2. Introduction
⢠Covered with skin : may be involved in most dermatoses
affecting the facial skin.
⢠Number of cutaneous and systemic conditions has predilection
for the nose, e.g. sarcoidosis and lupus vulgaris.
⢠As a characterstic deformity
⢠Saddle nose : congenital syphilis or Wegener's granulomatosis
⢠Beaked nose: scleroderma.
⢠A peculiar shape of nose : indicates genetic syndrome
⢠Pointed nose : Bloom's syndrome,
⢠Nasolabial angiofibromas : points towards tuberous sclerosis.
⢠Since nose occupies prominent anatomical position on the face,
early diagnosis and treatment of any scarring or ulcerative lesion
is imperative.
2
3. Conditions of external nose
⢠Infections:
⢠acute and chronic
⢠Neoplasm :
⢠benign and malignant
⢠Sarcoidosis and other connective tissue disorders
⢠Melanocytic lesions
⢠Kaposiâs sarcoma
⢠Vascular lesion
⢠Cysts
⢠Nasal destructive lesions
⢠Dermatological disease
3
4. ďą Acute infections
ďąFurunculosis:
⢠A furuncle or boil is an acute infection of a hair follicle with
Staphylococcus aureus.
⢠Trauma from nose picking or plucking the nasal vibrissae is the
usual predisposing factor
⢠It commences as a hard tender small red nodule which enlarges and
becomes more painful and fluctuant.
⢠The majority of vestibular furuncles discharge into the vestibule
and resolve.
⢠A serious and fortunately now very rare complication of nasal
furunculosis is the spread of infection via the valveless facial veins
and superior ophthalmic veins to the cavernous sinus.
4
5. ⢠Cavernous sinus thrombosis produces a severe illness with fever, vomiting,
prostration and convulsions.
⢠Local changes include oedema with cyanosis of the eyelids and base of the nose
and chemosis, due to obstruction of the ophthalmic veins.
⢠Ophthalmoplegia and pupillary changes (dilated or small and immobile) are
common. Retinal haemorrhages and papilledema are late events.
⢠Squeezing of nasal furuncles is to be avoided to reduce the risk of blood-stream
spread.
5
6. Treatment of furunculosis
⢠Local hot fermentation : Increases blood supply and drainage, also provides some
analgesic effects.
⢠Antibiotic ointment
⢠0.5% Neosporin, 2% mupirocin ( covers MRSA strains ) , 0.1% chlorhexidine ( thrice daily )
⢠Analgesics
⢠Systemic antibiotics: If above measures fails or in patients with facial cellulitis.
⢠Penicillin resistant antibiotics -clindamycin, cephalexin, cloxacillin , ciprofloxacin (
For MRSA)
⢠In facial cellulitis or severe cases : close observations and
1. Amoxyclav 1.2 g IV q 8hrly (40mg/kg/day q 8 hourly)
2. Clindamycin 600mg IV q 8hrly ( 10-20mg/kg/day q 8 hourly)
3. Ciprofloxacin 200mg IV q 12 hrly ( C/I in children)
4. Alternative : Vancomycin 500mg q 6hrly or 1g 12 hrly (10-20 mg/kg 8 hourly)
⢠If recurrent furunculosis : consideration of Diabetes mellitus
6
7. Vestibulitis
⢠Inflammation of the vestibule with recurrent
crusting and pain, usually due to infection with
Staphylococcus aureus.
⢠It may also be caused by an irritant dermatitis-type
reaction such as occurs in acute coryza, due to
watery rhinorrhoea and rubbing.
⢠Alternatively, it may be part of an atopic diathesis.
⢠Vestibulitis presents as crusting and irritation in the
anterior nares with resulting nasal obstruction.
⢠Examination shows excoriated vestibular skin and
septal mucous membrane.
7
8. ⢠Rubbing or over-diligent cleaning of the nose by the
patient usually causes vestibulitis, particularly if, a
septum is deviated anteriorly and impinges on the lateral
wall of the nose.
⢠A deviation of the septum has predisposed to a chronic
vestibulitis (induration of vestibular skin with painful
fissures and crusting)
⢠Nasal vestibulitis may present with squamous epithelium
replacing the mucosa.
