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women are similarly affected. Patients
may present with constitutional complaints like fever, night sweats,
fatigue, loss of appetite, and weight.
It is Multisystem autoimmune disease. Clinical features of WG can be
divided into three categories.
• Type 1 GPA—It is characteristic
by prolonged upper respiratory
tract infection.
• Type 2 GPA—Pulmonary involvement is often present and is associated with a cough, hemoptysis,
and cavitary lesions on chest
radiography.
• Type 3 GPA is a widely disseminated form of the systemic disease and commonly consists of
upper and lower airway involvement, cutaneous lesions, and progressive renal involvement.
History, examination, radiologic, and
biochemical data ndings help in diagnosis. The nasal cavity examination usually
shows septal perforation with or without
granulomatous tissue (Fig.4.5). Patients
also have abnormal erythrocyte sedimentation rate, hemoglobin, serum creatinine, and serum c-ANCA levels. These
serologic ndings in conjunction with
Fig. 4.5 Nasal endoscopy is showing large septal perforation with crusting and atrophy of surrounding tissue
(Courtesy—Dr. Hitesh Verma, Associate Professor,
AIIMS, New Delhi, India)
nasal biopsy can provide a denitive
diagnosis of WG. The c-ANCA test is
highly sensitive for GPA, but a negative
result does not exclude the diagnosis.
The main agents used to induce remission are glucocorticoids, cyclophosphamide, and/or methotrexate [7, 8].
(B) Sarcoidosis—It frequently involves
the lymphatic system, lungs, liver,
spleen, and bones. It occurs most
commonly between the ages of 20
and 40years with women are slightly
more often affected than men. The
etiology of sarcoidosis is unknown.
It is characterized by a seemingly
exaggerated immune response
against an unknown antigen.
Sarcoidosis is manifested by the
presence of multiple noncaseating
granulomas in affected organ tissues.
The sarcoid granuloma consists of a
central area of tightly packed epithelioid cells surrounded by lymphocytes and broblasts. The lung is the
primary organ affected by sarcoidosis. Approximately 40% of patients
have extrapulmonary involvement.
The involvement of the nose and
paranasal sinuses by sarcoidosis is
relatively infrequent with the incidence ranging between 1% and 6%.
Symptoms of nasal involvement are
nasal obstruction, epistaxis, dyspnea, nasal pain, epiphora, and anosmia. Nasal sarcoidosis commonly
affects the mucosa of the septum and
inferior turbinate. On examination,
the nasal mucosa is dry and friable
with crusts. Submucosal nodules
with a characteristic yellow color
may be noted. In more advanced disease, irregular polypoid, friable
mucosa is seen and bleeds readily.
More severe inltration may lead to
septal perforation or oronasal stulae. Diagnosis is based on a combination of histologic, radiographic,
immunologic, and biochemical data.
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Pulmonary ndings of either hilar
lymphadenopathy or pulmonary
brosis are common. Biochemical
examination shows elevated serum
or urinary calcium. Serum angiotensin-converting enzyme (ACE) elevations occur in 83% of patients with
active sarcoidosis, which has become
very useful for the diagnosis and for
monitoring of relapse. The diagnosis
of sarcoidosis is conrmed by the
presence of noncaseating granulomas, composed of multiple epithelioid cells and Langerhans giant cells
in the nasal mucosa. Negative stains
for fungus and acid-fast bacilli help
to support the diagnosis. Stage I sarcoidosis undergo spontaneous remission within 2years without specic
treatment. Sarcoidosis with elevated
ACE values or extrapulmonary
involvement usually requires treatment; this statement applies to most
cases of nasal sarcoidosis. The
mainstay of treatment for sarcoidosis is systemic corticosteroids.
Methotrexate has been used to treat
nasal sarcoidosis successfully. Nasal
symptoms may be treated with nasal
saline irrigations and topical nasal
steroids. Secondary infections
treated with culture-directed antimicrobial therapy. Surgery is advisable
in medically controlled symptomatic
nasal obstruction or chronic sinusitis, in selected patients [8, 9].
