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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4416_Библиотеки_им_академика_М_И_Перельмана
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377Chapter 26 Approach to Nasal Obstruction
Flowchart 26.1: Differential diagnosis of common erosive nasal lesions based on distribution.
*Can occur, although rare.
(GPA: Granulomatosis with polyangiitis).
Section 7 Clinico-Radiological Approach378
External Nose and Vestibular Lesion (Figs. 26.9 and 26.10)
e external nose and vestibular lesions are described in Table 26.6.
A
B
C
Figs. 26.9A to D: External nasal lesions. (A and B) Infected dentigerous cyst. Extensive
inammatory change in right maxilla and premaxillary spaces. Unerupted tooth in right
maxilla (arrows); (C) Nasal bone hemangioma. Expansile lytic sclerotic lesion of right nasal
bone with sun-burst appearance (asterisk); and (D) Heterogeneous contrast enhancement
(arrow).
D
379Chapter 26 Approach to Nasal Obstruction
A
B
C
Figs. 26.10A to D: Lesions of nasal vestibule. (A) Nasoalveolar cyst. Hypodense cystic lesion
(Cy) in left nasal vestibule; (B) Bony scalloping of the maxillary alveolus (arrow); (C) Basal cell
carcinoma. Mass lesion in left side of columella (asterisks in C and D) Bone erosion of left
maxillary alveolus (arrow).
D
Section 7 Clinico-Radiological Approach380
Table 26.6: External nose and vestibular lesions (see Figs. 26.9 and 26.10).
External nose lesions Vestibular lesions
Most diseases do not require imaging and
include cellulitis or deformities
Deformities often result from abnormalities of
the cartilage
• Saddle nose: Depression of the dorsum
due to involvement of bony/cartilaginous
part or both
• Following trauma or surgery or septal
hematoma, abscess or midline lesions
destroying the septum
• Masses:
– In the region of glabella:
- Congenital lesions: Dermoid
cyst, encephalocele, glioma,
hemangioma,andneurobroma
– In the region of vestibule:
- Malignant lesions: Basal cell
carcinoma, squamous cell
carcinoma, and melanoma
Most commonly infective: Vestibulitis,
furuncle
• Congenital: Stenosis, atresia
– Tumors/tumor-like condition:
Nasoalveolar cyst/squamous cell
carcinoma
• Nasoalveolar cyst:
– Seen as a smooth swelling in
nasalvestibule/lateralwall/oor
– Smooth,well-denedcysticlesion
at the nasolabial fold with no deep
extension
• Squamous cell carcinoma:
– Irregular,ill-denedsofttissue
masswithextensiontooorof
nasal cavity/collumella and
upper lip
MANAGEMENT
Management in nasal obstruction depends on the cause of obstruction. It can
be medical/conservative, endoscopic, or surgical.
DIAGNOSTIC ALGORITHM
■ Flowchart 26.2 summarizes the approach to unilateral nasal obstruction
associated with soft tissue/ ‘mass lesion’
■ Bilateral lesions are mostly infective or inammatory in nature.
■ However large masses which are initially unilateral become/appear
bilateral due to erosion/ displacement of the nasal septum.
SUGGESTED READING
1. Borges A, Fink J, Villablanca P, et al. Midline destructive lesions of the sinonasal
tract: simplied terminology based on histopathologic criteria. AJNR Am J
Neuroradiol. 2000;21:331-6.
2. Gupta A, Hawrych A, Wilson WR. Cocaine-induced sinonasal destruction.
Otolaryngol Head Neck Surg. 2001;124:480.
3. Provenzale JM, Allen NB. Wegener granulomatosis: CT and MR ndings. AJNR
Am J Neuroradiol. 1996;17:785-92.
4. Valencia MP, Castillo M. Congenital and Acquired Lesions of the Nasal Septum:
A Practical Guide for Dierential Diagnosis. RadioGraphics. 2008;28:205-23.
381Chapter 26 Approach to Nasal Obstruction
Flowchart 26.2: Diagnostic algorithm of unilateral soft tissue masses causing nasal obstruction.
(JNA:JuvenileNasopharyngealangiobroma).
27
CHAPTER
Approach to Epistaxis
David Victor Kumar Irugu, Manisha Jana, Ashu Seith Bhalla
• Introduction
• Epidemiology
• Relevant Anatomy
– External Carotid Artery
– Internal Carotid Artery
• Etiology
• Investigations
• Imaging
• Management
– Cauterization
– Nasal Packing
– Surgical Management
– Angiography and Embolization
– Others
• Prevention
INTRODUCTION
■ Epistaxis is dened as bleeding from nose or nasopharynx. e word
epistaxis originated from Greek word “epistazein” which means to ow
drop by drop.
■ In 1784 Vogel suggested that the term should be used specically for
nasal bleeding.
1,2
EPIDEMIOLOGY
■ Many people experience nose bleeding at some point in their life and
the prevalence of epistaxis is estimated to be about 108/100,000 per year.
■ Of these about 6% need medical management.
■ Epistaxis has bimodal age distribution and is most commonly seen
under the age of 10 years and over 40 years. ere is no race or gender
predilection.
1-3
RELEVANT ANATOMY
Blood supply to nose comes from both external and internal carotid arteries
(Fig. 27.1A), through the following branches.
