8-The Nose
8-The Nose
8-The Nose
Treatment : The aim is to stop the bleeding and treat the cause.
A- Control bleeding :
(1) Mild and moderate attack :
i- First aid :
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
- Chemical using chronic acid or silver nitrate crystals.
- 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 :
- Patient head down (elevation of foot of bed) to increase blood flow to the brain.
- I.V fluids and blood transfusion according to Hb %.
- Sedative as diazepam, avoide morphia (to avoid respiratory center depression).
- I.V corticosteroids.
- Monitoring vital signs e.g. pulse, blood pressure, temperature and urinary output.
ii- Anterior nasal pack.
iii- Posterior nasal pack :
- 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.
- Ligation of anterior ethmoidal artery via the orbit if bleeding is coming from above
the middle turbinate.
- Ligation of internal maxillary artery in pterygopalatine fossa through radical
antrostomy if bleeding comes from below the middle turbinate.
- 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.
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 :
- Positive family history.
- Psychogenic.
- Physical factors e.g. changes in temperature and humidity.
- 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 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.
Treatment :
A- Prophylaxis :
Avoid antigens exposure when the antigen is known.
Zaditen or sodium cromglycate (stabilize mast cells prevents 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 : (to relieve nasal obstruction)
Polypectomy.
Partial turbinectomy or submucous diathermy.
Septoplasty.
N.B : Medical treatment should be continued after surgery to avoid recurrence.
VASOMOTOR RHINITIS
Abnormal reaction of the nasal mucosa to non allergic factors.
Mechanism :
Unknown : may be due to over-activity of the nasal parasympathetic system :
Vasodilatation of the blood vessels (congestion).
Increased capillary permeability (oedema).
Increased secretion of the sero-mucinous glands (rhinorrhoea).
Etiology :
Environmental factors : irritants (as dust and tobacco) and changes in humidity or
temperature.
Endocrinal factors : pregnancy, menopause, puberty, old age and contraceptive
pills.
Drugs : anti-hypertensive and abuse of vasoconstrictive nasal drops (called rhinitis
medicamantosa).
Psychogenic.
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):
- Allergic rhinitis.
- Vasomotor rhinitis.
- Inflammatory e.g. antro-choanal polyp.
- 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 :
- Bilateral persistent nasal obstruction and hypo- or anosmia.
Signs :
- Bilateral, multiple, glistening, pale grayish, mobile and insensitive.
- Arises from the ethmoid sinuses due to loose submucosa (may arise from middle
turbinate and middle meatus).
- 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.
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-histaminics.
(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 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.
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 (danger. area) to avoid cavernous sinus thrombosis.
Septal abscess.
Treatment :
Systemic antibiotics 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 handkerchieves.
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, and influenza.
b- Specific e.g. diphtheria.
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 :
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 cold but the causative organism is influenza virus: types A,B & C.
Clinical picture: Similar to cold but the constitutional symptoms are more severe.
Complications :
Similar to cold but are more common and may also cause anosmia, labyrinthitis,
vestibular neuritis, meningitis, encephalitis, pericarditis, pneumonia and gastroenteritis.
Treatment and prophylaxis :
Similar to common cold but vaccines prepared from the prevalent strain of the
virus are available. They are used :
- during epidemics and
- for individuals with high risk of complications as elderly, children, medical staff
and immunocompromised patients.
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 :
- Nasal obstruction and mucoid discharge.
- 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.
- 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 rhinoscleromatous).
2-Biopsy :
- Shows (Mickulicz cells, Russel bodies, plasma cells, …etc).
- Diagnostic only in granulomatous stage.
Treatment :
Medical treatment :
- Antibiotics : rifampicin, quinolones, 3rd generation of cephalo-sporins or better
according to the results of sensitivity tests.
- In the atrophic stage : similar to atrophic rhinitis.
Surgical treatment :
- Removal of the granulomatous masses or fibrous tissue better by laser surgery.
- Rhinoplasty operation to correct nasal deformities.
- Reconstructive procedures for laryngeal and tracheal stenosis.
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.
4- Near by complications :
A- Orbital complications :
The commonest complications of sinusitis especially in children.
Etiology :
Commonly complicates ethmoidal sinusitis. Because the ethmoidal sinus are
separated from the orbit by a very thin bone (lamina papyracea).