(C) Churg–Strauss syndrome—
Eosinophilic granulomatosis with
polyangiitis (EGPA) traditionally
termed, Churg–Strauss syndrome is
a rare systemic necrotizing vasculitis
that affects small-to-medium-sized
vessels. It occurs equally among
men and women with mean age of
50 years. Autoimmunity is evident
with the presence of hypergammaglobulinemia, increased levels of
immunoglobulin E (IgE), rheumatoid factor, and Antineutrophil cyto-
plasm antibody (ANCA). CSS is
characterized by necrotizing vasculitis of small and medium-sized vessels, Necrotizing extravascular
granulomas, eosinophilia of the vessels and perivascular tissue. CSS
consists of three phases:
1. A prodromal phase with allergic
rhinitis and asthma
2. an eosinophilic inltrative phase
with chronic eosinophilic pneumonia (Loefer syndrome) or
gastroenteritis, and
3. A systemic, life-threatening vasculitis with granulomatous
inammation.
The patients presented with nasal crusing &
polyposis, distringuished from GPA is by
extensive polyposis on both side & asthma.
The c-ANCA test result is also negative in
CSS, although perinuclear antineutrophil
cytoplasmic antibodies (p-ANCAs) is
found in 70% of patients. Glucocorticoids is
the treatment for CSS whereas cyclophosphamide may be helpful in life- threatening
cases or in patients with poor prognostic
factors. Rituximab (B-cell- depleting monoclonal antibody) has been used with favorable responses in patients with CSS
refractory to conventional treatments. The
anti-IgE monoclonal antibody omalizumab
has demonstrated a corticosteroid-sparing
effect in refractory or relapsing
EGPA. Mepolizumab an interleukin-5
antagonist monoclonal antibody (IgG1
kappa) is being studied for its efcacy in
CSS [8, 10].
(D) T-cell lymphoma—It is extra-nodal
NK/T-cell lymphoma, nasal type
(ENKL) is a rare form of nonHodgkin’s lymphoma. Disease
causing destruction of the midline
structures of the palate and nasal
fossa, so it is also known as midline
lethal granuloma. Histopathology
shows the presence of polymorphic
lymphoid inltrate of mature,
immature, and atypical lymphocytes, plasma cells, histiocytes,
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eosinophils with necrosis of cells.
Immunohistochemical studies demonstrate positivity for T-cell markers like CD2, CD7, CD45RO, and
CD43 and natural killer cell marker
CD57.35. The causative role of
EBV in the pathogenesis of T-cell
lymphoma has been strongly suggested. Initial symptoms are nasal
obstruction, pus, and serosanguinous nasal discharge. As the disease
progresses, unilateral mucosal
ulceration with extension into the
palate, maxillary sinus, and upper
lip is seen (Fig.4.6). Oronasal stula and nasal septal perforations
are frequently present. The characteristic clinical feature with necrotizing atypical cell exudates on
histopathology suggests the diagno-
sis. Therapy for localized disease is
radiotherapy. Chemo-radiotherapy
is the treatment for advanced lesion
[11, 12]. The chemotherapy regimens are mentioned in Chap. 10.
4.1.2 Other Granulomatous
Pathology
Inammatory Pseudotumor (IPT)—It is benign
idiopathic non-neoplastic inammatory disease
and it can involve any organ. It presents with history of the progressive, locally destructive mass
lesion. Radiologically, it is inltrative in surrounding structures so it can mimic as skull base
osteomyelitis and invasive fungus sinusitis. It is
isointense on T1 and hypointense on T2 MRI
images. It most commonly involves orbit whereas
nose and paranasal sinus involvement are relatively rare. Immunoglobulin G4 level can be
raised in IPT.The nal diagnosis of IPT is based
on characteristic histopathology nding where
tissue shows the presence of dense lymphoplasmocytic inltration with obliterative phlebitis,
storiform brosis. Lymphoplasmocytic inltration is seen in IgG4 related granulomatous lesions
with serum IgG level above 135mg/dl. The most
accepted treatment modality is systemic steroid,
radiotherapy alone, or in combination. Surgery
and immune-suppression are also mentioned as
modality in few reports [13].