⢠Digital irritation, or the use of cocaine, which may also
lead to a septal perforation, may underlie this problem
8
9. Treatment
1. Suction cleansing of nasal discharge
2. Cleaning of crusts with hydrogen peroxide and antibiotic-steroid ointment
3. Oral antihistamines with decongestants ( 3- 5 days, TDS)
4. Antibiotics
⢠Amoxyclav 1g BD ( 40mg/kg/day BD in children)
⢠Clindamycin ( dalacin) 300mg TDS ( 10-20mg/kg/day TDS in children)
⢠Ciprofloxacin : 500mg BD ( contraindicated in childrens)
⢠Erythromycin : 500mg q 6hrly ( 30-50 mg/kg/day 6hrly in children)
⢠Azithromycin 500mg OD for 3 days ( 10mg/kg OD for 3 days)
⢠Cephalexin: 500mg q 6hrly ( 12.5-25mg/kg q 6hrly)
5. Chronic form : local steroid ointment and cauterization of base of fissure to promote
healing
6. In case of vestibular abscess : has to be drained
9
10. Erysipelas
⢠Bacterial infection of dermis and upper subcutaneous tissues usually caused by
group A streptococci.
⢠Most commonly affects infants, young children and older adults.
⢠Patients are usually febrile, swollen affected skin, indurated or peau d'orange
appearance , spreads peripherally.
⢠It is bright red, hot and shiny with a sharp border. Small vesicles, bulla ,
ecchymosis may develops.
⢠Occasionally involves the bridge of the nose and either sides in 'butterfly'
distribution.
⢠The diagnosis is clinical since bacteriological isolation of the offending
organism from the skin is unusual.
⢠Blood culture in the case of facial infections, Paired sera for antistreptolysin
(ASO) from days 1 and 14
⢠Treatment is with benzyl penicillin intravenously in the more severe cases.
⢠Mild cases may be adequately treated with oral antibiotics.
10
11. Cellulitis
⢠Cellulitis is an acute spreading inflammation of the skin involving the deeper
subcutaneous tissues, most commonly caused by group A streptococci and
Staphylococcus aureus.
⢠It resembles erysipelas, but as the inflammation is deep the margins tend to be ill-
defined, in contrast to the sharp margins of erysipelas.
⢠Facial cellulitis extending to involve the periorbital and orbital areas may be
complicated by cavernous sinus thrombosis
⢠Treatment is same as the erysipelas covering staphylococcus and streptococcus
with adequate analgesia.
11
12. Impetigo
⢠It is contagious superficial infection of the skin, can affect any
part of body, but particularly the face is involved.
⢠Bullous and non bullous types
⢠The bullous variety is caused by Staphylococcus aureus and non-
bullous impetigo may be caused by Staphylococcus aureus,
streptococcus or both together.
⢠Bullous impetigo is characterized by tense bullae 1-2 cm in
diameter or larger, which contain clear fluid initially. After
rupture, flat brownish crusts are formed.
⢠In non-bullous impetigo small pustules enlarge and rupture to
form the typical honey-coloured crusts.
⢠Except for the very localized cases impetigo should be treated
with systemic antibiotics (flucloxacillin or erythromycin)
12
13. Herpes simplex
⢠Herpes simplex type 1 or, 'cold sore' or 'fever blisterâ
⢠Most commonly affects the face ,lips, perioral area, cheeks and nose
⢠Initial prodrome of stinging / burning tiny grouped vesicles in skin , later becomes
cloudy and purulent, eventually dry and crust formations.
⢠Normally heals within 7-10 days.
⢠As herpes virus persists in sensory nerve ganglia the patient may suffer recurrent
episodes arising in the same area.
⢠Recurrences may be triggered by trauma, dental manipulation, strong sunlight, febrile
illnesses, upper respiratory tract infections, menses and stress.
Treatment
⢠Symptomatic treatment : mild uncomplicated herpes simplex requires no treatment.
