External nose
It is a pyramidal in shape upper boney pyramid and lower cartilaginous pyramid
Boney part consists of upper 1\3 and cartilaginous part consists of lower 2\3
Boney framework consists of
Pair of nasal bone
Frontal process of maxilla
Maxillary process of frontal bone
Cartilages of external nose
Pair of upper lateral cartilages
Pair of lower lateral cartilages(greater alar cartilage)
Part of septal cartilage
Vestibule is part of the nasal cavity just within the the external nose,the vestibular skin
contain hair follicles,hair and sebecious glands
Nasal cavity
Divided into two cavities by the nasal septum
It`s ant.openning called ant naris while it`s post. Opening called post.naris which open
into nasopharynx
Nasal septum
Formed by
Cartilaginous part anteriorly by quadrilateral cartilage
Boney part posteriorly which formed by
Perpendicular plate of ethmoid
Vomer
Nasal crest of maxilla
Nasal crest of palatine bone
Lateral nasal wall
Within the nasal cavity there are three turbinates (superior,middle and inferior) In the
inf.meatus
Opening of nasalcrimal duct
In the mid.meatus
There is bulge called bulla ethmoidalis below it there is Uncinate process between them
there is a fissure formed called hiatus similunaris
The following sinuses open in the middle meatus
Ant. Ethmoid air cell and frontal sinus in the anterior part of hiatus simlunaris
Maxillary sinus ostium and sometime accessory ostia open in the posterior part of hiatus
simlunaris
Superior and middle turbinate is part of ethmoid bone
Inferior turbinate is a separate bone
The air space beneath each turbinate is known as
the meatus of the corresponding turbinate.
i.e each meatus named after the turbinate above it
There are various ducts and sinuses open in the meati
Each turbinate is a cigar-shaed ridges or swellings are attached to the lateral nasal wall
,each is made of bone,superior and middle is part of ethmoid bone while inferior turbinate
is a separated bone,
All turbinates are coveres with vascular mucopreriostium and ciliated columnar
epithelium.
The space under each turbinate is called a meatus i.e inferior meatus lies under the
inferior turbinate etc…In the superior meatus
Posterior ethmoid sinus,sphenoid sinus drain in the sphenoethmoid recess which is a
small depression above and behind the superior turbinate
The vascular inferior turbinate contains the second errectile tissue in the body i.e it has
the ability to swell and shrink under autonomic nervous system control. Nasal resistance
The nose accounts up to half of the total airway resistance.
The resistance is made by two elements
A is essentially fixed made by bone,cartilage and attached muscle
B is variable made by mucosa
The nasal resistance is high in infants who initially are obligatory nasal breathers
Removal of nasal resistance by tracheostomy reduce the dead space but results in a
degree of alveolar collapse
Factors decrease nasal resistance
Exercise
Sympathmymetic
Rebreathing
Atrophic rhinitis
Erect position
Factors increase nasal resistance
Infective rhinitis
Allergic rhinitis
Vasomotor rhinitis
Aspirin
Ingestion of alcohol
Cold air
Supine position
Hyperventilation
Sympthatic antagonists
Factors that influence nasal resistance is nasal cycle
Nasal cycle
Demonstrated in over 80% of adults but it is more difficult to demonstrate in children.
The cycle consists of alternate nasal blockage between passages.
Cyclical changes occur between 4-12 hours;they are constant for each person
Various factors may modify the nasal cycle include
Allergy
Infection
Exercise
Hormones
Pregnancy
Fear
Emotiom
Autonomic nervous symptom vagal overactivity cause nasal obstruction
Drugs the anticholinergic effects of antihistamine can block the parasympthatic activity
and produce an increase of sympthatic tone ,hence improve airway
The function of the inferior turbinate is to control the passage of the air through the nose
via the nasal cycle,the inferior turbinate is one side enlarged,as and as aresult the air flow
through that nostril is restricted.
This reduse the drying effect of airflow and allows for rejuvenation of the nasal lining
and cilliary function.
After approximately 4 hours,the turbinate on the other side swells and on previously
rested side the turbinate shrinks.
This nasal cycle is a normal physiological mechanism that is present to some extent in all
of us but noticed only by some people.
Nasal epithelium is a pseudostratifi ed columnar ciliated mucous
membrane continuous throughout the sinuses. The epithelium contains
goblet cells, which produce mucus, and columnar cells with
mobile cilia projecting into the mucus, beating 12–15 times a second.