Fig. 4.6 The clinical photograph is showing reddish skin
over the right half of nose with widening of ala of the right
side (Courtesy—Dr. Hitesh Verma, Associate Professor,
AIIMS, New Delhi, India)
4.2 Part B: Atrophic Rhinitis
Atrophic rhinitis is a chronic inammatory condition characterized by progressive atrophy of the
nasal mucosa and underlying bone of the turbinates leading to the formation of thick crusts and a
constant foul smell (Ozaena) in the nose. The natural ostium of the sinuses is visible in routine nasal
endoscopy without effort. It can be of two types—
Primary and Secondary. Histopathological examination reveals the presence of squamous
epithelium instead of ciliated columnar epithelium. The choice of investigation is prescribed on
the basis of history for secondary atrophic rhinitis. The selection of management is based on
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symptomatology and response. The rst line of
management is to increase mucosal clearance by
nasal douches. The last management option is the
closure of the nasal cavity for certain period.
Primary Atrophic rhinitis is multi-factorial in
origin. Hereditary, as the disease is known to
involve more than one member in the same family.
In some cases, it usually involves females more
than males and starts at puberty. The disease is selflimiting, tends to cease after menopause thus hormonal inuence cannot be ruled out. It is more
common in hot and humid climate specially in the
low socioeconomic group. Nutrition has also been
shown to play a vital role as deciency of vitamin
A, D, or iron or some other dietary factors have
been associated with the disease and are likely
causes. Autoimmune process in which viral infection or some other unspecied agents trigger antigenicity of nasal mucosa. The antibody released
causes destruction of the nasal mucosa is also postulated. The most widely accepted fact is the infective process where in various organisms have been
cultured from cases which are Klebsiella ozaenae,
(Perez bacillus), diphtheroids, P. vulgaris, E. coli,
Staphylococci, and Streptococci. They are all considered to be secondary invaders responsible for
foul smell rather than the primary causative organism. Specic infections like syphilis, lupus, leprosy, and rhinoscleroma are the etiology for
secondary atrophic rhinitis which may cause
destruction of the nasal structures leading to atrophic changes. Atrophic rhinitis can also result from
long-standing purulent sinusitis, radiotherapy to
the nose, or excessive surgical removal of turbinates [14]. Unilateral Atrophic Rhinitis—changes
in the wider side of the nasal cavity is sometimes
seen in cases of marked septal deviation.
4.2.1 Pathology
The characteristic feature is squamous metaplasia of the normal ciliated columnar epithelium
along with its endarteritis obliterans is seen in the
mucosa, periosteum, and bone leading to atrophy
of seromucinous glands, venous blood sinusoids,
and nerve elements [15]. The bone of turbinates
undergoes resorption causing the widening of
nasal chambers. Paranasal sinuses are small due
to their arrested development. Young and Taylor
16] have proposed that atrophic rhinitis is of two
[
types, depending upon the vascular involvement
into two types. Type I is major subtype (50% to
80%) and is characterized by endarteritis obliterans, periarteritis, and periarterial brosis of terminal arterioles as a result of chronic infection
with round cell and plasma cell inltration. Type
II is minor subtype (20% to 50%) and shows capillary vasodilation with active bone resorption.
Infection affects the surfactant system leading to
surfactant decit [17] through several mechanisms including, the absence of noteworthy SP-A
gene up-regulation and diminution of SP-A protein reserves, also inammatory cytokines produced in response to sepsis inhibiting the
synthesis of surfactant leading to decrease the
efciency of mucociliary clearance also, surfactant deciency impairs opsonization and phagocytosis of bacteria thus developing into a vicious
cycle of colonization of nasal mucous by bacteria
and causing destruction overtime.
4.2.1.1 Clinical Features
The disease is commonly seen in females and
starts around puberty. Merciful anosmia is a term
characterized by the foul smell from the nose but
the patient herself is unaware of the smell due to
marked anosmia which accompanies these
degenerative changes thus making the patient a
social outcast. Patient may also complain of nasal
obstruction in spite of unduly wide nasal chambers. This is due to large crusts lling the nose
with atrophy of nerve ending. Epistaxis may
occur when the crusts are removed. Complain of
decreased hearing and fullness of ear due to
obstruction to eustachian tube. On examination,
anterior rhinoscopy shows the nasal cavity to be
full of greenish or grayish black dry crusts covering the turbinates and septum, which bleeds if
removed (Fig.4.5). On removal of crusts, nasal
cavities appear roomy with atrophy of turbinates
which may be reduced to mere ridges and the
posterior wall of nasopharynx can be easily seen.