Clinical picture :
Stage of orbital cellulitis :
- Pathology : Inflammation of the orbital contents without pus formation.
- Symptoms : Fever, headache, anorexia, malaise and pain in the eye.
- Signs : Conjunctival chemosis, limitation of eye movements, ophthalmoplegia and
diminution of vision. These manifestations are reversible with treatment.
Stage of sub-periosteal abscess :
- Pathology : Collection of pus between the orbital periosteum and lamina
papyracea.
- Symptoms : Throbbing pain in the eye.
- Signs : Proptosis and lateral displacement of the globe. These manifestations are
reversible with treatment.
Stage of orbital abscess :
- Pathology : Collection of pus within the orbit.
- Impaired vision, severe throbbing pain in the eye, irreversible ophthalmoplegia
and irreversible impairment of vision.
Investigation :
CT scan : diagnostic.
Fundus examination.
Complications :
Cavernous sinus thrombo-phlebitis.
Treatment :
Massive antibiotic therapy.
Surgical drainage of the paranasal sinuses and orbital infections (External fronto-
ethmoidectomy + FESS).
N.B. Posterior group of sinuses (posterior ethmoid and sphenoid) :
- Infections of these sinuses which are closely related to the orbital apex (optic
foramen, superior and inferior orbital fissure) causing orbital apex syndrome : ptosis,
ophthalmoplegia, impaired vision and trigeminal pain (ophthalmic). If vision is normal
these symptoms are called superior orbital fissure syndrome.
- Treatment is drainage of posterior group by FESS.
B- Intracranial complications :
Every sinus shows a tendency to be associated with a particular intracranial lesion.
1-Frontal sinusitis : can cause frontal lobe abscess, via an osteitis of the posterior
sinus wall.
2-Ethmoidal sinusitis : can cause meningitis, via a perforation near the cribriform plate.
3-Sphenoidal sinusitis : can cause cavernous sinus thrombosis via thrombophlebitis of
the diploic venules in the sinus wall.
4-Maxillary sinusitis : rarely causes any intracranial lesion.
Frontal lobe abscess :
Signs of increased ICT.
Its focal symptoms and signs are difficult to be recognized by clinical means
because this is a silent area of the brain. There may be personality changes and
memory defects.
Treatment : Surgical drainage of the paranasal sinus and brain abscess.
Clinical picture :
Classic migraine :
- Recurrent attacks of unilateral severe temporal or frontal pulsating pain. It lasts
for few to several hours. It is associated with photophobia, nausea and vomiting.
- It may be preceded by an aura as flashes of light or numbness in face and hand.
It lasts for minutes. It is due to vasoconstriction of the intracranial blood vessels.
Common migraine : Similar to classic migraine but has no aura and may be
bilateral.
Treatment :
During the attack : Ergotamine.
In between the attacks (i.e prophylaxis) : beta blockers and calcium channel
blockers.
b- Facial pain of neural origin (Neuralgia).
Unilateral sudden severe sharp pain that occurs in short lived attacks along the
distribution of the involved sensory nerve.
a- Trigeminal neuralgia (Tic Douloureux) :
Usually elderly females.
Recurrent attacks of unilateral sudden severe brief (seconds)
sharp pain in the sensory distribution of maxillary and/or
mandibular divisions of the trigeminal nerve.
It is induced by stimulation of a trigger zone as during shaving
or teeth brushing.
Treatment :
Medical : Carbamazepine (Tegretol).
Surgical : Decompression or section of the sensory root of the trigeminal nerve in
resistant cases.
b- Glosso-pharyngeal neuralagia :
Recurrent attacks of unilateral sudden severe brief (seconds) sharp pain in the
tonsil and may be referred to the ipsilateral ear.
It is induced by swallowing or talking.
The cause is unknown but long styloid process compressing the nerve.
Treatment :
Medical : Carbamazepine (Tegretol).
Surgical : Section of the glosso-pharyngeal nerve in resistant cases or fracture of
long styloid process.
II-Secondary facial pain :
1-Intracranial causes : Pain may originate from the dura and blood vessels (middle
meningeal arteries) e.g.
- Inflammations as meningitis, encephalitis and extradural abscess.
- Increased intracranial tension as tumours.
- Decreased intracranial tension as after lumbar puncture or CSF rhinorrhea.
- Head trauma.