⢠Topical acyclovir improves recurrent cutaneous infections ( twice daily for 7 days)
⢠Oral acyclovir 200-400mg five times a day for 7-10 days if severe constitutional
symptoms present
⢠Patients with eczema herpeticum should receive intravenous acyclovir as early as
possible
13
14. Herpes zoster
⢠Varicella zoster virus reactivation
⢠Erythematous macular or papular lesions painful within
distribution of nerve âmaxillary and ophthalmic nerve --
common
⢠Vesicles appear after 24 hrs, become purulent, rupture and
crust formation â disappear after 1 to 2 weeks
⢠Tip of nose- nasocilliary branch of ophthalmic nerve-
consultation to ophthalmologist also.
⢠Cheek, nose ,vestibule, palate- maxillary divison
⢠Treatment : Acyclovir, steroids along with analgesia
14
15. Warts
⢠Warts or verrucae are benign epithelial proliferations of the skin and mucosae caused by
infection with papillomaviruses.
⢠The common wart is caused by types 2 and 4 .
⢠Rough papules or distinctive filiform surface.
⢠Patients with warts on the nose are likely to request treatment for cosmetic reasons
⢠Liquid nitrogen cryotherapy is usually effective
⢠Other modalities
⢠Cautery
⢠Topical application of salicylic acid
⢠Laser therapy
⢠Pulse dye laser or carbon dioxide (CO2) laser.
15
16. Molluscum contagiosum
⢠Molluscum contagiosum is a common benign viral (poxvirus)
disease of the skin and mucous membranes that predominantly
affects children.
⢠Individual lesions usually 3-6 mm in size, are characteristic pink
or flesh-coloured dome-shaped papules with central umbilication.
⢠Patients with atopic dermatitis and those who are
immunosuppressed may develop persistent and extensive lesions.
Treatment
⢠In the majority of immunocompetent patients the condition is self-
limiting but resolution may be aided by liquid nitrogen
cryotherapy or by curettage
16
17. Chronic infections
Lupus vulgaris
⢠Rare, painful cutaneous infection with Mycobacterium
tuberculosis .
⢠By haematogenous, lymphatic or contiguous spread or latent
activation . Rarely lupus vulgaris may follow primary inoculation
tuberculosis or BCG vaccination.
⢠The lesions are usually solitary but two or more sites may be
involved simultaneously.
⢠Lupus vulgaris shows a predilection for the head and neck (90%).
⢠The initial lesion starts on the nose or cheek and slowly extends
into adjacent areas. The early lesion is a reddish-brown papule
with a gelatinous consistency. This gradually extends and
becomes more infiltrated.
17
18. ⢠The typical appearance later is of an irregular reddish-brown nodular plaque with a scaly
surface. When pressed with a glass slide (diascopy) the brown nodules, referred to as 'apple
jelly nodules', are more easily seen.
⢠The natural course of these lesions is slow peripheral extension.
⢠In ulcerative lupus vulgaris the underlying tissue may be affected by progressive necrosis,
and, if the nasal or auricular cartilage is involved, extensive destruction takes place. Scarring
is a prominent feature of lupus vulgaris.
⢠Atrophic scars occur subsequent to or independent of ulceration, and new 'apple jelly' nodules
develop within the scarred areas destruction.
⢠There is a risk that aggressive squamous cell carcinomas or, less commonly, basal cell
carcinomas and rarely sarcomas will develop in the scar tissue
Treatment
⢠Antituberculous chemotherapy is indicated, usually for 9 months.
⢠The clinical response to treatment is usually satisfactory.
⢠However, there may be residual hyperpigmentation
18
19. Syphilis
⢠The characteristic lesion of primary syphilis, the chancre, is a painless firm
button-like nodule at the site of treponemal penetration.
⢠Extragenital chancres usually occur on or close to the lips and may very
rarely involve the nose or nasal vestibule.
⢠Untreated chancres persist for 3-6 weeks while, with treatment, they
resolve in 1-2 weeks.
⢠The lesions of secondary syphilis are papular and involve the trunk, limbs,
palms and soles
⢠The lesion of tertiary syphilis, the gumma- painless nodule which breaks
down to leave a 'punched out' ulcer with a ragged necrotic floor. It heals
with scarring and tissue destruction.
⢠Snuffles or syphilitic rhinitis is an early and important sign of congenital
syphilis.
⢠Fissures or 'split' papules may develop at the angles of the mouth or lateral
to the external nares.
⢠Late congenital syphilis produces the classical stigma of saddle nose
deformity.
