Congenital Nose Anomalies & Trauma
Congenital Nose Anomalies & Trauma
CONGENITAL ANOMALIES
OF THE NOSE
Congenital posterior choanal atresia.
It is the commonest congenital anomaly of the nose.
Aetiology :
• Persistence of bucco-nasal membrane (between the nose and
nasopharynx).
Types :
• Bony or membranous.
• Unilateral or bilateral.
• Partial or complete.
The commonest type is unilateral complete bony atresia.
Clinical picture :
• Unilateral : may not be noticed until late in childhood when the patient
notices permanent unilateral nasal obstruction and discharge which
does not move on blowing the nose.
• Bilateral :
1- Early :
- at or soon after birth.
- Cyanosis which may be cyclical or during suckling.
- Asphyxia and death may occur because infant is obligatory nasal
breather. It takes about 2 weeks to learn breathing by mouth.
2- Late : If the infant passed asphyxia, there may be :
- Nasal discharge.
- Mouth breathing.
- Failure to develop taste and smell.
Diagnosis :
• Mirror test: No condensation of air on a cold mirror.
• Catheter can not pass into the nasopharynx.
• X-ray with lipidol (dye): The dye cannot pass to the nasopharynx.
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• C.T determines the thickness of the bony atresia and differentiate
between bony and membranous atresia.
• Endoscopic examination.
Treatment :
• Bilateral cases is a neonatal emergency : oral air way or endotracheal
intubation.
• Transnasal endoscopic (preferred) or transpalatal excision of the atretic
plate (obsolete).
Chapter III
TRAUMATIC CONDITIONS
OF THE NOSE
(A) Foreign body in the nose :
Most commonly children.
Types :
• Vegetable foreign bodies: such as pea and bean. Their fatty acids are
irritating → inflammatory reaction.
• Non-vegetable foreign bodies: such as button and bead.
Clinical picture :
• Unilateral offensive purulent nasal discharge: may be blood-stained
(pathognomonic).
• Unilateral persistent nasal obstruction.
• The foreign body is seen by clinical or endoscopic examination.
Complications :
• Rhinitis and sinusitis.
• Formation of rhinolith i.e a nasal stone. Due to precipitation of calcium
salts from the nasal secretions on a foreign body, blood clot or
inspissated mucus.
Treatment:
• Removal by a hook or forceps.
• General anesthesia with cuffed endotracheal intubation is necessary:
- If the patient is uncooperative.
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- If the foreign body is impacted and it is necessary to push it back to
the pharynx to get it through the mouth.
- To avoid inhalation of the foreign body in the lower airway.
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• Traumatic : is the most common. Trauma may be accidental (skull
base fractures) or surgical (during sinonasal surgery).
• Neoplastic : due to invasion of anterior skull base by malignant tumors.
• Inflammatory : e.g. gumma of syphilis.
• Spontaneous or idiopathic : no cause can be detected.
Clinical picture :
• Unilateral watery nasal discharge : which is clear, colourless, has
salty taste, dose not stiffen the handkerchief increased by coughing,
straining and leaning forwards.
• Headache : may be due to high CSF pressure (caused by Brain tumor
or idiopathic) or low CSF pressure (caused by CSF leakage).
Complications : Meningitis.
Investigations :
1- Biochemical analysis of discharge, CSF is characterized by :
- Clear, colourless and contain no mucus.
- Contain sugar more than 30 mg%.
- Reduce Fehling's solution.
- Contain B2 transferrin, which is diagnostic (B2 only in CSF).
2- CT with intrathecal metrizamide: can detect the site of leakage.
3- MRI
Treatment :
A- Conservative : Most traumatic cases heal spontaneously :
- Bed rest in semi sitting position with the head-up.
- Avoid coughing and straining.
- Avoid blowing of nose.
- Avoid nasal medications (drops or packing).
- Prophylactic antibiotics to prevent meningitis.
B- Surgical: Covering the defect by a graft (fat or fascia) or flap
(mucoperiosteal flap); if conservation failed. It can be done
endoscopically and rarely through external approach.
THE NASAL SEPTUM
(A) Deviated nasal septum :
Etiology :
a- Developmental : most common. b- Traumatic.
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Types :
a- C-shaped : deviation to one side.
b- S-shaped : deviation to both sides.
c- Spur : sharp angulation at bony cartilaginous junction.
d- Dislocation of septal cartilage from the maxillary crest (traumatic).
Clinical picture :
a- Asymptomatic : most cases.
b- Persistent nasal obstruction which :
• Unilateral in C-shaped septum.
• Bilateral in S-shaped septum.
c- Hyposmia.
d- Epistaxis from :
• A prominent vessel over a bony spur.
• Kinking of a vessel on the convex side.
• Separation of a crust on the concave side.
e- Headache: due to contact between deviated septum and middle
turbinate (irritating anterior ethmoidal nerve).
f- Secondary effects: atrophic rhinitis in the wider side and hypertrophy
of inf. turbinate on the wide side.
