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Epistaxis
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AhmedShaikh, HamadAl Saey, SaraAshkanani,
MashaelAlhail, MansourAl Sulaiti,
MaryamAbdulraheem, EmadAl Duhirat,
andShanmugamGanesan
31
31.1 Introduction
Epistaxis is a common ENT emergency. The
estimated lifetime incidence of epistaxis is
approximately 60% [1]. Most episodes are
minor in nature, self-limiting and do not
require intervention. Minor bleeding episodes
occur more frequently in children and adoles-
External Carotid Artery Internal Carotid artery
Facial ArteryInternal Maxillary artery ophthalmic artery
Superior Labial artery
Sphenopalatine artery septal br greater palatine artery
Kiesselbach’s Plexus / littles area
K
Nasal Septum
s
a
cents, whereas severe bleeds requiring intervention often occur in individuals older than
50years. Peaks in incidence are seen in those
less than 10 years of age and aged over
40years [2].
For management of epistaxis, it is imperative
to learn about the vascular supply to the nose.
Blood supply to the nose:
Anterior Ethmoidal
n
r
r
h
Posterior Ethmoidal
A. Shaikh (*) · H. Al Saey · S. Ashkanani
M. Al Sulaiti · S. Ganesan
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
Department of Otolaryngology-Head and Neck Surgery
Division, Weill Cornell Medicine-Qatar, Doha, Qatar
e-mail: Halsaey@hamad.qa;
unknown_user_499795@meteor.springer.com;
Malsulaiti1@hamad.qa; sganesan@hamad.qa
© Springer Nature Switzerland AG 2021
M. Alhail · M. Abdulraheem · E. Al Duhirat
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
e-mail: malhail@hamad.qa;
Ashaikh4@hamad.qa; EAlDuhirat@hamad.qa
347
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_31
348
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31.2 Woodrus Plexus
Mainly a venous plexus situated at the posterior
and inferior end of the inferior turbinate.
31.3 Classication ofEpistaxis [3–5]
A. Shaikh et al.
• Pollution
• Altitude
Postoperative/iatrogenic
• Nasal surgery
• Nasal crustations
Anterior epistaxis: anterior to pyriform aperture
which can be visualised by head light.
Posterior epistaxis: posterior to pyriform aperture the source of which cannot be visualised by
head lamp. Some authors [6] describe the maxillary ostium as landmark to differentiate anterior
from posterior nasal bleeding.
31.3.1 Causes ofNasal Bleeding
Epistaxis can result from multiple causes both
local and systemic, most of the time epistaxis is a
manifestation of underlying disease, hence in all
cases of epistaxis underlying cause should be
investigated and treated.
Local Causes (Nasal) of Epistaxis
Idiopathic/spontaneous
Trauma
• Nose picking
• Foreign body
• Nasal oxygen and continuous positive
airway pressure
• Nasal fracture
Inammatory/infectious
• Common cold, viral rhinosinusitis
• Allergic rhinosinusitis
• Bacterial rhinosinusitis
• Granulomatous diseases
• Wegener granulomatosis
• Sarcoid
• Tuberculosis
Environmental irritants
• Smoke
• Chemicals
Primary neoplasm
• Haemangioma of the septum, turbinates
• Haemangiopericytoma
(glomangiopericytoma)
• Nasal papilloma
• Pyogenic granuloma
• Angiobroma
• Carcinoma and other nasal malignancies
Structural
• Septal deformity, spurs
• Septal perforation
Drugs
• Topical nasal steroids
• Cocaine abuse occupational substances
General Disorders, Systemic Causes
Hypertension
Arteriosclerosis
Platelet deciencies or dysfunction
Coagulopathies (e.g. warfarin, liver
disease)
Leukaemia
Von Willebrand disease
Hereditary hemorrhagic telangiectasia
Organ failure (e.g. liver, kidney)
31.3.2 Management
31.3.2.1 General Management
ABC: Airway Breathing andCirculation
Assessment
Patient should be quickly assessed for any hypovolemic shock; the signs include tachycardia,
pale, cold extremities, sweating and hypotension.
AL GRAWANY
31 Epistaxis
349
Blood should be collected for haemoglobin,
coagulation, cross matching and platelet function
test and peripheral line should be secured.
After stabilisation of vitals, assessment
includes
1. History taking: includes the history of onset,
amount of blood loss, laterality and any systemic or family diseases.