19
20. Treatment of syphilis
⢠Inj Benzathine penicillin G 2.4 Million units IM single dose
⢠Penicillin allergic cases
⢠Cap doxycycline100mg BD orally for 14 days
⢠Tab erythromycin 500mg q6 hourly orally for 14 days
⢠Inj ceftriaxone 1g daily iv/im for 14 days
⢠Childrens
⢠Single Im injection of benzathine penicillin 50000 units/kg upto 2.4 million
units
20
21. ďą Vascular lesions
ďąCapillary hemangioma
Affect 2.6% of all live births
⢠Seen after birth as pink to red macular lesion , that rapidly
increases in size.
⢠Lesions becomes raised and polypoidal
⢠Then attains the plateau size and resolves at the age of 7 years
⢠Treatment : Usually not required , if results in pressure effects of
important structures â surgery is treatment of choice
21
22. ďąCavernous haemangiomas
⢠Less common
⢠Large dilated or sinusoidal venous channels
⢠Lies deeper in dermis
⢠Appear in 1st month of life
⢠Ill defined smooth bluish red growth
⢠Involution less common
⢠Rx : unsatisfactory âcryotherapy, radiotherapy or surgery
difficult
ďąPyogenic granuloma
⢠Is common in nose and is common in children, young adults
and pregnant womens
⢠Treatment : Excision f/b cauterization of base
⢠If present on septum : excised with perichondrium
leaving cartilage intact
22
24. Dermoid cyst
⢠Cystic swelling lined by squamous epithelium containing desquamated cells
⢠Along the line of embryonic fusion â congenital / sequestration dermoid
⢠Root of nose at fusion lines of frontal process
⢠Fusion lines of frontonasal and maxillary processes
⢠Contains mixtures of hairs, sebum , desquamated cells, sweats.
It is of two types:
⢠Simple dermoid. Midline swelling under the skin but in front of nasal bones with no
external opening.
⢠Dermoid with a sinus. In infants and children, represented by a pit or sinus in the
midline of dorsum of nose.
24
25. ⢠Hair may be seen protruding through the sinus opening.
⢠In these cases, the sinus track may lead to a dermoid cyst
lying under the nasal bone in front of upper part of nasal
septum or may have an intracranial dural connection.
⢠In those with intracranial extension, sinus tract passes
through the cribriform plate or foramen caecum and is
attached to dura or has other intracranial connection.
⢠Meningitis occurs if infection travels along this path.
⢠Treatment of such cysts may necessitate splitting of the
nasal bones to remove any extension in the upper part of
the nasal septum.
⢠A combined neurosurgicalâotolaryngologic approach is
required in those extending intracranially so as to close
simultaneously any bony defect through which the
fistulous tract passed.
25
26. Encephalocele or
meningoencephalocele
⢠Neural tube defect , due to incomplete closure of neural tube during
development
⢠Is a herniation of brain tissue along with its meninges through a
congenital bony defect ( frontal , ethmoidal , temporal , occipital bone)
⢠An Extranasal meningoencephalocele presents as a subcutaneous
pulsatile swelling in the :
⢠At the root of nose (nasofrontal variety),
⢠Side of nose (nasoethmoid variety) or
⢠On the anteromedial aspect of the orbit (naso-orbital variety).
⢠Swellings show cough impulse and may be reducible.
⢠Treatment is neurosurgical; severing the tumour stalk from the brain
and repairing the bony defect through which herniation has taken place
26
27. Glioma
⢠Arises from glial cell (supporting cell) of brain or
spinal cord
⢠It is a nipped off portion of encephalocele during
embryonic development.
⢠Most of them (60%) are extranasal and present as
firm subcutaneous swellings on the bridge, side of
nose or near the inner canthus.
⢠Some of them are purely intranasal (30%), while
10% are both intraand extranasal.
⢠Extranasal gliomas are encapsulated and can be
easily removed by External nasal approach
27
28. Rhinophyma
⢠Rhinophyma or potato tumour is a slow-growing benign tumour
due to hypertrophy of the sebaceous glands of the tip of nose often
seen in cases of long-standing acne rosacea.
⢠It presents as a pink, lobulated mass over the nose with superficial
vascular dilation; mostly affects men past middle age.