2-Cranial causes :
- Trauma e.g. head and facial trauma or postoperative pain.
- Inflammations e.g. petrositis.
- Tumours of skull base e.g. nasopharyngeal carcinoma.
- Ear diseases e.g. otitis externa, complications of otitis media.
- Sino-nasal diseases :
In sinusitis its site depends on the affected sinus, it is more severe in
the morning and increased by coughing, straining and leaning forwards.
Vacuum headache caused by obstruction the frontal recess which is
the opening of the frontal sinus as in frontal sinusitis and deviated septum
causing obstruction of the recess. It is characterized by periodic attacks (starts
in the morning, increases in the mid-day, and subsides by the end of the day)
this is due to absorption of air in the sinus.
Contacted headache caused by contact of medial wall (septum) and
lateral wall (middle turbinate) in deviated septum.
3-Extracranial causes :
- Dental causes : caries.
- Tempanomandibular joint disorders e.g. arthritis.
- Ocular : glaucoma, errors of refraction.
- Cervical : spondylosis, myositis.
- Temporal arteritis : affect old patients due to acute inflammation of the branches
of superficial temporal arteries, may be autoimmune. The sup. Temporal arteries
become tender and cord like. The condition treated by corticosteroids.
4-General causes :
- Tension headache : due to fatigue, most common, starting from the back of the
neck and occiput.
- Hypertension and hypotension.
- Renal and hepatic disorders.
- G.I.T disturbance e.g. constipation.
- Withdrawal of chemical substance e.g. Nicotine and caffeine.
Clinical evaluation of headache :
A- History :
Time of onset, duration and intensity.
What precipitate ? Trigger zones in neuralgia, fatigue, noise, eye strain, sinusitis,
drugs.
Relieved by : Medications, sleep, rest.
Localization and radiation of pain.
Associated symptoms e.g. nasal, ocular, dental, gastrointestinal.
B- Examinations :
General exam : B.P, anaemia, gastrointestinal, diabetes, cervical spine, T.M.J.
E.N.T exam :
- Ant. rhinoscopy : Discharge, septal deviation, frunclosis.
- Oropharyngeal exam : Dental infection, swellings, ulcers.
- Ear exam : Mastoiditis, otitic intracranial complications.
Ophthalmological exam : Iritis, error of refraction, glaucoma.
Neurologic or psychiatric evaluation.
C- Investigations :
Laboratory : Haematological, liver and kidney function …etc.
Radiological : Paranasal sinuses, spines …. etc.
(D) SMELL
Smell is the process by which an odorous substance stimulates the olfactory mucosa.
Smell pathway :
1-The olfactory nerve transmits the odorous impulses from the olfactory mucosa to the
olfactory bulb.
2-The olfactory bulb transmits the impulses to the smell center in the brain (uncus and
hypocampic gyrus).
Smell disorders :
Most patients of olfactory disturbance will fall into one of 4 groups.
1-After head trauma.
2-After viral infection.
3-Poor odorant access to the olfactory mucosa.
4-As manifestation of other diseases.
Types :
1-Anosmia : means loss of the sense of smell. Smell is perceived when the air-borne
odoriferous particles dissolve first in the mucus to reach the olfactory endings,
impulses hence travel by the olfactory nerves to the brain.
The causes of anosmia may be classified as :
A- Nasal :
a- Obstruction : the smell particles do not reach the olfactory mucosa,e.g. acute
rhinitis, deviated septum and nasal polypi.
b- Maldirection of the air current, e.g. after removal of the inferior turbinate.
c- Causes in the mucus : in allergic rhinitis there is excess secretion which washes the
smell particles. In atrophic rhinitis the mucus is too thick to dissolve the smell particles.
d- Interference with nerve endings :
- Degeneration : in atrophic rhinitis.
- Irritant vapours : e.g. sulphuric acid, benzene, formaldehyde, and many industrial
dusts ..etc.
- Post-influenza neuritis, has been observed more often in the last few years, some
cases recover, but if persists more than 3 months it is unlikely to recover.
B- Intracranial :
a- Fracture base involving the cribriform plate and olfactory nerves.
b- Senile atrophy.
c- Tumours of the anterior cranial fossa, e.g. meningioma, neuroblastoma.
N.B : Patients with anosmia are at a risk from dangerous fumes and gases and also from fires
as they cannot detect the smoke odour.