2. Examination: examination of nasal septum
should be done to visualise the little area which
is commonest site of nasal bleeding; nasal septal deviation and nasal turbinates should be
inspected, if the source of bleeding is not visualised by the head light, then nose should be
decongested and nasal endoscopy should be
done for visualisation of posterior aspect of
nasal cavity.
31.3.3 Specic Management
Trotter’s manoeuvre: cartilaginous part of the
nose should be compressed for at least 15–20min
most of the time the anterior pressure stops the
nasal bleeding.
Cauterisation of anterior nasal bleeding [7]: if
the source of the bleeding can be seen, attempt
should be made to cauterise it after local anaesthesia; silver nitrate cautery and the bipolar cautery are effective to control the bleeding from the
anterior nasal septum.
Failure of cauterisation or medical manage-
ment leads a clinician to consider packing as the
next treatment option. Many different types of
packs have been developed over the years, including no absorbable, anterior, and posterior packs.
Absorbable gelatin foams (Gelfoam): act by
temponade effect and promote the platelet aggregation (Fig.31.1).
Floseal: combination of thrombin with gelatin
to promote the coagulation, it is easier to use with
least patient discomfort, drawback is oseal and
more expensive than other traditional packing
materials.
31.4.1.2 Non-absorbable Packs
Carboxymethylcellulose Sponge (Merocel)
Usually used as rst-line anterior nasal packs,
they act by mechanical compression of the bleeding point, usually they are lubricated with antiseptic ointment for easy insertion and preventing
the secondary infection. Once inserted they are
left for 24–48h. They are inserted along the oor
of the nose. Side effects include patient discomfort at the time of insertion and removal of pack.
They can act as focus of infection and can cause
toxic shock syndrome, hence patient with nasal
packs should be covered with antibiotics and
Staphylococcus aureus.
Inatable balloons: Rapid rhino they are
inserted along the oor of the nose and inated
with normal saline. They also act by direct compression of bleeding site and promote the
coagulation.
Impregnated gauze packing: This is a traditional way of nasal packing where impregnated
gauze is used as layers for packing the nasal cavity; it caused signicant pain to the patient and
needs expertise for packing. They have fallen out
31.4 Nasal Packing
31.4.1 Anterior Nasal Packs
31.4.1.1 Absorbable [8]
Oxidised cellulose (e.g. Surgicel): it is local
hemostatic agent which acts by pressure compression and promotes the coagulation at the
bleeding site.
Fig. 31.1 Nasopore (absorbable haemostat)
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A. Shaikh et al.
of favour as more easy methods of anterior packing like merocel is available. One of the packs
which is used for long-term packing is gauze
impregnated with BIPP (Bismuth Iodine Parafn
Paste); BIPP is an antiseptic pack and can be left
upto 7days inside the nasal cavity (Fig.31.2).
Posterior nasal packing: posterior packing is
not as commonly used; it is used with anterior
packing when anterior packing alone fails to stop
the bleeding.
A Foleys catheter of size 14 or 12 is used,
catheter is inserted along the nasal oor into the
choana, the position is conrmed after visualisation of the tip in the posterior pharyngeal wall
through the oral cavity, 5 to 10 ml of saline is
used to fully inate the balloon and catheter is
pulled to hinge over the choana there by occupying the nasopharynx and putting a tamponade
effect on posterior end of the nasal cavity. An
artery forceps or vascular clip is used to keep the
traction. The nasal cavity around the catheter is
packed with impregnated gauze strips.
The side effects of posterior nasal packing are
severe nasal pain, necrosis of columella and
necrosis of posterior part of nasal septum by
pressure effect. Posterior packs also lead to
obstructive sleep apnoea and arrhythmia in some
patients; the patients with posterior packs should
be admitted and regular monitoring is needed for
oxygen saturation.
Documented success rate of posterior packing
is around 75%. Failure of posterior packing warrants surgical management of epistaxis.
Fig. 31.2 BIPP (Bismuth Iodine Parafn Paste) Pack
31.4.2 Surgical Management
ofEpistaxis [
Surgical management includes the cauterisation
or ligation of major vessels in the nose, as discussed earlier nose is mainly supplied by anterior
ethmoidal artery, posterior ethmoidal artery and
sphenopalatine branch of internal maxillary
artery.
9–13]
31.5 Anterior Ethmoid Artery
Ligation
Anterior ethmoidal artery [14] is a branch of ophthalmic artery which is branch of internal carotid
artery; the course of AEA is described in three
parts intraorbital, intranasal and intracranial.