⢠Patient seeks advice because of the unsightly appearance of the
tumour, or obstruction to breathing and vision due to large size of
the tumour.
Treatment modalities :
1. Decortication of thickened skin
2. Dermabrasion
3. Harmonic knife
4. Sometimes excision with skin grafting
28
29. Actinic/solar keratoses
⢠Actinic or solar keratoses are areas of dysplastic epithelium
arising in sun-damaged skin.
⢠They are ill-defined red or pink scaly patches which are rough
to touch.
⢠They have a predilection for the forehead, temples, tip of the
nose, vermilion of the lower lip and dorsum of the hands
⢠They are premalignant, progressing to low grade invasive
squamous cell carcinomas in approximately 10% of cases
⢠Actinic keratoses respond well to treatment with liquid nitrogen
cryotherapy.
⢠Other modalities : curettage or local 5- FU for large areas
29
30. Bowen's disease
⢠Bowen's disease refers to squamous cell carcinoma in situ and is characterized
clinically by a well-defined red scaly plaque.
⢠It responds to treatment with liquid nitrogen cryotherapy or topical 5-fluorouracil
⢠Other modalities : photodynamic therapy , excision
⢠Outstanding results has been noted with Imiquinod , which is not approved by
FDA
30
31. Basal cell carcinoma
⢠Synonym: basal cell epithelioma, rodent ulcer.
⢠Malignant tumour of the skin that arises from the basal cell
layer.
⢠Most commonly affect the face, 25% involving the nose
⢠Predisposing factors:
⢠Light skin color, poor tanning ability, freckling in childhood
⢠AIDS, immunosuppresive therapy
⢠Arsenic exposure
⢠Vaccination sites
⢠Chronic ulcers or burn scars
⢠Inactivation of tumor suppressor gene on chromosome 9.
31
32. ⢠A typical basal cell carcinoma is of Nodular variety : shiny papule with a pearly
translucent surface traversed by telangiectasia
Other types :
⢠Superficial type - Scaly plaque with raised edge
⢠Morpheaform BCC - White or yellow plaque with telangiectasia âulcerates and
form scar like lesion
⢠The typical pearly feature may be accentuated by either compressing or stretching the
surrounding skin and viewing the lesion with the aid of a side lamp.
⢠When the basal cell carcinoma becomes ulcerated (rodent ulcer), the raised rim of the
tumour retains the typical pearly telangiectatic features.
⢠Typically slow growing, if neglected can be destructive and locally invasive, but very
rarely metastasize
32
33. ⢠Small basal cell carcinomas involving the nose may be effectively treated by
curettage and cautery, excision, cryosurgery or radiotherapy in extensive
lesions.
⢠It is important that surgically removed specimens include an adequate margin (
minimum 4 mm healthy margin) of normal skin to reduce the risk of local
recurrence.
⢠The relative risk for recurrence of tumour on the nose is particularly high compared
to other locations.
⢠Ulcerative and sclerosing lesions may be deceptively extensive, and those extending
inside the nose should ideally be managed by microscopically controlled surgery-
mohs micrographic surgery
⢠Photodynamic therapy : As an adjunct in tumor recurrence case , elderly patients or
patients with medical conditions preventing surgery
⢠Pharmacological therapy : topical 5-FU , 5% imiquimod, tazarotene
33
34. Squamous cell carcinoma
⢠This is the second most common malignant tumour
(11%),equally affecting both sexes in 40â60 age group.
⢠It occurs as an infiltrating nodule or an ulcer with
rolled out edges affecting side of nose or columella.
⢠Nodal metastases are seen in 20% of cases.
⢠Early lesions respond to radiotherapy; more advanced
lesions or those with exposure of bone or cartilage
require wide surgical excision margin of 5mm of
normal tissues and plastic repair of the defect.
⢠Enlarged regional lymph nodes will require block
dissection
34
35. Fibrous papule of the nose
⢠This benign papule develops slowly in middle-aged
persons as a dome-shaped flesh-coloured, pink or
pigmented lesion which is usually sessile.
⢠It occurs as a single lesion on the nose, but occasionally
there are multiple papules which involve other parts of the
face.
⢠Most are asymptomatic and may be removed by excision
or 'shave' removal for cosmetic reasons or because of
bleeding.