Nasal mucosa appears pale and dermatitis of the
nasal vestibule may be present. Septal perforations can be seen leading to saddle nose deformity. Atrophic changes may also be seen in the
pharyngeal mucosa which appears as dry and
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glazed with crusts leading to atrophic pharyngitis. Sometimes the atrophic changes may extend
to the laryngeal mucosa causing cough and
hoarseness of voice typical of Atrophic Laryngitis.
middle ear effusion, tympanic membrane retractions due to obstruction to eustachian tube causes
hearing-impairment in the minority of cases [18].
Paranasal sinuses are usually small and underdeveloped with thick walls. The presence of 2 or
more features beyond 6 months are in favor of
atrophic rhinitis: recurrent epistaxis, episodic
anosmia, nasal purulence, crusting, surgical
intervention in two or more sinuses, and presence
of chronic inammatory disease [19].
4.2.1.2 Investigations
Mainly aim to establish the diagnosis by excluding secondary causes of atrophic rhinitis and other
granulomatous conditions. Low hemoglobin and
peripheral blood smear show microcytic hypochromic picture pointing towards iron deciency
anemia. As bacterial infection is seen, there is
raised total leukocyte count (TLC) and differential leukocyte count (DLC) show lymphocytosis.
Commonly, low Serum protein and plasma vitamin levels are seen due to malnutrition. Other
tests done to rule out secondary causes are the
erythrocyte sedimentation rate (ESR) which is
raised in tuberculosis and granulomatous infection. Blood sugar is to rule out diabetes mellitus.
VDRL test is to diagnose secondary to syphilis.
Chest X-ray and Mantoux test/enzyme-linked
immunosorbent assay (ELISA) for tuberculosis.
Skin biopsy is to get the diagnosis of leprosy.
Nasal biopsy is for granulomatous diseases such
as lupus, leprosy, scleroma, and gumma. CT scan
of paranasal sinuses shows mucoperiosteal thickening of paranasal sinuses, loss of denition of
osteomeatal complex due to resorption of ethmoidal bulla and uncinate process, hypoplastic
maxillary sinuses, enlargement of the nasal cavity
with the erosion of the lateral nasal wall, and atrophy of inferior and middle turbinates.
crusts and the associated infection, putrefying
smell, and to further check crust formation. alkaline nasal douching solution is made by dissolving a teaspoonful of powder containing soda
bicarbonate one part, sodium biborate one part,
sodium chloride two parts in 280 ml of water.
Saline acts as solvent and it washes thick mucus,
crust, and debris. Nasal douches also increase
mucosal humidication and ciliary function. The
solution is run through one nostril and comes out
from the other. It loosens the crusts and removes
thick tenacious discharge. Initially, irrigations are
done two to three times a day but later once every
2–3days is sufcient. After crusts are removed,
the nose is painted with 25% glucose in glycerine. This inhibits the growth of proteolytic organisms which are responsible for foul smell. In
place of this antibiotic spray can also be used like
Kemicetine antiozena solution contains chloromycetin, oestradiol, and vitamin D2 but antibiotics are not having much role in the treatment of
atrophic rhinitis. Budesonide based nasal wash
(2ml in 1000ml saline irrigation solution) is also
recommended after saline nasal douches to
improve symptomatology.
Other treatment strategies that have shown
benet are oestradiol spray which has been found
to increase vascularity of nasal mucosa and
regeneration of seromucinous glands for Young
and Taylor Type1 not Type 2. Placental extract,
when injected submucosally in the nose may provide some relief. A potassium iodide oral preparation promotes and liquees nasal secretion
[20]. Mitomycin C, platelet-rich plasma, and
ozone were tried as an adjuvant treatment with
nasal douches but both medications were not
showed any signicant benet. Nasal endoscopic
surveillance is recommended twice a year to
clear crusting and to remove adhesion till symptoms persist.