The artery pierces the periorbital and enters
the nose through anterior ethmoidal foramen.
Anterior ethmoidal foramen is located at 24mm
distance from the lacrimal crest. The artery exits
the orbit between medial rectus and superior
oblique muscles; at the level of ethmoidal foramen lamina papyracea is dehiscent with projection that can be appreciated on CT sinus. The
level of artery in relation to the skull base in the
ethmoidal sinus is variable; the artery is covered
with a thin bony canal which also contains the
anterior ethmoidal nerve. Artery enters the cranium through lateral lamella of cribriform plate.
Anterior ethmoidal artery supplies the nasal septum. Intracranial part of anterior ethmoidal artery
gives anterior meningeal and anterior falcine
artery which supplies the falx cerebri (Fig.31.3).
The anterior ethmoidal artery ligation is considered in cases of refractory epistaxis when
either the bleeding is seen coming from AEA or
sphenopalatine artery ligation does not control
the nasal bleeding. Embolization is not an option
for AES bleed as there is high risk of blindness.
Traditionally ligation has been performed via
an open approach using a Lynch-type incision
[15] with the placement of the vascular clip on
the AEA between the periorbital fascia and its
entrance into the lamina papyracea. Now many
endoscopic approaches have been described for
ligation of AEA avoiding external scar.
AL GRAWANY
31 Epistaxis
Fig. 31.3 Anterior ethmoidal artery (AEA, red),
Olfactory Cleft (yellow Olf Cleft) and Fovea Ethmoidalis
(Blue FE)
Retraction of the AEA into the orbit can lead
to permanent vision loss, hence in case of failed
endoscopic approach external approach is used
(Figs.31.4 and 31.5).
The posterior ethmoidal [16] artery which is a
branch of ophthalmic artery passes through the
posterior ethmoidal canal and enters the dura at
the posterior margin of the cribriform plate and
supplies the dura of the medial third of the oor
of the anterior cranial fossa; PEA is seen at the
roof of posterior ethmoidal cells and most of the
time is covered with bone; the bleeding from posterior ethmoidal artery is rare and usually iatrogenic as PEA is a small artery as compared to
AEA (Fig.31.6).
351
Figs. 31.4 and 31.5 Anterior ethmoidal artery at the
skull base with anterior ethmoidal nerve with dehiscent
lamina (RED ARROW)
31.6 Endoscopic Sphenopalatine
Artery Ligation
31.6.1 Anatomy ofSphenopalatine
Artery
Sphenopalatine artery is [17, 18] a terminal
branch of the internal maxillary artery originating from the external carotid artery system. The
SPA is the major blood vessel to the nasal cavity
mucosa: supplying the superior, middle, and
inferior turbinate; lateral nasal wall; and nasal
Fig. 31.6 Posterior ethmoidal artery (PEA red)
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A. Shaikh et al.
septum. The sphenopalatine artery travels within
the pterygopalatine fossa and enters the nasal
cavity through the sphenopalatine foramen within
the superior meatus between the middle turbinate
and the posterior end of the superior turbinate on
the lateral nasal wall; the shape of the sphenopalatine foramen predicts the size of the sphenopalatine artery and branches. The SPA branches
into two major vessels, the septal artery and posterior lateral nasal artery, before exiting the sphenopalatine foramen. The septal artery exits the
sphenopalatine foramen, courses through the
anterior inferior wall of the sphenoid sinus and
distributes on the nasal septum. The posterior lateral nasal artery exits the sphenopalatine foramen, courses downward anteriorly to the posterior
end of the middle turbinate along the lateral nasal
wall, and runs inferiorly on the perpendicular
plate of the palatine bone giving off branches to
the inferior and middle turbinate.
Surgical management [19, 20] of epistaxis is
typically only for those patients whose bleeding is
refractory to more conservative therapies.