⢠Diagnosis may be confirmed by the histological findings
which are characteristic.
35
36. Angiofibromas
⢠Firm discrete telangiectatic papules with a predilection for the
nasolabial furrows and chin and usually developing in
childhood or adolescence should raise the possibility of
tuberous sclerosis (epiloia).
⢠The presence of other stigmata of this autosomal dominant
condition like periungual fibromas or ash-leaf macules makes
the diagnosis easier, but there is a range of severity and the
condition may remain latent until adult life.
⢠Mental deficiency is present in 70% of cases and epilepsy is
also common.
⢠Angiofibromas may be few in number or numerous and
conspicuous.
⢠In cases of diagnostic doubt a skin biopsy should be carried out.
⢠The cosmetic appearance of angiofibromas may be improved by
the use of diathermy or laser.
⢠Lesions tend to recur after dermabrasion.
36
37. Naevi and lentigo maligna
⢠Naevi Compound, junctional and dermal naevi may
involve the nose.
⢠Junctional naevi:
⢠Dark brown macules with spots of black pigment
⢠Intradermal naevi:
⢠Solely in dermis with macule, papule or warts like
⢠Compound naevi :
⢠Mixed of both with raised brown lesions
⢠Spitz naevus:
⢠Rapidly growing red papule or nodule on the face in
children.
⢠Atypical naevi:
⢠Unevenly pigmented, large and more irregular than
the usual pigmented naevi
37
38. Congenital naevi
⢠Present at birth or appear upto 5 yrs
- Pale, enlarged ,darken and develop terminal hairs
- Giant form up to 20cm, disfiguring
- Malignant transformation in 4-6 percent cases
Acquired naevi
⢠Present mostly during childhood
⢠20-30 in no, smaller forms, remain stable through life
⢠Rarely become malignant.
⢠Lentigo maligna most commonly affects the cheek in elderly
persons. Clinically it is a flat pigmented patch with various
shades of brown and an irregular edge
⢠Its importance lies in its potential to develop into invasive
melanoma, usually after many years
38
39. Melanoma
⢠Melanoma, a malignant proliferation of melanocytes, affects the head and neck in 10-20% of cases.
⢠The commonest type is the superficial spreading melanoma which manifests as a pigmented lesion with
colour variegation and an irregular edge.
⢠However, unusual and some non-pigmented melanomas (desmoplastic and amelanotic) may
particularly affect the head and neck.
⢠Clinical stages of malignant melanoma
⢠Stage I â Primary lesion only
⢠Stage II â Regional nodal disease
⢠Stage III â Distant disease (nodal or visceral)
⢠Features of malignant melanoma:
⢠Asymmetry, irregular outline, varying colour and size
⢠Diameter > 1cm
⢠Superficial and nodular types.
⢠Superficial- common in face.
39
40. ⢠Histological diagnosis required
⢠Suspicious lesions: 1-2 cm diameter: excised with clear circumferential margin of
1-2 mm
⢠Confirmed lesion: Less than 1mm deep: can be removed with a 1cm margin of
normal tissue
⢠>1mm deep: excisions margins of 1-3 cm
⢠Special techniques are often required to perform successful reconstruction of the nose.
⢠Primary closure is not usually possible and the best reconstructions are performed with
the use of local flaps
40
41. Kaposi's sarcoma
⢠Kaposi's sarcoma is a multifocal neoplasm originating from the vascular endothelium.
⢠It may involve the nose in patients with acquired immune deficiency syndrome (AIDS).
⢠The early lesions are macules with a reddish-salmon colour. Within a week the colour
changes to purplish or brown and the lesions become nodular.
⢠Rarely there may be a single growth.
⢠The majority of patients develop multiple lesions
Treatment
⢠Chemotherapy : intralesional vinblastine
⢠External beam radiotherapy
⢠Argon laser therapy
⢠Systemic chemotherapy
⢠Radical surgical procedure rarely indicated due to systemic nature of this malignancy
41
42. Sarcoidosis
⢠Sarcoidosis is a chronic granulomatous disease of
unknown aetiology.
⢠Slight female preponderance , 20-40 years of age
⢠It is a 'multisystem' disorder but cutaneous disease may
occur without systemic involvement.