Treatment :
a- No treatment for minor symptomless deviation.
b- Septoplasty which preferred now over submucous resection (S.M.R)
operation.
c- Septo-rhinoplasty : if there is associated ext. deformity.
(B) Septal hematoma :
Collection of blood between the septal cartilage and its perichondrium.
Etiology :
1- Traumatic : accidental or following septal surgery e.g. SMR or
septoplasty.
2- Spontaneous : blood diseases.
Clinical picture :
1- Bilateral persistent nasal obstruction.
2- Smooth red soft swelling on both sides of the nasal septum.
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3- Aspiration → blood.
Treatment :
1- Prophylactic antibiotics.
2- Incision and drainage of the haematoma with tight nasal packing to
prevent recollection of blood.
(C) Septal abscess :
Collection of pus between septal cartilage and its perichondrium.
Etiology :
Secondary infection to septal hematoma
Clinical picture :
• Fever, headache, anorexia and malaise.
• Severe throbbing nasal pain.
• Bilateral persistent nasal obstruction.
• Tender nasal dorsum.
• Bilateral smooth red tender soft swelling of the septum.
• Aspiration → pus.
Complications :
• Cartilage necrosis : supra-tip depression of the nasal dorsum.
• Cartilage and mucosal necrosis : septal perforation.
• Spread of infection : cavernous sinus thrombo-phlebitis.
Treatment : Similar to septal haematoma.
(D) Septal perforation :
Etiology :
1- Traumatic :
a- Septal operations e.g. S.M.R (common cause).
b- Repeated cauterization or cauterization of both sides at the same time.
c- Habitual nose picking.
2- Inflammatory :
a- Septal abscess.
b- Chronic specific inflammation e.g. lupus and syphilis.
3- Cocaine addiction (ischemia).
Clinical picture :
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• It may be symptomless.
• Small perforation : may be cause whistling on inspiration.
• Large perforation : crusting and epistaxis after separation of the crusts.
• Site: bony part in syphilis and cartilaginous part in other causes.
Treatment :
• No treatment if a symptomatic.
• Alkaline nasal wash to diminish crusting.
• Surgical closure by mucosal flaps or grafts or an obturator (button-like).
Epistaxis
Bleeding from the nose.
Causes :
(A) Local causes :
1- Idiopathic :
- Bleeding from little area.
- The commonest cause of epistaxis 90%.
- Occurs spontaneously, may be initiated by slight trauma or change of
atmosphere.
- Occurs mainly in children and adolescents.
2- Congenital : hereditary haemorrhagic telengiectasia.
3- Traumatic :
- Accidental : nose picking, foreign body, fracture nasal bones and fracture
skull base.
- Post nasal operations.
4- Inflammatory : acute rhinitis and sinusitis.
5- Neoplastic :
- Benign (haemangioma) and malignant (carcinoma).
- Nasopharyngeal angiofibroma (severe epistaxis).
- Nasopharyngeal carcinoma.
6- Septal deviation.
(B) General causes :
1- High arterial blood pressure (hypertension) :
ff- Mostly from the posterior part of the nose.
gg- The commonest cause of epistaxis in elderly patients.
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2- High venous blood pressure due to heart failure and mediastinal
tumours.
3- Fevers e.g. rheumatic fever and exanthemata due to toxic capillarities
(vasculitis).
4- Haemorrhagic blood diseases e.g. purpura, haemophilia, leukaemia and
vit. C or K deficiency.
5- Drugs as anti-coagulants, non steroidal anti-inflammatory drugs and
salicylate.
6- Hormonal: during menses.
Site of bleeding:
1- Little's area: is the commonest site.
2- Above the middle turbinate (upper part of the nasal cavity). From the
anterior and posterior ethmoidal arteries.
3- Below the middle turbinate (posterior part of the nasal cavity): from the
sphenopalatine artery (artery of epistaxis).
4- The middle meatus, the inferior turbinate and floor: are rare sites.
Clinical picture :
hh- Bleeding may be anterior (nasal) or posterior (post-nasal) or with
both.
ii- Unilateral or bilateral.
jj- Mild or severe.
Investigations :
1- Blood pictures (anemia, leukemia).
2- Coagulation profile for bleeding tendency.
3- Liver function tests.
4- CT scan (nose and nasopharynx).
5- Biopsy : if tumour is seen.
Treatment : The aim is to stop the bleeding and treat the cause.
A- Control bleeding :
(1) Mild and moderate attack :
i- First aid :
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The patient sites with the head leant forwards (to prevent swallowing of
blood), the nostrils are compressed by the fingers (to compress little's area),
apply cold compresses over forehead and nasal bridge (to induce reflex
vasoconstriction), packing nasal fossae using piece of cotton soaked with
vasoconstrictor solution.
ii- Cautery : Under local anesthesia
kk- Chemical using chronic acid or silver nitrate crystals.
ll- Electrical (diathermy).
iii- Anterior nasal pack :
When above lines fails using Vaseline gauze, inflatable tampons or merocel
sponges for 24-48 hours under antibiotic cover.