The direction of ciliary beats is organized into well-defi ned pathways,
present at birth. These mucociliary pathways ensure drainage of the
sinuses through their physiological ostium into the nasal cavity
‫المحاضره الثانيه‬
The middle meatus is of special signifi cance as it contains the ostiomeatal
complex (OMC). This is an anatomical area in the bony
lateral nasal wall comprising narrow, mucosal lined channels and
recesses into which the major dependent sinuses drain. The OMC
acts physiologically as an antechamber for the frontal, maxillary
and anterior ethmoid sinuses. Irritants and antigens are deposited
there and may cause mucosal oedema. As the clefts in the OMC are
narrow, small degrees of oedema may cause outfl ow tract obstruction
with impaired ventilation of the major sinuses
The configuration of the structure of the middle meatus are complex and variable,in
disarticulated skull ,the maxillary bone has a large opening in its medial wall,the
maxillary hiatus.
In articulated skull this is filled by adjacent bones
1 inferior: maxillary process of inferior turbinate bone
2 posterior:perpendicular plate of palatine bone
3Anterosuperior:lacrimal bone
4superior:UP and Bulla ethmoidalis
So portion of maxillary hiatus is left open these osseous attachment which in life filled
wth mucous membrane of
1 Mucous membrane ofMM
2Mucous membrane of maxillary sinus
3 Intervening connective tissue and membranous portion of lateral wall
It is the site for the common pathway of the anterior group of sinuses(frontal,anterior
ethmoid,mawillary) structure contribute to this area:
Uncinate process
Thin bony structure runs anterosueriorly to psteroinferioly.it articulate with the ethmoidal
process of inferior turbinate,it artly cover the oening of maxillary sinuse
Hiatus similunaris
It is a semilunar groove which leads anteriorly to the ethmoidal infundibulum
Ethmoidal infundibulum
It is a short passage at the anterior end of the hiatus
Frontal sinus,maxillary and anterior ethmoid drain into it
Bulla ethmoidalis
It ia a round prominence formed buldging of ethmoid sinus
Frontal recess
Maxillary sinus
Middle Meats
Middle Meatus
Lies lateral to the MT
Structure important in the MM:
UP
HS
BE
Ethmoid infundibulum
Anterior and posterior fontanelle:
Are membranous areas between the interior turbinate and uncinated process,accessory
ostia are found mostly in the posterior fontanelle Arterial supply
external carotid arteryfacial arterysuperior labial artery
nasal branch
maxillary arterysphenopalatine
greater
palatine artery
internal carotid arteryanterior ethmoid artery
posterior ethmoid artery
Little`s area or Kiesselbach`s plexus
It is an area in the anterior part of the septum just behind the skin margin contain
aggregation of poorly supported blood vessels represents the most important and
commonest site of epistaxis
It formed by anastamasis of
*Septal br.of sphenopalatine artery
*Superior labial artery
Greater palatine artery*
*Ant.ethmoid artery
Nerve supply
Autonomic supply either1
Sympthatic
Parasympthatic
Special sence2
By olfactory nerve that supply olfactory mucosa which located in the sup.portion of the
nasal cavity
3 sensory supply mainly by branches of trigeminal nerve
Anterior ethmoid nerve from ophthalmic division which has medial branch supply
ant.end of the septum and lateral branch supply mid.&sup. Turbinate
Branches from sphenopalatine & greater palatine nerve which supply most of turbinate
4 motor nerves from facial neve for elevate and dilate nasal ala
‫المحاضره الثالثه‬
Rhinosinusitis
Rhinitis is defined as inflammation of the lining of the nose,characterized by one or more
of the following symptoms
Nasal congestion
Rhinorrhea
Sneezing and itching
The term sinusitis refers to a group of disorder charecterized by inflammation of the
mucosa of paranasal sinuses.
Because the inflammation always also involve the nose ,it is now generally accepted that
"Rhinosinusitis" is preferred term to desecribe the inflammation of the nose and paranasal
sinusesThe ciliated mucosa of the nose and paranasal sinuses are contiguous and it would
be rare for one to be affected without the other so the term rhinosinusitis always
usedDifferential diagnosis
Polyp
Mechanical factors
NSD
Hypertrophic turbinate
Obstruction OMC
F.B
Choanal atrasia
Tumours..Benign or malignant
Granuloma
CSF Rhinorrhea
Acute rhinosinusitis ARS is acute infection of sudden onset with duration of less than
four weeks, 7 days to four weeks as viral rhinosinusitis follow viral URTI and mimic it`s
symptoms so five to seven days was recommended perior to an acute bacterial
rhinosinusitis.