Knowledge of the vascular anatomy and important
landmarks is necessary to avoid intraoperative
bleeding and to lower the risk of postoperative
bleeding. The sphenopalatine artery can be exposed
endoscopically by raising a posterolateral mucosal
ap over the orbital process of the palatine bone. A
maxillary antrostomy is done to visualise the posterior maxillary wall and palatine bone. A vertical
incision is made inferior to the posterior portion of
the middle turbinate, 1cm anterior to its posterior
tip. Raising the mucoperiosteal ap posteriorly and
superiorly will expose the ethmoid crest [21]. The
ethmoid crest represents a signicant landmark for
locating the position of the sphenopalatine artery
and is consistently anteromedial to the sphenopalatine foramen. Resection of the ethmoid crest
enhances exposure of the sphenopalatine artery
and helps identify its branches to ensure appropriate vessel ligation. As the ap is raised and ethmoid
crest resected, the broneurovascular bundle
including the SPA and nasopalatine nerve will be
reachable at the sphenopalatine foramen. After isolating the artery and its branches, the next step is
either cauterising them with bipolar forceps,
occluding with clips, or using a combination of
both. Upon attaining bleeding control, the mucoperiosteal ap is put back in place and covered with
surgicel (Figs. 31.7 and 31.8).
31.6.2 Embolization
Embolization for epistaxis was rst performed by
Sokoloff in 1974 [22]. Since then, embolization
has become an accepted treatment for posterior
epistaxis, where available. Common embolization
targets include the IMA and facial artery. These
Fig. 31.7 Sphenopalatine artery and ethmoidal crest
Fig. 31.8 Sphenopalatine artery exiting from the pheno-
palatine foramen (red) NLD: Nasolacrimal Duct
AL GRAWANY
31 Epistaxis
353
vessels can be embolised with various materials,
including cyanoacrylate glue, polyvinyl alcohol
sponges, metal coils, or gelatin foam. Bilateral
IMA ligation is often used for cases in which the
exact source is unidentiable. Success rates have
ranged from 79 to 96% in multiple studies.
However, complication rates as high as 24% have
been reported. Complications from embolization
include rebleeding, stroke, blindness, facial numbness, skin sloughing, carotid artery dissection, and
groin haematoma. Embolization is expensive.
Miller and colleagues showed that embolization
was twice as costly as modern surgical treatment
for recurrent epistaxis. Another drawback for
embolization is its inability to control bleeding
from the ethmoidal arteries. Embolization needs
expertised and trained intervention radiologists
are not available at many centres. In this situation,
if packing fails to control the bleeding, surgical
treatment may become necessary [23].
Take Home Messages
• The estimated lifetime incidence of epistaxis is approximately 60%.
• All cases of epistaxis should be investigated and treated for underlying cause.
• Otolaryngologist should be well aware
about the anatomy of major vessels in
the nose.
References
1. Weiss NS.Relation of high blood pressure to headache, epistaxis, and selected other symptoms. The
United States Health Examination Survey of Adults.
N Engl J Med. 1972;287:631–3.
2. Massick D, Tobin EJ.Epistaxis. In: Cummings CW,
Haughey BH, Thomas JR, etal., editors. Cummings
otolaryngology: head and neck surgery. Philadelphia:
Mosby; 2005. p.942–61.
3. Tan LK, Calhoun KH.Epistaxis. Med Clin North Am.
1999;83:43–56.
4. Wormald PJ.Epistaxis. In: Bailey BJ, Calhoun KH,
Derkay C, et al., editors. Head and neck surgeryotolaryngology. Philadelphia: Lippincott Williams &
Wilkins; 2006. p.505–14.
5. Orlandi RR, Lanza DC.Is nasal packing necessary
following endoscopic sinus surgery? Laryngoscope.
2004;114(9):1541–4.
6. Floreani SR, Nair SB, Switajewski MC, et al.
Endoscopic anterior ethmoidal artery ligation: a
cadaver study. Laryngoscope. 2006;116:1263–7.
7. Douglas R, Wormald PJ. Pterygopalatine fossa
inltration through the greater palatine foramen: where to bend the needle. Laryngoscope.
2006;116(7):1255–7.
8. Hanif J, Tasca RA, Frosh A, etal. Silver nitrate: histological effects of cautery on epithelial surfaces with
varying contact times. Clin Otolaryngol Allied Sci.
2003;28(4):368–70.
9. Brouz D, Charakidas A, Androulakis M, et al.
Traumatic optic neuropathy after posterior ethmoidal
artery ligation for epistaxis. Otolaryngol Head Neck
Surg. 2002;126(3):323–5.
10. Thornton MA, Mahesh BN, Lang J. Posterior epistaxis: identication of common bleeding sites.
Laryngoscope. 2005;115(4):588–90.
11. Pope LE, Hobbs CG.Epistaxis: an update on current
management. Postgrad Med J. 2005;81:309–14.
12. Srinivasan V, Sherman IW, O’Sullivan G. Surgical
management of intractable epistaxis: audit of results.