(2) Sever attack :
If the patient is shocked, treatment of shock should start immediately.
i- Treatment of shock :
mm- Patient head down (elevation of foot of bed) to increase blood
flow to the brain.
nn- I.V fluids and blood transfusion according to Hb %.
oo- Sedative as diazepam, avoide morphia (to avoid respiratory
center depression).
pp- I.V corticosteroids.
qq- Monitoring vital signs e.g. pulse, blood pressure, temperature and
urinary output.
ii- Anterior nasal pack.
iii- Posterior nasal pack :
rr- Used if anterior pack fail or if the bleeding is posterior – using
Vaseline pack (under general anesthesia), inflatable balloon or
fooly's catheter.
iv- Surgical control :
When nasal packing fails to control bleeding.
ss- Ligation of anterior ethmoidal artery via the orbit if bleeding is
coming from above the middle turbinate.
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tt- Ligation of internal maxillary artery in pterygopalatine fossa through
radical antrostomy if bleeding comes from below the middle
turbinate.
uu- Endoscopic ligation of sphenopalatine artery.
N.B. Ligation of external carotid artery in the neck is less effective due to
cross anastmosis.
v- Emoblization : Angiography to detect the bleeding vessel then injection of
embolus (e.g. Gelatin sponge) to occlude it.
B- Treatment of the cause e.g. tumours, hypertension.
Chapter IV
ALLERGIC RHINITIS
Abnormal reaction of nasal mucosa due to exposure to antigenic substances.
Pathogenesis : (Type I hypersensitivity reaction) :
1- When the patient exposed to the antigen, the body produces IgE.
2- IgE + mast cells (in nasal mucosa) → mast cell bound IgE.
3- Antigen + mast cell bound IgE → rupture of mast cell with release of
chemical mediators as histamine, serotonin, prostaglandins and
leukotrienes. These mediators will act on :
• Nerve ending causing itching and sneezing.
• Smooth muscles causing bronchospasm.
• Seromucinous glands causing increased secretions (rhinorrhea).
• Blood vessels causing vasodilatation (congestion) and increased
capillary permeability (oedema).
• Eosinophilic infiltrate.
Types :
• Seasonal: occurs in seasons e.g. hay fever which occurs in spring.
• Perennial: persistent all over the year.
Etiology :
• Predisposing factors :
vv- Positive family history.
ww- Psychogenic.
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xx- Physical factors e.g. changes in temperature and humidity.
yy- Infection which decrease tissue resistance.
• Precipitating factors : Exposure to allergens which may be
- Inhalant : the commonest. It may be :
a- Seasonal as pollens, grasses and moulds.
b- Perennial as house dust, dust mite, animal dander and feather.
- Ingestant as egg, milk and wheat.
- Injectant as penicillin.
- Contactant : as face powders.
- Infectants : parasites end fungi.
Clinical picture :
• Paroxysmal attacks of prolonged sneezing, profuse watery rhinorrhea
and nasal obstruction.
• Anosmia or hyposmia
• Palatal itching.
• Allergic conjunctivitis and bronchial asthma may be associated.
Anterior rhinoscopy :
• Swollen and pale bluish nasal mucosa.
• Hypertrophy of turbinate especially inferior turbinate.
• Nasal polyp may be present.
Investigations :
A- To confirm the diagnosis :
• Microscopic examination of a nasal smear → excess eosinophils.
• Blood examination : eosinophilia and increased total plasma IgE level.
B- To define the offending allergen :
• Nasal provocation tests.
• Skin sensitivity tests.
• Radio-allergo-sorbent test (RAST) to detect plasma IgE to a specific
allergen.
C- To detect complications :
• CT scan for paranasal sinus to detect sinusitis or polypi.
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Treatment :
A- Prophylaxis :
• Avoid antigens exposure when the antigen is known.
• Zaditen or sodium cromglycate (stabilize mast cells prevents their
degranulation).
B- Medical :
• Antihistamine : local or systemic.
• Steroids : local or systemic.
• Immunotherapy (desensitization) by using small repeated doses of
the antigen. It is useful in seasonal allergy (grass pollen) but
anaphylaxis may occur.
C- Surgical (in resistant cases): (to relieve nasal obstruction)
• Polypectomy.
• Turbinate reduction surgery.
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Clinical picture: Similar to allergic rhinitis but:
- No itching. - Tests of allergy are negative.
Treatment :
• Prophylaxis : avoidance of predisposing factors.
• Psychological treatment (very important in many cases).
• Medical : antihistamines and steroids.
• Surgical :
- For nasal obstruction : Polypectomy, partial turbinectomy and septoplasty.
- For rhinorrhea : Vidian neurectomy : cutting of the nerve leads to
vasoconstriction of the nasal mucosa.