⢠Fibrinoid necrosis with non caseating granuloma
⢠Where cutaneous and systemic disease coexist, there is
poor correlation between the extent of the cutaneous
lesions and the severity or extent of systemic disease.
42
43. ⢠However, nasal involvement in sarcoidosis, particularly the lesions of lupus pernio)
and nasal rim papules have been associated with significant sarcoidosis of the upper
respiratory tract.
⢠These cutaneous lesions are markers of possible granulomatous infiltration of the
nasal mucosa and upper airway.
⢠Histological diagnosis is most important and based on evidence sarcoid granuloma
⢠Lupus pernio : nasal mucosa biopsy
⢠Other investigations : Chest xray, kveim test , ESR , serum calcium
⢠Treatment
⢠Cutaneous lesions: Local or intralesional steroids
⢠Persistent or disfiguring disease : systemic steroid therapy
⢠In lupus pernio: MTX , chlorambucil and azathioprine as immunosuppressive therapy
⢠As a adjunct laser therapy is implicated
43
44. SLE and DLE
Systemic lupus erythematosus (SLE) is a generalized autoimmune disorder with a
predilection for young females.
⢠It shows a spectrum of severity from a mild recurring illness to a fulminant rapidly
fatal disease.
⢠Multiple organ system involved : m/c joints, kidney and cardiopulmonary mainly.
⢠Psoriasiform, verrucous and lupus-erythematosus-like lesions may occur in addition
to patches of hypopigmentation.
⢠Characterstic butterfly rash which is intensely red on both cheeks , sharply
demarcated at nasolabial and cross bridge of the nose
⢠Nasal septal ulceration and perforation in form of epistaxis is rare( 5%)
44
45. CDLE
⢠Characterized by well-defined red scaly plaques which tend to heal by atrophy,
scarring and pigmentary change.
⢠Removal of the adherent scale may reveal horny plugs in the under surface -'carpet-
tack' sign.
⢠There may be areas of follicular plugging and hyperkeratosis.
⢠Facial lesions most commonly affect the cheeks, bridge of the nose, tip of the nose
and the ears.
⢠Examination of the scalp may show well-defined areas of scarring alopecia.
⢠CDLE-type lesions may occur in patients with SLE, but less than 5% of patients with
CDLE will progress to SLE.
⢠The overall prognosis for CDLE is good.
⢠However, there may be considerable psychological morbidity due to facial scarring
45
46. Diagnosis
The cutaneous lesions of SLE and CDLE may be histologically indistinguishable.
⢠The histological features hyperkeratosis, follicular plugging, epidermal degeneration
of the basal layer lymphocytic inflammatory infiltrate.
⢠Antinuclear antibodies are present in high titre in patients with active SLE and
antibodies to double-stranded DNA are specific to SLE.
⢠Other abnormalities include elevated ESR, hypergammaglobulinaemia, hy-
pocomplementaemia, anaemia, leukopenia, thrombocytopenia, positive rheumatoid
factor, a false positive test for syphilis and urinary abnormalities.
⢠Approximately 50% of patients with CDLE have haematological and serological
abnormalities.
⢠Antinuclear antibody, when positive, is usually present in lower titre than in SLE
and antibodies to double-stranded DNA are negative
46
47. Treatment
⢠The wide range of involvement and severity in SLE means that treatment must be
tailored to the individual's needs.
⢠Choice of therapy is dictated by the extent of vital organ involvement.
⢠Corticosteroids in high dose are required in acute disease, and may be combined
with azathioprine or cyclophosphamide.
⢠Lupus nephritis may respond to a combination of prednisolone and chlorambucil
⢠Patients must be advised to avoid strong sunlight which is well known to provoke
exacerbations of SLE
⢠Lesions of CDLE will improve with potent topical corticosteroids
⢠Active cutaneous lesions warrant topical corticosteroids under occlusion,
intralesional triamcinolone or hydroxychloroquine. Patients with active facial
CDLE or with residual scarring often gain considerable benefit from the use of
cosmetic camouflage.