383Chapter 27 Approach to Epistaxis
A
B
Figs. 27.1A and B: (A) Blood supply of nasal septum from external and internal carotid
artery systems; and (B) Little’s area and Kiesselbach’s plexus.
External Carotid Artery
■ Internal maxillary artery: It supplies blood to nose through its branches.
• Greater palatine artery
• Pharyngeal artery
• Posterior nasal artery
• Sphenopalatine artery (SPA) is the major supply to nasal cavity and to
superior and medial turbinates.
■ Superior labial artery branch of facial artery supplies to nasal vestibule.
Internal Carotid Artery
Ophthalmic artery, a branch of internal carotid artery (ICA) provides blood
supply through:
■ Anterior ethmoidal artery gives branch to superior turbinate.
■ Posterior ethmoidal artery supplies to sphenoethmoidal recess area.
Both anterior and posterior ethmoidal arteries give medial and lateral
branches. e medial branches supplies the superior septum and Little’s area.
Section 7 Clinico-Radiological Approach384
Anatomically important structures which are involved in epistaxis are
(Fig. 27.1B):
■ Little’s area: Situated in the anteroinferior part of septum, described by
James Little in 1879.2 It contains Kiesselbach’s plexus, a vascular network
formed by branches from septal branches of SPA, greater palatine artery,
and septal branch of superior labial artery, anterior, and posterior
ethmoidal arteries. e vascular anatomy of this plexus was described by
Wilhelm Kiesselbach in 1884.
2
■ Woodru plexus: Situated at inferoposterior end of inferior turbinate;
and formed by branches from ascending pharyngeal artery, posterior
nasal branch of sphenopalatine and SPA.
ETIOLOGY
Epistaxis can be classied depending on anatomical location, onset, severity,
causing/risk factors, and age as:
■ Anterior or posterior
■ Primary or secondary
■ Traumatic or nontraumatic
■ Acute or chronic
■ Pediatric or adult.
About 90% of nose bleeding originates from Little’s area.
■ e most common cause of epistaxis in children is digital trauma and
hypertension in people over 40 years of age. Most often primary epistaxis
is idiopathic and the various causes of bleeding are documented in
Table 27.1 and Figures 27.2 to 27.5.
■ It is frequently seen in dry season and in less humid environments.
ese factors increase excoriation and cracking of nasal mucosa, loss
Table 27.1: Causes of epistaxis.
Traumatic Nontraumatic
• Nose picking
• Facial injury
• Impacted foreign body
• Surgery: Ear-nose-throat
(ENT)/maxillofacial/
ophthalmic
• Nasal intubation
• Septal spur/septal deviation/septal perforation
• Allergic rhinosinusitis
- Nasal polyps
• Rhinosporidiosis
• Benign tumors (e.g. inverted papilloma, juvenile
angiobroma) (Figs. 27.2 and 27.3)
• Malignant tumors (e.g. squamous cell carcinoma)
• Hereditary hemorrhagic telangiectasia
• Vascular malformations (Figs. 27.4 and 27.5)
• Granulomatosis with polyangiitis
• Hypertension
• Coagulopathies: Hemophilia, thrombocytopenia
• Liver disease
• Drugs: Nasal sprays, drug abusing, anticoagulants
(heparin, warfarin)
• Antiplatelet (e.g. aspirin, clopidogrel)
385Chapter 27 Approach to Epistaxis
of mucosal integrity causing exposure of underlying vessels to trauma
leading to nose bleeding.
1,2
INVESTIGATIONS
e following investigations should be performed after stabilizing the patient
(detailed later):
■ Endoscopic examination to locate the site of bleed
■ Complete blood picture to determine amount of blood loss
■ Renal function tests to assess the renal damage in severe epistaxis
■ Liver function tests for coagulation factors
A
Figs. 27.2A and B: Juvenile nasopharyngeal angiobroma. (A) Enhancing mass in the
nasopharynx (asterisk). Widening of pterygomaxillary ssure (arrow); and (B) Extension into
pterygopalatine fossa (block arrow) and sphenoid (arrowhead).
A
Figs. 27.3A and B: Magnetic resonance imaging (MRI) of juvenile nasopharyngeal
angio broma. (A) T2W hyperintense mass lesion located in left nasopharynx. Widening of
pterygo maxillary ssure (arrow); and (B) Intense enhancement after contrast administration
(arrow).
B
B
Section 7 Clinico-Radiological Approach386
A
Figs. 27.4A and B: (A) High ow arteriovenous malformation (arrow) of nose causing
epistaxis; and (B) Computed tomography (CT) angiogram showing large feeder from left
linguofacial trunk.
A
Figs. 27.5A and B: Arteriovenous malformation of nose causing epistaxis. (A) Multiple
tortuous ow voids over root of nose on T2W fat suppressed MRI (arrow); and (B) MR
angiography: Feeding artery from ICA (arrow) and ECA (block arrow).
(ECA: External carotid artery; ICA: Internal carotid artery; MRI: Magnetic resonance imaging).
B
B
■ Prothrombin time (PT), activated partial thromboplastin time (APTT),
and platelet counts
■ Coagulation prole such as serum brinogen, plasminogen, brin
breakdown products (FBPs), von Willebrand factor (VWF) antigen, etc.
■ Imaging (vide infra)
■ Diagnostic angiography if planning to embolize the patient.
IMAGING
■ Cross-sectional imaging protocol for epistaxis depends on the severity of
epistaxis and suspected cause based on clinical evaluation
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