NASAL POLYPI
Edematous pedunculated mucosa of the nose or paranasal sinuses.
Etiology (Causes – Types) : (Figs. 135, 136)
zz- Allergic rhinitis.
aaa- Vasomotor rhinitis.
bbb- Inflammatory e.g. antro-choanal polyp.
ccc- Malignant : polyp may accompany malignant neoplasm of the
nose due to lymphatic obstruction.
N.B. : Bleeding polyps :
a- Bleeding polyps of the septum (angioma).
b- Fungal (Rhinosporidosis).
(A) Ethmoidal polyp :
The commonest type (allergic)
Symptoms :
ddd- Bilateral persistent nasal obstruction and hypo- or anosmia.
Signs :
eee- Bilateral, multiple, glistening, pale grayish, mobile and insensitive.
fff- Arises from the ethmoid sinuses due to loose submucosa (may arise
from middle turbinate and middle meatus).
ggg- In long standing cases : broadening of the nose and polyps may
protrude through anterior nares.
Investigations : CT to show origin and extent of the polyp.
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Treatment :
- Surgical treatment : Endoscopic removal (treatment of choice).
- Medical treatment :
• Systemic steroids for small polypi (called medical polypectomy) and
local steroid sprays postoperatively to avoid recurrence.
• Anti-histamines.
(B) Antro-choanal polyp :
• Unilateral single polyp which arises within the maxillary sinus (antrum)
then passes through its ostium to enter the nasal cavity → then passes
backwards through the choana to enter the nasopharynx.
• Much less common than the ethmoidal polypi and occurs in teenagers
(13-20 years).
Etiology : Unknown. May be inflammatory or a retention cyst.
Symptoms :
• Unilateral persistent nasal obstruction.
• Unilateral mucoid nasal discharge.
Sign :
• Unilateral single pale grayish glistening smooth soft pedunculated mass
which arises from the middle meatus → passes backwards to the
choana, it may be seen in the oropharynx during oropharyngeal
examination (if large).
Investigation : C.T scan : Diagnostic.
Treatment :
• Endoscopic polypectomy with widening of the natural ostium of the
maxillary sinus (treatment of choice).
• Radical antrum (Caldwell-Luc) operation may be done in recurrent
cases.
INFLAMMATION OF THE NASAL CAVITY
(A) Acute inflammation :
1- Vestibulitis :
a- Localized (Frunclosis) : Staphylococcus infection of a hair follicle in the
nasal vestibule.
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Predisposing factor :
• Trauma (nose picking), diabetes or lowered immunity.
Clinical picture :
• Pain and tenderness.
• Swelling and redness (usually at nasal tip).
• Pus pointing (usually at nasal vestibule).
• It may be recurrent in diabetes.
Complications :
• Do not squeeze the furuncle (dangerous area) to avoid cavernous sinus
thrombosis.
• Septal abscess.
Treatment :
• Systemic antibiotics (penicillinase resistant) e.g. flucloxacillin or
cephalexin) and local antibiotic cream.
• Analgesics.
• Incision if there is pus.
b- Diffuse :
Predisposing factor : Rhinorrhoea lead to skin maceration and skin
laceration due to repeated rubbing with handkerchiefs.
Clinical picture : Nasal pain and diffuse redness, oedema and tenderness of
the skin lining of the vestibule.
Treatment :
• Treatment of the cause.
• Systemic treatment : Antibiotics and analgesics.
• Local treatment : Antibiotics and steroid cream.
2- Rhinitis :
a- Non specific e.g. common cold, influenza and rhinitis due to exanthemata.
b- Specific e.g. diphtheria (very rarely seen after vaccination).
COMMON COLD (Coryza)
Caused by rhinovirus followed by secondary bacterial infection, transmitted
by droplet infection. Incubation period 1-3 days.
Predisposing factors :
1- General factors :
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a- Over-crowding and poor personal hygiene.
b- Fatigue and low immunity.
c- Exposure to temperature changes i.e a cold air after a hot bath.
2- Local factors : Allergic and vasomotor rhinitis.
Clinical picture : 4 stages :
1- Ischaemic stage : dryness, burning sensation and sneezing.
2- Hyperemic stage : nasal obstruction, watery discharge and mild fever
(nasal mucosa congested and swollen).
3- Secondary infection stage : thick mucopurulent discharge with more
obstruction, more fever and toxemia.
4- Stage of resolution : recovery by gradual improvement within 5 days.
Complications :
1- Vestibulitis due to rhinorrhea and repeated rubbing of the nose.
2- Spread of infection e.g. sinusitis, otitis media, bronchitis.
3- Anosmia due to viral neuritis of the olfactory nerve.
Treatment :
• Avoid predisposing factors.
• Rest, fluid and analgesics.
• Antihistamines.
• Nasal vasoconstrictors.
• Antibiotics for secondary infection.
• No vaccine is available against common cold virus because large number
of the causative viruses and their continuous mutation.