J Laryngol Otol. 2000;114(9):697–700.
13. Klotz DA, Winkle MR, Richmon J, et al. Surgical
management of posterior epistaxis: a changing paradigm. Laryngoscope. 2002;112:1577–82.
14. Mathiasen RA, Cruz R. Prospective, randomized,
controlled clinical trial of a novel matrix hemostatic
sealant in patients with acute anterior epistaxis.
Laryngoscope. 2005;115(5):899–902.
15. Pletcher SD, Metson R. Endoscopic ligation
of the anterior ethmoid artery. Laryngoscope.
2007;117(2):378–81.
16. Douglas SA, Gupta D. Endoscopic assisted external approach anterior ethmoidal artery ligation
for the management of epistaxis. J Laryngol Otol.
2003;117(2):132–3.
17. Smith TP.Embolization in the external carotid artery.
J Vasc Interv Radiol. 2006;17(12):1897–912.
18. Miller TR, Stevens ES, Orlandi RR.Economic analysis of the treatment of posterior epitaxis. Am J Rhinol.
2005;19:79–82.
19. Kumar S, Shetty A, Rockey J, et al. Contemporary
surgical treatment of epistaxis. What is the evidence
for sphenopalatine artery ligation? Clin Otolaryngol
Allied Sci. 2003;28(4):360–3.
20. Budrovich R, Saetti R. Microscopic and endoscopic
ligature of the sphenopalatine artery. Laryngoscope.
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21. Orlandi RR. Endoscopic sphenopalatine artery
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2001;12(2):98–100.
22. Morgan MK, Aldren CP. Oroantral stula: a complication of transantral ligation of the internal
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crista ethmoidalis in endoscopic sphenopalatine
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The Nasal Septum andTurbinates
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MansourAl Sulaiti, EmadAl Duhirat,
HamadAl Saey, ShanmugamGanesan,
andAbdulazizAl Jufairi
32
32.1 Introduction
The sensation of normal nasal ow happens when
the ow receptors in the nasal valve area are
stimulated. The normal perception of ow
requires a background level of resistance with the
presence of a laminar air ow pattern.
Nasal resistance is the difference between air
pressure at the nasal vestibule and air pressure in
the nasopharynx, which is normally between 8
and 20mm H2O.This is why conditions with low
resistance like “empty nose syndrome” are associated with the sensation of nasal obstruction,
because a minimum level of resistance (normally
greater than 6–8mm H2O) is needed for the normal perception of ow.
The internal nasal valve plays a major role in
the resistance of the airways as it is the narrowest
M. Al Sulaiti · H. Al Saey · S. Ganesan
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
Department of Otolaryngology-Head and Neck
Surgery Division, Weill Cornell Medicine-Qatar,
Doha, Qatar
e-mail: Malsulaiti1@hamad.qa;
Halsaey@hamad.qa; sganesan@hamad.qa
E. Al Duhirat (*) · A. Al Jufairi
Otolaryngology-Head and Neck Surgery Division,
Department of Surgery, Hamad Medical Corporation,
Doha, Qatar
e-mail: EAlDuhirat@hamad.qa; aaljufairi@hamad.qa
portion of the nasal cavity and, therefore, any
compromise of the components of the valve creates symptoms of nasal obstruction. The angle is
bound medially by the septum and laterally by
the inferior edge of the upper lateral cartilages
and the anterior aspect of the inferior turbinate.
Another factor affecting the physiological air
ow is the nasal cycle, during which each side of
the nasal airway undergoes an alternating cycle of
congestion and decongestion. Normally, this cycle
is not noticeable, but when accompanied by disorders affecting the nasal airway, cyclical alternating
nasal obstruction may become apparent. The regulation of the nasal cycle is by the parasympathetic
and sympathetic nervous systems on vascularity of
the erectile tissue of the inferior turbinate and septum, causing a variation in the respective nasal
resistance of each nasal airway. This explains the
positive inuence of exercise, during which
increased sympathetic nervous system tone
enables vasoconstriction via stimulation of nasal
mucosal vascular α-adrenergic receptors.
Adrenaline analogue drugs such as xylometazoline work in the same way. This demonstrates why
intranasal vasoconstrictors may relieve nasal
obstruction by causing mucosal decongestion. The
turbinates in the dependent nasal fossa become
congested when the patient is in the lateral decubitus position. The nasal cycle is an alternating one,
with the total resistance in the nose remaining constant. In patients with a xed septal deviation and
intermittent nasal obstruction, the interplay of the
© Springer Nature Switzerland AG 2021
A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_32
AL GRAWANY
355
356
M. Al Sulaiti et al.
nasal cycle becomes evident; the sensation of
obstruction frequently mirrors the congestion
phase [1–6].