Subacute rhinosinusitis SRS the duration is last for 4- 12 weeks
Recurrent acute infection RARS are defined by four or more episodes per year
Chronic rhinosinusitis CRS occur when the duration of symptoms is greater than 12
weeks
Acute exacerbation of chronic rhinisinusitis AECRS is is sudden worsening of CRS with
return to baseline CRS
Signs and symptoms
Rhinosinusitis requires two major factors,or one major and two minor
Major symptoms
Facial pain\ pressure
Facial congestion/fullness
Nasal obstruction
Nasal discharge/purulent/posterior drainage
Hyposmia/Anosmia
Purulence on nasal examination
Fever (acute rhinosinusitis only
Minor symptoms
Headache
Fever (non acute)
Halitosis
Fatigue
Dental pain
Cough
Ear pain/pressure/fullness
Microbiology of acute bacterial rhinosinusitis
Streptococcus pneumoniae 20-43%
Haemophilus influenzae 22-35%
Strep species
Anaerobes
Moraxella catarrhlis
Staphylococcus aureas
Predisposing factors
Either
Local or general
◙ mucosal obstruction ,deviation,polyp
◙ obstruction of the sinus ostea by allergic rhinitis
◙ neighbouring infection especially in children
General factors
◙immunedifficiancy
◙mucocilliary disorder
◙ allergy
Treatment
Medical
1 treatment of infection
Systemic penicilline always effective
If not do culture and sensitivity
2 treatment of pain
Asprin or codien
3 establishment of drainage of sinus
Either local like ephedrine and normal saline or systemic by pseudoephedrine and
antihistamine.
Always be aware of Rebound phenomenon on using common nasal decongestant
Surgical operations for chronic sinusitis
█ maxillary sinuses
►antral washout
►►intranasal antrostomy
●Middle meatus antrostomy (endoscopic)
●Inferior meatus antrostomy
►Caldwell-Luc operation
Frontoethmoidosphenoid
►Trephenation of frontal sinuses
►►Intranasal ethmoidectomy
►►►FESS Functional endoscopic sinus surgery
►►►►Transnasal ethmoidectomy
►►►►►external frontoethmoidosphenoidectomy
‫المحاضره الرابعه‬
Allergy and Allergic Rhinitis
Atopy is a tendency to develop an exaggerated IgE response while allergy is the clinical
resentation of atopic disease in the presence of allergen
Aetiology
A genetic and family history
Environmental factors like exposure to allergen ,air pollution and irritant, occupational
allergen like flour, wood dust, latex in surgical gloves,tobacco,detergents and
bleach.Food occasionally provoke IgE allergic rhinitis, it may be due to sensitivity to
preservatives, some type of food contain histamine like cheese and wine
Drugs like penicilline, asprin, antihypertensive, B-blocker, ACE inhibitor
The allergic responses can be divided into two phases. The first is an acute response that
occurs immediately after exposure to an allergen. This phase can either subside or
progress into a "late phase reaction" which can substantially prolong the symptoms of a
response, and result in tissue damage
Pathogenesis
IgE has a property of binding to high affinity receptor on the mast cell and basophil .the
interaction of allergen with IgE initiate secretion of active mediators that cause clinical
manifestation,thes mediators either preformed mediators (histamine, proteases,
chemokines, heparine); or newly formed mediators (prostaglandins, leukotrienes,
thromboxanes
Rhinitis if defined clinically by a combination of two or more nasal symptoms
Nasal obstruction…….blocking
Rhinorrhea…………...running
Itching and sneezing
Allergic rhinitis occur when these symptoms are the result of IgE mediated inflammation
following exposure to allergen
Classification
Seasonal
Perennial
New classification by ARIA guideline (allergic rhinitis and its impact on asthema)
Mild
Normal sleep
Normal daily activities
Normal work and school
No troublesome symptoms
Moderate or severe
Abnormal sleep
Impairment of daily activities
Problems caused at school and work
Troublesome symptoms
Intermittent symptoms
Less than 4 days/week
Or less than 4 weeks
Persistent symptoms
More than 4 days/week and more than 4 weeks
Co-morbidities
Other conditions associated with allergic rhinitis are asthema,sinusitis,otitis media,sleep
disorder,lower respiratory tract infection
Rhinitis and asthma are linked by epidemiological,pathophysiological characteristics and
by common therapeutic approach.