INFLUENZA :
Etiology : Similar to common cold but the causative organism is influenza
virus : types A,B & C.
Clinical picture : Similar to common cold but the constitutional symptoms are
more severe.
Complications :
Similar to common cold but are more common and may also cause anosmia,
labyrinthitis, vestibular neuronitis, meningitis, encephalitis, peri-carditis,
pneumonia and/or gastro-enteritis.
Treatment and prophylaxis :
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• Similar to common cold but vaccines prepared from the prevalent
strain of the virus are available. They are used :
hhh- during epidemics and
iii- for individuals with high risk of complications as elderly,
children, medical staff and immunocompromised patients.
RHINITIS OF EXANTHEMATA
As influenza but with skin rash e.g. chicken pox, measles and rubella.
Secondary bacterial infection and complications are more common and more
severe than those of common cold.
Chronic non-specific rhinitis :
(A) Atrophic rhinitis :
Chronic non specific inflammation characterized by atrophy of nasal mucosa
and underlying bone.
Etiology : 2 types
1- Primary : cause unknown may be :
• Hormonal theory : it is common in females at puberty due to oestrogen
deficiency.
• Infection theory : infection by klebsiella ozaena and other gram –ve
organisms.
• Autoimmune theory.
• Vitamin A and iron deficiency.
• Autonomic imbalance with sympathetic overactivity.
2- Secondary :
• Deviated nasal septum on the wider side or large septal perforation on
both sides.
• Postoperative : Excessive inf. turbinate removal after total and even
partial turbinectomy.
• Inflammatory : Lupus, syphilis and scleroma.
• Post-irradiation for malignant disease.
Pathology :
Endarteritis or peri-artenitis → ischaemia (if prolonged) → dryness (if
prolonged) will cause atrophy of :
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a- Glands leading to diminished secretion.
b- Mucosa leading to destruction of cilia and stasis of secretions.
c- Turbinal bones leading to wide (roomy) nose.
d- Secondary infection by klebsiella ozaena → offensive smell (ozaena).
Clinical picture :
• Nasal discharge : greenish, crusty and has foul odour.
• Nasal obstruction (inspite of the roomy nose) due to accumulation of
crusts or dullness of the sensation of air as a result of atrophy of the
sensory nerves.
• Anosmia due to atrophy of the olfactory mucosa the patient does not
smell his own bad odour.
• Epistaxis due to separation of the crusts.
Ant. Rhinoscopy :
• The nasal cavity is roomy and lined with greenish offensive crusts.
• The nasal mucosa and the turbinates are atrophic.
Treatment :
A- Medical treatment :
• Treatment of the cause in case of secondary atrophic rhinitis.
• Alkaline nasal lotion to separate the crusts.
• Oily nasal drops as paraffin (lubricant) to prevent adherence of the new
crusts.
• Menthol nasal drops to mask the foul odour.
• Glucose 25% in glycerine nasal pack to diminish foetor. How ? It
inhibit growth of the proteolytic saprophytic organisms which are
responsible for the foul odour.
• Local oestrogen and oral potassium iodide to stimulate the nasal glands.
B- Surgical treatment :
Narrowing the roomy nasal cavities till the nasal mucosa regenerates. If
medical treatment fail to control the patient's symptoms by :
• Submucosal insertion of a graft as fat, bone, cartilage or Teflon.
• Closure of the nostril(s) for 6-24 months by skin flaps from the
vestibule.
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(B) Hypertrophic rhinitis :
Etiology :
• Recurrent attacks of rhinitis or sinusitis.
• Prolonged allergic or vasomotor rhinitis.
• Septum deviation may cause hypertrophic rhinitis on the wider side.
Clinical picture :
• Bilateral persistent nasal obstruction and mucoid or muco-purulent
nasal discharge.
• Hypertrophy of the nasal mucosa, especially the inferior turbinates. It
does not shrink on application of a vasoconstrictor solution (indicating
irreversible changes).
Treatment :
• Medical treatment :
jjj- Treatment of the cause. - Steroids sprays.
• Surgical treatment :
kkk- Reduction of the size of the inferior turbinate by submucous
diathermy, laser, radiofrequency or partial resection (partial
turbinectomy).
Chronic specific inflammation
(Granuloma of the nose)
(A) Rhinoscleroma :
Chronic specific inflammation of the upper respiratory tract especially the
nose by klebsiella rhinoscleroma (Gram negative Frisch bacillus).
It may affects :
lll- The nose : Rhinoscleroma.
mmm- The pharynx : Pharyngoscleroma.
nnn- The larynx : Laryngoscleroma.
ooo- The trachea : Tracheoscleroma.
ppp- The lacrimal apparatus : Dacryoscleroma.
Pathology :
1- Stage of invasion : similar to acute non-specific rhinitis.
2- Active stage : Either atrophic or nodular form :
a- Atrophic : similar to atrophic rhinitis.