4.2.3 Surgical Management
4.2.2 Management Aim
Complete cure is not yet possible. Goal of treatment is to maintain nasal hygiene by removal of
The surgeries can be broadly classied into four
categories with different aims.
1. Surgeries for narrowing the nasal cavities—
Nasal chambers are very wide in atrophic rhi-
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nitis and air currents dry up secretions leading
to crusting. Narrowing the size of the nasal
airway helps to relieve the symptoms. Among
the techniques followed for narrowing the
nasal cavities initially Wilson injected
Submucosal a mixture of 50% Teon in glycerin paste. Then insertion of the implant under
the mucoperiosteum of the oor and lateral
wall of the nose and the mucoperichondrium
of the septum was done and the types of
implants used can be classied into two
(a) Living tissue implants
(i) Autogenous—dermofat, bone,
cartilage
(ii) Homogenous—placenta
(iii) Heterogenous—bioimplant
(b) Synthetic implants—acrylic, silicone,
Teon, proplast
2. Surgeries to promote regeneration of normal
mucosa: Young’s operation [21]—In it both
the nostrils are closed completely just within
the nasal vestibule by raising aps. They are
opened after 6months or later. In these cases,
mucosa may revert back to normal and crusting reduced. To avoid the discomfort of bilateral nasal obstruction, modied Young’s
operation was devised which aims to partially
close the nostrils instead of complete closure.
It is also claimed to give the same benet as
Young’s (Fig.4.7).
Fig. 4.7 The clinical photograph is showing modied
Young’s operation. The catheter is placed to prepare small
size nostril (Courtesy—Dr. Hitesh Verma, Associate
Professor, AIIMS, New Delhi, India)
3. Surgeries to increase lubrication of dry nasal
mucosa: There are two main techniques used
one is Raghav Sharan’s operation [22], in which
implantation of maxillary sinus mucosa is done
in the nostril. And the other is Wittmack’s technique, where implantation of the Stenson’s duct
is done (parotid duct) into the maxillary antrum.
4. Surgeries to improve the vascularity of the
nasal cavities: Sympathetic tone causes vasoconstriction and emptying of the venous
sinusoids via the arteriovenous anastomosis.
A reduction in sympathetic tone causes venous
sinusoids dilatation along with the increase in
blood supply by decreasing the vasoconstriction which is being utilized in these procedures that are satellite ganglion block, cervical
sympathectomy, pterygopalatine fossa block,
and juxta-nasal sympathectomy.
Number of surgical options is mentioned in
literature but no control trial is performed till
date for the efcacy of different procedures
[20].
4.3 Part C: Maxillofacial Trauma
4.3.1 Introduction
Maxillofacial trauma presents in emergency as
part of polytrauma or standalone facial trauma.
The common causes include motor vehicle accidents, fall from height, or assault. Maxillofacial
trauma is very commonly associated with neurological and eye trauma, along with possibility of
solid viscera injury. This necessitates team
approach to this entity. Like any trauma, principles of Advanced Trauma Life Support (ATLS)
should be followed and attention to Airway,
Breathing, Circulation, Disability, and Exposure
(ABCDE) be done appropriately.
Non-comminuted maxillary fractures seldom
bleed profusely. At the same time, in severe fractures nasal packing alone to control bleeding may
be insufcient as splayed walls of the nasal cavity and/or palatal process of maxilla will not
allow the packing to generate enough pressure to
control bleeding. In such cases, airway securing
followed by both oral and nasal packing can be
considered (Fig.4.8a, b).