█Rhinitis is a risk factor for the development of subsequent asthma ,
█is a frequent cause of asthma exacerbations ,and
█effective rhinitis treatment reduce asthma
So patient with persistent allergic rhinitis should be evaluated for asthma and the
converse is true
Clinical presentation
Immediate type allergic symptoms of sneezing ,rhihinorrhea and itching are easily
recognized
Perennial allergic inflammation is mainly expressed as nasal obstruction,hyperreactivity
and poor sense of smell,the sinus lining is also usually involved so that the picture is of
one of a chronic inflammatory rhinosinusutus,in those patient immediate symptom not
present and may undergo unnecessary operations for septal deviation or turbinate befor
the true nature of the problem is diagnosed properly
Pharmacotherapy
Antihistamine
It relieve running,itching,and sneezing but have little or no effect on blockage
First generation like chlorpheneramine,diphenhydramines should be avoided because of
sedation,psychomotor retardation and learning impairment because it cross the BBB and
interact with histamine receptors
Second generation antihistamine act with an hour topical ones within 15 minutes
Terfenadine,astemazoleblock potassium channel and cause cardiac arrhythmia, QT
prolongation,so care taken not overdose and nor to combine with
erythromycin,ketokanazole,grapefruit juice,antiarrythmia .
Citrizine,fexofenadine,and desloratidine not block potassium channels even at
supranormal dose
Desloratidine is exception that affect on nasal blockage
Topical corticosteroid
Are the most effective treatment of rhinitis especially if started prior to allergen exposure
it reduce the relative risk of asthma exacerbation by 50%
Side effects are minor include epistaxis and nasal irritation
Sodium cromoglicate
It is weakly effective against all rhinitis but safe means it is useful for small children less
than four years for whom a topical corticosteroid is not available
Decongestants
Used topically reduce nasal obstruction but increase rhinorrhea,regular use for more than
few days result in rhinitis medicamentosa
Systemic decongestant are relatively ineffective with side effects like
hyperactivity,insomnia in children and hypertension in adult
Ipratropium bromide
Response in patients who do not response to topical corticosteroid alone
Systemic corticosteroid
Used to unlock the nose at start of treatment or for sever symptoms,used for few days
Depot injection not recommended because they are not if side effects occur
Antileukotriens LRA
Recently been licensed in rhinitis it can also be helpful in polyposis
Nasal douching
Immunotherapy
‫المحاضره الخامسه‬
Epistexis
Epistaxis is the commonest otolaryngologic emergency, affecting up to
60% of the population in their lifetimes, with 6% of cases requiring
medical attention.
The nasal cavity is extremely vascular.
Terminal branches of the
external
and internal carotid arteries supply the mucosa of the nasal cavity
with frequent anastomoses between these systems
The anterior nasal septum is the site of a plexus of vessels called Little’s or
Kiesselbach’s area, which is supplied by both systemsThe maxillary sinus ostium
serves as the dividing line between
“anterior” and “posterior” epistaxis. Anterior bleeding is usually easier
to access and is therefore less dangerous. Posterior epistaxis is more
difficult to treat because visualization is more difficult and blood is often swallowed,
making it more difficult to gauge the amount of
blood loss
The
term “posterior bleeding” is all too often used incorrectly to
label bleeding that cannot be visualized with a head lamp. It transpires
in many cases that endoscopic examination shows the bleeding to be
located high on the septum Primary No proven causal factor
Secondary Proven causal factor
Childhood <16 years
Adult >16 years
Anterior Bleeding point anterior to piriform aperture
Posterior Bleeding point posterior to piriform aperture
Aetiology:
A idiopathic---------from little`s area
B Trauma
Nose picking
F.B
Maxillofacial trauma
Itrogenic
C infection acute or chronic.viral or
bacterial
D Inflammatory
Rhinosinusitis
Nasal polyp
E Neoplasm
Benign angiofibroma, papilloma
Malignant
sq.cellcarcinoma,adenocarcinoma,
lymphoma
F Drug induced
Cocaine abuse
Rhinitis medicamentosa
medicamentosa,asprin,anticoagulant.chloramphinicol,immunosuppressant,alcohol
G inhalant
Tobacco
H endocrine
2 General
A atherosclerosis
B bleeding disorder
A coagulopathy
1inhereted coagulation factors deffeciancy like
factor vii,factor ix
2acquired :anticoagulant,liver disease,vitamin
k defficiancy