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b- Nodular : The submucosa is infiltrated by granulomatous tissue
characterized by :
i- Mikulicz cells : large foamy cell with a central nucleus and
vacuolated cytoplasm. The vacuoles contain the Frisch bacilli
(gram negative intracellular diplo-bacilli). These cells are
diagnostic.
ii- Russell bodies : bright red oval or rounded bodies devoid of
nuclei. They represent plasma cells undergoing hyaline
degeneration.
iii- Plasma cells and lymphocytes.
Clinical picture :
1- Stage of invasion : similar to prolonged attacks of acute non specific
rhinitis that does not respond to treatment.
2- Atrophic stage : similar to atrophic rhinitis.
3- Active granulomatous stage :
qqq- Nasal obstruction and mucoid discharge.
rrr- Bilateral discrete reddish non ulceration of firm nodules at the
muco-cutanous junction between the nasal cavity and the vestibule,
the nodules coalesce to fill the nasal cavity.
sss- It may extend into surrounding structures: upper lip, larynx and a
trachea (air way obstruction) and lacrimal passages (epiphora).
4- Fibrotic stage : narrowing of the nasal cavity and external nasal
deformity. It may extend to the pharynx (shortening of the soft palate),
subglottic stenosis and tracheal stenosis.
Investigations :
1- Culture and sensitivity : shows gram –ve diplobacilli (Klebsiella
rhinoscleromates).
2- Biopsy :
ttt- Shows (Mickulicz cells, Russel bodies, plasma cells, fibroblast,
dense fibrous tissue and less vascularity).
uuu- Diagnostic only in granulomatous stage.
Treatment :
• Medical treatment :
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vvv- Antibiotics : rifampicin, quinolones, or better according to the
results of sensitivity tests.
www- In the atrophic stage : similar to atrophic rhinitis.
• Surgical treatment :
xxx- Removal of the granulomatous masses or fibrous tissue better by
laser surgery.
yyy- Reconstructive procedures for laryngeal and tracheal stenosis (in
laryngotracheal involvement).
• Radiation therapy : was used in active stage to induce fibrosis – now
it is not used, it may induce malignancy in other area e.g. cancer
thyroid.
(B) Nasal syphilis :
Etiology :
• Causative organism : spirochaete Treponema pallidum.
• Mode of transmission :
zzz- Acquired syphilis : Sexual transmitted.
aaaa-Congenital syphilis : Trans-placental.
Clinical picture :
A- Acquired syphilis :
1- Primary acquired syphilis : very rare.
Chancre : Single reddish firm painless papule in the vestibule which may
ulcerate.
2- Secondary acquired syphilis :
Persistent rhinitis with multiple white mucous patches. These patches may
ulcerate forming snail track ulcers.
3- Tertiary acquired syphilis : commonest. Either
a- Diffuse lesion : atrophic rhinitis.
b- Gumma : single or multiple reddish rubbery painless ulcerating swellings.
The ulcers are deep with punched-out edges with destruction of the bony walls
of the nose :
• Perforation of the bony part of the septum.
• Perforation of the hard palate (oro-nasal fistula).
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• Depression of the nasal bridge (saddle nose deformity).
• Destruction of the cribriform plate (cerebro-spinal rhinorrhoea).
B- Congenital syphilis :
1- Early congenital syphilis : First three months.
• Similar to secondary acquired syphilis : Persistent rhinitis →
vestibulitis with fissuring of the vestibule and upper lip (snuffle).
2- Late congenital syphilis : After the age of three years.
• Similar to tertiary acquired syphilis: Diffuse lesion or gumma.
• Other stigmata of congenital syphilis : Hutchinson's teeth, interstitial
keratitis and sensori-neural hearing loss (called Hutchinson's triad).
Investigations :
• Serological tests for syphilis
• Biopsy : shows granuloma with endarteritis (not diagnostic).
• Smears from chancer or mucus patch (T. pallidum).
Treatment :
• Medical treatment :
bbbb-Antibiotics : Penicillin is the drug of choice.
cccc- In the atrophic stage (similar to atrophic rhinitis).
• Surgical treatment :
dddd-Removal of the granulomatous masses (better by laser surgery).
eeee-Rhinoplasty operation (to correct nasal deformities).
ffff- Reconstruction of septal perforation, oro-nasal fistula and
cerebro-spinal rhinorrhoea.
(C) Nasal lupus vulgaris :
Chronic specific form of T.B infection that affects skin and mucous
membrane.
Etiology :
• Causative organism : attenuated tuberculous bacilli.
• Mode of transmission : Direct inoculation as nose picking.
Clinical picture :
• Prolonged nasal obstruction, discharge and crustation.
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• Bilateral discrete firm nodules at mucocutaneous junction of the
vestibule and skin of butterfly area of the face.
• On pressure over these nodules with glass slide (or apply
vasoconstrictor) it will shows apple-jelly appearance.
• It may ulcerate shows shallow undermind ulcers.
• Perforation of the cartilaginous part of the nasal septum or scarring of
the nasal vestibule may occur.
