 SEQUELAE OF CSOM-
O-CART
Quote:
Ossicular necrosis
Cholesterol granuloma
Atrophic tympanic membrane and atelactatic middle
ear
Retraction pockets and cholesteatoma
Tympanosclerosis
 Gradenigo's triad
EAR
Quote:
 E-Ear discharge
A-Abducens palsy
R-Retro orbital pain(5th nerve involved)
 indications of tympanoplasty-
ABCDES
Quote:
 A- age should be above 10yrs when sufficient
resistance develops
B- benign (tubotympanic disease) can be corrected
C- conductive deafness can corrected
D- dry perforation gives best results
E- eustachian tube should be functioning properly
S- stapes should be mobile
Menier's disease :Features
' VAST men'
 Vertigo
 Aural fullness
 Sensorineural hearing loss
 Tinnitus
 Little's area: Arteries
" LEGS "
 L - superior Labial artery
 E - anterior Ethmoidal artery
 G - Greater palatine artery
 S - Sphenopalatine artery
The four arteries anastamose at Little's area to form a
vascular plexus called Kiesselbach's plexus.
 Auditory pathway
 ' E.COLI-MA'
 Eighth nerve
 Cochlear nuclei
 Olivary complex
 Lateral lemniscus
 Inferior colliculus
 Medial geniculate body
 Auditory cortex
The area of cortex ,concerned with hearing is
Brodmann's area located in the Superior temporal
gyrus. Each ear is represented in both hemispheres.
EAR:BONES OF MIDDLE EAR:
' MIS '
 Describes the inner ear bones from out to in:
 Malleus
 Incus
 Stapes
 Alternatively, 'Mailing Includes Stamps' .