By-Dr. Sudeep K.C.. 1) VIRAL RHINITIS 1)COMMON COLD(CORYZA) Aetiology: it is caused by virus usually...
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ACUTE AND CHRONIC RHINITIS By-Dr. Sudeep K.C.
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,
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 2- 3 weeks.
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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. TREATMENT: Bed rest
Plenty of fluids. Antihistamine and nasal decongestant. Analgesics
to relieve headache and antibiotics if secondary infection.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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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.
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TREATMENT: First is to discover the cause and remove it. Nasal
obstruction can releived by reduction in size of turbinates by
various methods.
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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.
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.
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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.
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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.
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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.
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PROGNOSIS The disease persists for years but there is a
tendency to recover spontaneously in middle age.
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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
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Local therapy Irrigations Saline Mixtures Sodium bicarbonate
Shehata: Sodium Carbonate 25g, Sodium Biborate 25g, and Sodium
Chloride 50g in 250ml water. Antibiotic solution Moore: Gentamycin
solution 80mg/L Anti-drying agents Glycerine Mineral Oil Paraffin
with 2% Menthol Other Acetylcholine Pilocarpine
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Systemic therapy Oral antibiotics 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
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SURGICAL: A) Youngs 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. Youngs 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
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Modified youngs operation: To avoid discomfort of B/L nasal
obstruction, modified youngs operation aims to partially close the
nostrils. It is also claimed to give the same benefit as youngs.
Modified Youngs 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 Not possible with large septal defects Does
not allow for cleaning Does not allow for periodic examination
Recurrence after flap takedown
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Modified Young
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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.
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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
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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.
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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.
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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
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PNEUMONICS
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THEORIES FOR ORIGIN OF CHOLESTEATOMA:- CRUSH- Congenital theory
Ruedi's theory Wittmaacks's theory(use W instead of U) Saade's
theory Habermann's theory
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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)
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SEQUELAE OF CSOM- O-CART Quote: Ossicular necrosis Cholesterol
granuloma Atrophic tympanic membrane and atelactatic middle ear
Retraction pockets and cholesteatoma Tympanosclerosis
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