B platelate disorders
●thrombocytopenia
●●platelate disfunction
►congenital like vonwillbrand disease
►► acquired like leukemia,uremia,drugs as
NSAID
C blood vessel disorders
●congenetal----osteogenesis imperfecta
●●acquired-----amyloid,vasculitis,vit.K
D hyperfibrinolysis
●congenital------αantitrypsin deficiency
●● acquired------malignant DIC
asprin &
defeciancy
Management
Initial Assessment
The amount of blood loss should be estimated (the physician should
ask about whether the patient has lost enough to soak a handkerchief,
a facecloth, or a towel; the last would indicate a significant loss), and
over what period (a regular minor bleed can cause anemia). A clinical
assessment of the patient’s cardiac status and circulating blood volume
should include looking to see if the patient is pale, sweating, or cool,
or has tachycardia; any of these findings would indicate significant
hypovolemia. A reduction in blood pressure is often a late sign, particularly
in young people, who can maintain blood pressure until the
circulatory volume is critical.
Obtaining intravenous access, checking for and correcting any
clotting abnormalities, and taking blood for “group and save” and/or
crossmatching may be required. In our unit patients admitted via the
emergency department can be “fast-tracked” to the otorhinolaryngo- logic
emergency unit if stable (Box 45-1). This practice helps avoid
unnecessary and counterproductive nasal packing in the emergency
department as well as transfer of patients before they are fit enough to
travel.
The clinician must remember that epistaxis is frequently idiopathic
but can be a manifestation of a possible underlying pathology
(see Fig. 45-12). Your patient should undergo further investigation
First aid measures include asking the patient to apply constant firm
pressure over the lower (non-bony) part of the nose for 20 minutes and
to lean forward with the mouth open over a bowl so that further blood
loss can be estimated. Otherwise, blood dripping postnasally will be
swallowed, and the next warning sign of a serious loss could be several
hundred milliliters of blood being vomited up.
It is important to establish both the site and the cause
The philosophy of this approach can
be summarized as follows:
1. Establish the site of bleeding.
2. Stop the bleeding.
3. Treat the cause.
Headlamp Examination Using Local Anesthesia—
Initial Overview
The key to controlling most epistaxis is to find the site of the bleeding,
and although chemical cautery with silver nitrate can be used, bipolar
diathermy is more effective for stopping the bleeding. Protection from
blood contamination is important. A plastic apron for both parties is
helpful in order to avoid staining of clothes, and eye protection is advisable
if there is active bleeding because some patients have a reflex to
blow away any fluid dripping down the upper lip, which can create a
bloody aerosol. Once the clots have been sucked out, the nasal airway
should be inspected, initially with a headlamp and then, if the bleeding
point cannot be located, with an endoscope
Epistaxis in Children
Young children usually bleed from a vessel just inside the nose at the
mucocutaneous junction on the septum, and the bleeding invariably
stops spontaneously. In children with epistaxis in whom no prominenvessel can be
seen, the regular local application of a cream can help,
but petroleum jelly (Vaseline) alone does not.
As many as 5% to 10% of children with recurrent nosebleeds
may have undiagnosed von Willebrand’s disease.
Children
who have leukemia or are undergoing chemotherapy often have
epistaxis associated with thrombocytopenia. Older children, adolescents,
and adults often bleed from Little’s area or a maxillary spurt
Epistaxis in Adults
The caudal end of the septum, where several branches of the external
and internal carotid anastomose in Little’s area or Kiesselbach’s plexus,
is the most common site of bleeding in adultsLess commonly bleeding,
comes from further back on the septum, and a septal deviation
may make it difficult to visualize Some patients with
seasonal allergic rhinitis complain of more nosebleeds in the hay fever
season, and topical nasal steroids aggravate the bleeding in approximately
4% of users. Many people believe that a nosebleed signifies a
release of pressure and may herald a stroke, and it is important for the
clinician to address these anxieties for the patient. Although many
patients are found to be hypertensive during nosebleeds, few remain so on followup. The association between hypertension and epistaxis is
disputed.