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ba
Fig. 4.8 (a) Patient with nasoethmoidal and bilateral
maxillary fracture who needed securing of airway and
oral and nasal packing to control bleeding. (b) 3D CT
reconstruction of the same patient shows severely com-
4.3.1.1 Assessment ofaMaxillofacial
Trauma Patient
The mechanism of injury is crucial to understanding the extent and pattern of trauma. The
direction, amount of force, and object with which
trauma is sustained gives an insight into the pattern of injury, hence a careful history about the
circumstances how the trauma was sustained
needs to be enquired. Careful attention to the
scalp and facial wounds for laceration, contamination, and foreign material/debris impaction is
needed. Facial skeleton should be assessed in a
structured protocol to evaluate frontal bones,
supra, and infraorbital margins, nasal bones,
zygomatic arch and mandible. Observe for any
step deformity or discontinuity. Intraoral assessment for occlusion, hematoma in the oor of
mouth, missing/fractured/avulsed teeth is imperative (Fig.4.9). Orbital assessment for telecanthus, mobility, acuity, pupillary size, and reaction
should be done. Anterior rhinoscopy is done for
septal fracture/hematoma. Sensation over the
face along the distribution of infraorbital and
mental nerves is important in preoperative period
in a conscious patient. This may prevent potential
postoperative medicolegal issues. Coexistent
medical conditions like renal, hepatic, or cardio-
minuted nasoethmoidal complex and bilateral maxillary
fractures leading to splaying of lateral nasal wall. Bleeding
in such a case may not be controlled by nasal packing
alone
Fig. 4.9 Hematoma in oor of mouth of and edentulous
patient who had fracture mandible
vascular ailments along with any coagulopathies,
should be ruled out which may have a bearing on
wound healing and postoperative complications.
4.3.2 Imaging
Multidetector CT scan with three-dimensional
shaded surface display is standard for evaluation
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Fig. 4.10 3D shaded surface display with fractures
involving left fronto-zygomatic buttress, left angle of
mandible, right parasymphysis, midline maxillary, and
left frontal process of the maxillary bone
(Fig.4.10). X-ray of the skull in anteroposterior,
lateral, and submentovertical view along with
X-ray mandible lateral oblique view may be done
if CT scan is not available.
4.3.3 Timing ofSurgical
Intervention
In cases of midfacial, nasal, zygomaticomaxillary complex, and frontal fractures, early operative intervention may not be feasible due to
concomitant signicant facial swelling and/or
intracranial trauma. Hence, the surgical intervention is planned after the reduction in swelling. In
patients with solid organ or hollow visceral
trauma too, a denitive management of these
injuries takes priority. Only after any other vital
organ injury has been assessed and addressed,
facial trauma care should be planned.
G. Gupta et al.
Fig. 4.11 Image shows fracture of right ramus of mandible. Also seen are midline maxillary fracture, right side
Le Fort 2 maxillary fracture, and fracture of the frontal
bone
nasotracheal intubation is adequate. For Le Fort 2
and Le Fort 3 fractures, a submental intubation or
tracheotomy is considered.
4.3.4.1 Mandibular Fractures
Based on the location, they are divided into condylar/subcondylar, parasymphyseal (between
mandibular canines)/symphyseal (between central mandibular incisors), ramus (Fig. 4.11)
(posterior border of masseter to height of sigmoid notch), angle (third molar to posterior border of masseter), body (distal part of mandibular
canine to distal mandibular second molar), and
alveolus [
23].
Condylar fractures may be intracapsular or
extracapsular. Since these are often missed, a
keen observation is needed during clinical examination. A small wound on the chin, malocclusion
with otherwise preserved mandibular arch, diffuse parotid swelling, and parotid area crepitus
are subtle pointers (Fig.4.12a, b).
Intermaxillary xation is done by closed
(tooth-borne/bone-borne) or open techniques.
4.3.4 Airway Management During
Surgery
For isolated mandibular, zygomaticomaxillary
complex, and Le Fort 1 fractures of midface, an
1. Tooth-borne closed techniques—Erich arch
bars, interdental wires (Ivy loops/eyelet wires,
etc.) or lingual splints.
2. Bone-borne techniques—skeletal suspen-
sion wires, IMF screws, external xators,
hybrid systems.