Investigations :
• Biopsy : diagnostic, shows tuberculous granuloma.
• Bacteriological exam. for T.B bacilli.
Treatment :
• Anti-tuberculous drugs.
• Vit. D.
• Surgical reconstruction of nasal deformities.
INFLAMMATION OF THE PARANASAL SINUS
a- Acute sinusitis
b- Chronic sinusitis
c- Fungal sinusitis
(A) Acute sinusitis: Acute inflammation of the muco-periosteal lining of one
or more of the paranasal sinuses.
Causative organisms:
• Streptococcus pneumoniae, Haemophilus influenzae and Moraxella
catarrhalis.
• Anaerobic organisms in maxillary sinusitis of dental origin.
Routes and sources of infection:
• Nasal route: infection reaches the sinus via its ostium:
gggg-Acute rhinitis (commonest).
hhhh-Swimming and diving in polluted water.
iiii- Nasal packing.
jjjj- Nasal foreign body.
• Dental route: Causes maxillary sinusitis:
kkkk- Infection of the 2nd premolar or 1st molar teeth.
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llll- Oro-antral fistula.
• Trauma:
mmmm- Compound fracture of the sinus.
nnnn-Penetrating foreign bodies as gunshots.
oooo-Sinus barotrauma due to rapid changes in an pressure during
flight leading to edema and obstruction of sinus ostium.
Predisposing factors:
1- General :
pppp-Bad hygienic conditions and overcrowding.
qqqq-Low general resistance as in diabetes and immuno-compromized
patients.
2- Local : Any conditions that leads to obstruction of sinus ostia will
predispose to infection e.g. septal deviation, allergic rhinitis and nasal
polypi.
Pathology :
The inflammatory changes of the mucosa of the affected sinus include :
• Hyperaemia and oedema leading to obstruction of the sinus ostium and
stasis of secretions.
• Exudation, first mucous (catarrhal) then purulent (suppurative)
inflammation.
Symptoms :
• General symptoms : Fever, headache, anorexia and malaise.
• Local symptoms :
1- Nasal obstruction usually bilateral and may alternates from side to
side.
2- Nasal discharge :
rrrr- Muco-purulent or purulent.
ssss- Scanty or profuse.
tttt- Post-nasal or nasal in sinusitis of the anterior group of
sinuses and post-nasal in sinusitis of the posterior group of sinuses.
uuuu- Offensive in maxillary sinusitis of dental origin (anaerobic
organisms).
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3- Hyposmia or anosmia due to nasal obstruction. Dental maxillary
sinusitis causes cacosmia.
4- Facial pain : severe and increases by straining and leaning forwards.
It is due to accumulation of discharge in the sinus under tension
(tension pain).
vvvv- Ethmoidal sinusitis between the eyes.
wwww- Maxillary sinusitis over the cheek.
xxxx- Frontal sinusitis over the forehead. It is characteristically,
periodic i.e starts in the morning, decreases at noon and subsides in
the afternoon.
yyyy- Sphenoidal sinusitis behind the eye.
5- Facial swelling : edema over the affected sinus may occurs specially
in infants and children.
Signs :
1- External examination : Tenderness over the affected sinus :
zzzz- Ethmoidal sinusitis (over the medial canthus).
aaaaa- Maxillary sinusitis (over the cheek).
bbbbb- Frontal sinusitis over the floor of the sinus (at the roof of
the orbit).
2- Anterior rhinoscopy :
ccccc- Congestion and edema of the nasal mucosa.
ddddd- Muco-purulent or purulent discharge :
o In the middle meatus (infection of anterior group of paranasal
sinus).
o Above the middle turbinate in (in posterior and ethmoidal
sinusitis).
Investigations :
• Radiological examination : CT scan used only :
a- In case of failure of medical treatment : for proper assessment of the
disease.
b- In case of suspected complications.
• Culture and sensitivity tests : of the discharge.
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Treatment :
1- Medical : main treatment
eeeee- Antibiotics for 10 days.
fffff- Nasal decongestants (local and systemic) to open the sinus ostia.
ggggg- Analgesic, antibiotics and bed rest.
hhhhh- Anti-inflammatory drugs.
iiiii- Mucolytics : to liquefy viscid discharge to facilitate drainage.
2- Surgical :
jjjjj- Indicated in case of failed medical treatment as in impending
complications. Surgery in the form of endoscopic widening of the
natural ostium of the affected sinus.
(B) Chronic sinusitis :
Chronic inflammation of the mucoperiosteal lining of the penanasal sinus.
Causative organism :
Gram –ve (H. influenza, pneumocci, proteus, pseudomonas) and Gram +ve
bacteria.
Etiology : (Causes of Chronicity)
1- Persistent obstruction of the sinus ostium e.g. deviated septum, allergic
rhinitis and polypi.
2- Incomplete resolution of recurrent acute sinusitis due to inefficient
treatment, virulent organism and low resistance of the patient.