Many clinicians report that hypertension is not related to
Nosebleed
However, nosebleeds in patients with hypertension
are more likely to lead to admission and to be associated with
comorbidity.
In over-anticoagulated
patients, fresh frozen plasma, clotting factor extracts, and vitamin K
help. Vitamin K takes more than 6 hours to work, however, and it can
delay anticoagulation for 7 days after warfarin is started.
. Tranexamic cyclocapron
acid, an antifibrinolytic agent, has not been shown to help.
But other litriture advice to give it Scott brown) Tranexamic
acid has been shown to reduce the severity and risk of rebleeding in epistaxis at a
dose of 1.5 g
three times a day. These drugs do not increase fibrin deposition and so do not
increase the risk of
thrombosis. Preexisting thromboembolic disease is a contraindication.
Other drugs associated with bleeding are aspirin, which interferes with
platelet function for up to 7 days, clopidogrel, and nonsteroidal antiinflammatory
drugs.27,28 In patients who do not have a history of a
bleeding disorder or undergoing anticoagulant therapy, routine clotting
studies do not add to the management.22,24 There is a higher incidence
of epistaxis in patients with a high alcohol intake, even when there is
no laboratory evidence of a coagulation abnormality.29,30
Topical Treatment
Topical Treatment
A randomized controlled trial of silver nitrate cautery with topical
antiseptic nasal carrier cream versus topical alone showed both to be
effective
Use of cold pack is advisable although hot water irrigation 50c has been proposed as
an alternative to packing
Cautery
Most anterior epistaxis can be controlled with identification of the
bleeding point and cautery using a headlamp. The vast majority of
posterior bleeding sites can be identified by endoscopy without the use
of general anesthesia
After cautery the patient should be advised against blowing the
nose for about 10 days to allow the area to heal. A greasy antiseptic barrier cream
should be applied several times daily for 2 weeks to
prevent the eschar from drying and coming off with a resulting rebleed.
The ointment should not be placed directly on the area treated but is
best placed inside the rim of the nostril with the tip of the finger, and
“milked up” by massaging the nostril rims, and then sniffed up. This
advice can also be given to patients with a crusted septal area from
picking or excessive drying.
Nasal Packing
If a bleeding point cannot be found, ideally the nose is packed with an
absorbable hemostatic agent that produces minimal mucosal trauma.
Various nonabsorbable packs have been used, but their insertion is
uncomfortable, as is their presence once in position. The insertion of
a pack can cause local mucosal trauma and complicate localization of
the bleeding point The insertion of a nasal pack has
conventionally meant that the patient has to be admitted, although one
study discharged 46 of 62 patients whose nasal airways had been
packed, with outpatient follow-up arranged for 48 hours later If anterior packing
fails, a posterior balloon may have to
be placed and inflated in the postnasal space. An anterior pack is then
placed, and gentle traction used to pull the balloon forward against the
anterior pack this arrangement is held by placement of a clip over the
catheter anteriorly as it emerges through the anterior pack The morbidity and
physical discomfort
associated with nasal packing includes pain, hypoxia, alar necrosis, and
toxemia, and is well described in the literature; Packing not only traumatizes the
nasal lining but also can
cause cardiorespiratory complications and local infection.
The role of prophylactic systemic antibiotics in patients who have
nasal packs is not well established. If the patient does not experience rebleeding
within 12 to 24
hours, the packs should be removed
removal.” Endoscopic sphenopalatine
artery ligation (ESPAL; see later) has replaced the need for
posterior nasal packs, oLigation od sphenopalatine arteryLigation of ant ethmoid
artery
Ligation of posterior ethmoid artery
Ligation of external carotid artery
Angiography and embolization
Septal surgery
When epistaxis originates behind a prominent septal deviation or vomeropalatine
spur, septoplasty
or submucosal resection (SMR) may be required to access the bleeding point. Some
authors have
advocated septal surgery as a primary treatment for failed packing. The rationale is
that by
elevating the mucoperichondrial flap for septoplasty or SMR, the blood supply to
the septum is
interrupted and haemostasis secured. Cumberworth et al. showed a strategy
involving SMR and
repacking to be more effective and economic than ligation in patients who had failed
with packing.
[***]
Embolization
Embolization under angiographic guidance has been shown to control severe
epistaxis in between
‫المحاضره السادسه‬
Nasal obstruction