32.2 The Nasal Septum
The nasal septum functions include separation of
the nasal two nasal cavities, support of the nasal
framework including the nasal tip and formation
of part of the nasal valves.
The nasal septum consists [7] of (Fig.32.1):
• Bony part:
– The perpendicular plate of the ethmoid
bone forms the upper one third of the nasal
septum. Attached to the cribriform plate
superiorly and posteriorly attached to the
sphenoid rostrum, posteroinferiorly with
the vomer, and anteroinferiorly with the
septal cartilage.
– The Vomer: forms the posterior and infe-
rior nasal septum and articulates with the
sphenoid rostrum, articulates with the nasal
crest (the maxillary and palatine bones)
and anteriorly articulates with the septal
cartilage, and the posterior edge forms the
posterior free edge of the septum.
– Maxillary crest and palatine bone.
• Cartilaginous part: the septal or quadrilateral
cartilage attached rmly to the nasal bones,
perpendicular plate of the ethmoid and vomer.
Inferiorly seated within the nasal crest of the
maxilla.
• Membranous portion: the connective tissue
between the caudal portion of the septal cartilage and columella.
32.3 Embryology
The nasal septum grows inferiorly from the nasofrontal prominence to the level of the palatal
shelves following fusion to form the secondary
palate. Anteriorly, the septum is contiguous with
the primary palate originating from the nasomedial processes. At the end of its development, the
nasal septum divides the nasal cavity into two
separate chambers [8].
32.4 Blood Supply
• The external carotid artery:
– The sphenopalatine: supplies the postero-
inferior septum by a branch called the posterior septal artery (the base of the
nasoseptal ap).
Fig. 32.1 Anatomy of
the nasal septum
32 The Nasal Septum andTurbinates
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– The greater palatine arteries supply the
anteroinferior portion of the septum.
– The superior labial artery (facial artery):
supplies the caudal septum and columella.
• The internal carotid artery:
– The anterior ethmoid artery (branch of the
ophthalmic artery)
– The posterior ethmoid artery (branch of the
ophthalmic artery)
Kiesselbach’s plexus (Little’s area): The anterior ethmoid artery, posterior septal artery, greater
palatine artery, and septal branch of superior
labial artery.
357
32.5 Venous Drainage
The venous system drainage:
• The sphenopalatine vessels into the pterygoid
plexus posteriorly and into the facial veins
anteriorly.
• The ethmoidal veins communicate with the
superior ophthalmic system and there are some
direct intracranial connections through the
foramen caecum into the superior sagittal sinus.
32.6 Nasal Valves (Table32.1)
32.7 Nasal Septal Deviation
A physiological septum deviation is dened as a
deviation without subjective or objective reduction of the nasal breathing (Fig.32.2). A pathological septum deviation has to be dened as a
Table 32.1 Comparison between the internal nasal valve
and the external nasal valve [1, 9]
Internal nasal valve External nasal valve
Medial wall: septum
Lateral wall: anterior
part of the inferior
turbinate
Nasal oor: oor of the
bony aperture
Medial wall: septum
Lateral wall: lateral crus of
the lower lateral cartilage
(LLC)
Nasal oor: Floor of the
nasal vestibule
Fig. 32.2 Image of a deviated nasal septum to the right
side
Table 32.2 Mladina classication of the nasal septal
deviation [10]
Mladina classication for nasal septal deviation
Type 1 Unilateral vertical ridge in the valve region
Type 2 Similar to type 1 but more severe
obstruction and disturbance of nasal valve
Type 3 Unilateral vertical ridge at the level of the
head of the middle turbinate
Type 4 Combination of type 3 with either type 1 or
2
Type 5 Prominent maxillary crest contralateral to
the deviation with a septal crest on the
deviated side
Type 6 Combination of previously described septal
deformity types
septum deviation with subjective reduction of
nasal breathing [2] (Table32.2).
32.8 Nasal Septal Surgeries
(Table32.3)
32.9 Indications forSeptoplasty
The nasal septum very rarely lies absolutely
straight within the skull but usually shows a more
or less pronounced deviation that can be found in
up to 90% of cases investigated [10, 12].
AL GRAWANY
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