3- Persistence of the predisposing factors e.g. dental.
Pathology :
1- Early : congestion, edema and cellular infiltration (reversible).
2- Late : hypertrophic or atrophic mucosa (irreversible).
Clinical picture :
1- Similar to acute sinusitis.
2- Headache : dull ache, may be tension, vaccum or toxic types, periodic
(more in the morning) may occur with chronic frontal sinusitis.
3- Symptoms of septic focus : fatigue, malaise, mental dullness.
4- Symptoms of descending infection : pharyngitis, laryngitis.
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Investigations :
• CT scan : should be done because it shows :
a- Opacity or thickening of the mucosal lining of the affected sinus for
proper assessment of extent of the disease.
b- Cause of ostium obstruction.
c- Exclude complications.
d- Avoid false +ve results of plain x-ray.
• Culture and sensitivity tests : of the discharge.
Treatment :
(A) Medical : Antibiotics, anti-inflammatory drugs and mucolytics.
(B) Surgical : aims at
1- Correcting a predisposing factors e.g. deviated septum, polypi.
2- Clearance of the sinus disease by :
a- Functional endoscopic sinus surgery (FESS)
• Using sinoscope of different angles.
• Restore ventilation and drainage of blocked sinuses by
removal of polypi, granulations and thick secretions and
widening of sinus ostea.
b- Conventional surgery : uncommonly practiced now :
• For maxillary sinusitis :
kkkkk- Repeated puncture and lavage (by creation of
small temporary opening in the medial wall of the
maxillary sinus) for temporary drainage and lavage.
lllll- Intranasal antrostomy (creating an artificial
opening for the sinus in the inferior meatus).
mmmmm- Radical antrostomy i.e. Caldwell-Luc or
through sublabial incision (a hole in the anterior sinus wall
is made) through which the diseased sinus mucosa is
removed.
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• External fronto-ethmoidectomy : for ethmoid sinuses,
frontal and sphenoid can be approached by the same
procedures.
• Obliterative operations : when radical operations fail, the
sinus cavity is closed completely by implantation of fat e.g.
osteoplastic flap for the frontal sinus.
(C) Fungal sinusitis :
• Recently there are increasing incidence of fungal sinusitis (7-10% of
cases of sinusitis).
• Aspergillus is the commonest but mucor species (mucormycosis)
causing fulminating fungal sinusitis.
• It is either invasive or non invasive.
(1) Invasive : Occurs in :
a- Immunocompromised patient e.g. elderly diabetics, AIDS patients and
those receiving immunosuppressive therapy (acute fulminating type).
b- Immunocompetent patients (chronic indolent type) :
Caused by mucor (Acute fulminating) or Aspergillus (Chronic indolent).
Clinical picture :
nnnnn- As in bacterial sinusitis followed rapidly (or slowly in chronic
type) by extension of infection to the orbit or intracranially.
Investigations :
ooooo- CT scan : Unilateral opacity involving most of the sinuses and
extending beyond the sinuses.
ppppp- Detection of fungi in smears from nasal discharge or by fungal
cultures.
Treatment :
qqqqq- Systemic antifungal therapy: Amphotercin-B (Nephro and
hepatotoxic).
rrrrr- Surgical debridment of necrotic tissue and bone sequestra.
(2) Non-invasive :
a- It is either mycetoma (Fungal ball)
sssss- Patient's immunity : Immunocompetent.
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ttttt- Causative organisms : Aspergillus species.
uuuuu- Pathology : Accumulation of fungal hyphae within the
paranasal sinuses (maxillary or sphenoid), with minimal mucosal
reaction (it is infestation not infection).
vvvvv- Clinical picture : Unilateral nasal discharge.
wwwww- CT scan : Unilateral sinus opacity.
xxxxx- Treatment : Endoscopic removal of the fungal ball.
b- Allergic : It is allergic reaction of the sinonasal mucosa due to contact with
specific fungus (type I and II allergic reactions).
Clinical picture :
yyyyy- Common in atopic patients.
zzzzz- Unilateral nasal polypi
aaaaaa- CT scan : unilateral sinus opacity with characteristic focal
hyperdense spots (microcalcification).
bbbbbb- Skin tests +ve for fungal extracts.
Treatment :
cccccc- Endoscopic sinus surgery followed by systemic and local
steroids for a long time to avoid recurrence.
SINUSITIS IN CHILDREN
• The maxillary and ethmoids are the commonest.
• Frontal sinusitis is rare, as the frontal sinus is poorly developed before 5th
year of life.
Etiology :
A- Predisposing factors :
• Dietary deficiency and poor social conditions.
• Exanthemata e.g. measles.
• Kartagener's syndrome (immobile cilia syndrome) consists of sinusitis,
bronchiectasis and dextrocardia.
• Adenoid which acts as a source of infection and obstruct drainage.
• Local causes : choanal atresia and foreign body.
B- Organisms : Streptococcus pneumonia and haemophilus influenza.
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