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Fig. 4.12 (a) Left parotid swelling and ear bleeding in a
patient with the left condylar fracture. The patient was
otherwise well preserved with no other apparent facial
Open techniques are preferable and are based
on AO/ASIF guidelines. These methods includetwo plate xation, reconstruction plate, lag
screws. Fracture line can be accessed by transoral/transbuccal approach (body/symphysis/
parasymphysis), transcervical-submandibular
approach (angle), transcervical-retromandibular
approach (ramus/subcondylar), or endoscopic
approach (subcondylar). Some fractures of
ascending ramus and angle can be plated by transoral approach using a transbuccal device for
xation.
4.3.5 Management ofNasal Bone
Fractures
Nasal fracture is classied into ve subtypes on
clinical basis
• Grade 0—No displacement.
• Grade 1—The deviation of nose is less than
50% of width of bridge of nose.
• Grade 2—The deviation of nose is more than
50% to almost equal of width of bridge of
nose.
• Grade 3—The deviation of nose is more than
width of bridge of nose.
• Grade 4—It almost reaching to the cheek.
Nasal fractures are also divided on the basis of
patterns of damage.
injury. (b) Same patient showing malocclusion due to
condylar fracture
Category 1 Fracture
In this, fracture segments
are generally maintained position by their inferior attachment with upper lateral cartilage. It
occurs in less severe form of trauma and grade 1
fractures come under category 1 fracture.
Chevallet was the rst documenting person so it
was also known as Chevallet fracture.
Category 2 Fracture Nasal bones, frontal process of the maxilla, and septal bones are involved
in this fracture. It is seen in the more severe form
of trauma. Grade 2 and above fractures come
under category 2 fractures. It is also known as
Jarjavay fracture (C shaped fracture).
Category 3 Fracture
It involves all nasal bone
with orbit, ethmoid bone, and any other facial
bone. Clinically, patient may have pig-like
appearance. It is also classied into two, depending upon skull base involvement. In type 2, anterior cranial base, posterior wall of frontal sinus,
and optic nerve is involved.
For evaluation of nasal bone fractures, clinical
assessment is most informative. Additionally,
X-rays (Water’s view, lateral view) and in select
cases (nasoethmoidal fractures, minimally
depressed fractures at rhinion/ nasion) CT may
be requisitioned.
For simple fractures, closed reduction with
Asch or Walsham forceps with digital manipulation is carried out (Fig.4.13a, b). Septal straight-
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Fig. 4.13 Preoperative (6a) and postoperative (6b) image of a patient with nasal bone fracture who underwent closed
reduction
G. Gupta et al.
ening is done if required. If signicant septal
cartilage and septal fracture are present, emergency septoplasty can be considered. Telescoping
of fragments with signicant comminution may
merit external xation using lead plates or orthopedic plates [24].
4.3.6 Zygomatic Fractures
Fractures of zygomaticomaxillary complex (ZMC)
(also called trimalar, tripod, tetrapod, quadrapod)
may lead to infraorbital anesthesia, trismus, diplopia, enophthalmos, palpable bony suture line
abnormalities, and attened malar prominence.
Clinical evaluation includes the assessment of
malar depression, mouth opening, ocular examination for mobility and diplopia, and sensation over
area of V2 division. Open reduction and xation by
miniplates of ZMC fractures are carried out by
using a combination of approaches: vestibular for
zygomaticomaxillary buttress, subciliary/subtarsal/
transconjunctival for infraorbital rim, and brow/
eyebrow for lateral orbital rim [23]. Comminuted
and displaced fracture of zygomatic arch are
reduced and xed by coronal approach. Noncomminuted depressed fractures of arch that are
cosmetically and functionally signicant can
undergo closed reduction by temporal (Gilles) or
vestibular (Keen) approach using periosteal or
Rowe zygoma elevator.
4.3.7 Fractures ofMidface
These are usually classied as Le Fort 1 (oating
palate), Le Fort 2 (oating maxilla), and Le Fort 3
(craniofacial dysjunction). However, in the current
scenario of high-velocity injuries, fracture lines
may not follow lines of least resistance, which was
the basis of this classication, and mixed fractures
are more common presentation [23].
Impacted maxillae need to be disimpacted
using Rowe disimpaction forceps. Denitive
management is preferably by intermaxillary xation and open reduction and internal xation
using miniplates. Fractures can be accessed by
vestibular incision (Le Fort 1), a combination of
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