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48. Wegener's granulomatosis
⢠Rare granulomatous necrotizing condition of the upper and lower
respiratory tract associated with generalized arteritis and focal or
diffuse glomerulitis
⢠Rhinological symptoms include nasal crusting, bloody rhinorrhoea,
progressive nasal obstruction and vague pain and tenderness of the
dorsum of the nose.
⢠Papular, plaque-like and ulcerative lesions are the most common
cutaneous signs.
⢠Granulomatous involvement of the nasal septum with dissolution of
cartilage leads to typical saddle nose deformity, and necrotizing
granulomatous lesions may lead to complete destruction of the nose.
⢠The skin elsewhere may show the 'palpable purpura' of cutaneous
vasculitis
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49. Diagnosis
⢠Antineutrophil cytoplasmic antibody with cytoplasmic staining (C-ANCA) has a
high sensitivity (96%) in patients with generalized active Wegener's
granulomatosis.
⢠Positivity is seen less commonly in active localized diseas
⢠e.
Treatment
⢠Systemic corticosteroids and cyclophosphamide .
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50. Relapsing polychondritis
⢠Relapsing polychondritis is a rare disease characterized by recurring episodes of inflammation
in cartilaginous tissues.
⢠Patients usually present with auricular chondritis and arthritis
⢠The chondritis manifests as acute onset of redness, heat, swelling and tenderness of the affected
part, mimicking cellulitis.
⢠Eventually more than 50% of affected patients will have involvement of the nasal cartilage.
⢠With recurrent bouts of inflammation the cartilage is destroyed and replaced with fibrous tissue,
resulting in 'cauliflower' ears and a deformed and obstructed nose.
⢠There may be collapse of the cartilages of the larynx and trachea.
⢠Other features include aortic aneurysm, mitral regurgitation and eye inflammation.
Treatment
⢠Systemic corticosteroids are used to control acute disease.
⢠The course of relapsing polychondritis is highly variable and spontaneous remission may occur.
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51. Other diseases affecting external nose
ďą Centrofacial ulcerations:
⢠Destructive processes of facial midline may signify any of a
range of infective, malignant or autoimmune diseases
⢠Term 'lethal midline granuloma' is a clinical description,
embraces Wegener's granulomatosis, polymorphic reticulosis
granulomatosis and idiopathic midline destructive lymphoid
disease.
⢠The majority of lymphoid granulomatosis are peripheral T-cell
lymphomas (occasionally B-cell lymphomas) causing
ulceration and destruction of the nose and paranasal sinuses.
⢠Treatment is with radiotherapy and initial treatment with oral
alkylating agents and steroids useful in newly diagnosed case
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52. ⢠Idiopathic midline destructive disease commences insidiously with oedema of nose
and nasal congestion f/b perforation of nasal septum, ulceration of hard palate and
extensive mutilation of centre of the face
⢠Histology of involved tissue shows a diffuse infiltrate of lymphocytes, leucocytes
and histiocytic-type giant cells.
⢠It may be distinguished from Wegener's granulomatosis by the absence of
necrotizing granulomas.
⢠The disease lasts from 3 to 20 months.
⢠Local high dose radiation offers the best hope of amelioration.
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53. Rosacea:
⢠Chronic disease of unknown aetiology , centre of face is most involved site
⢠Clinical features : erythema, crops of red papules and small pustules,
telangiectasia and facial oedema .
⢠In the most severely affected patients disfiguring enlargement of the nose,
paranasal areas may be affected in some patients
⢠The diagnosis is a clinical one.
Treatment
⢠Most stages of rosacea will improve with oral tetracycline 1 g/day.
⢠Topical metronidazole is also beneficial.
Seborrhoic dermatitis
⢠Disorder typically affecting sebaceous follicles rich area of face and trunk,
caused by yeast pityrosporum ovale
⢠Classically involves nasolabial folds as a red eruption with greasy scalehigh
prevailences in patients with AIDS
Treatment
oral and topical ketoconazole
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54. ďą Contact dermatitis
⢠Dermatitis localized to the nose and paranasal skin may be allergic due to contact with
nose drops or plants or irritant due to rubbing.
ďą Dermatitis artefacta
⢠Usually women who produces factitious disease to satisfy a psychological need .
Lesions may be produced by cutting , scratching , picking , burning or damaging the
skin with chemical
⢠Treatment of underlying psychological disorders.
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