DISEASES OF PINNA AND EXTERNAL EAR CONTD.

Dr.pournamy mohan

Haematoma auris

• Haematoma auris is a collection of blood between the auricular cartilage and perichondrium.

AETIOLOGY

• trauma

• occasionally the spontaneous rupture of a blood vessel

PATHOGENESIS• Pandya demonstrated experimentally in rabbits-

components of fibrosis, immature chondrogenesis and osteogenesis in the organizing haematoma.

• Ohlsen et al. demonstrated the subperichondrial site of the haematoma in rabbits

• and that, while subcutaneous haematomas resorb without consequence,

• subperichondrial serosanguinous fluid stimulates the proliferation of mesenchymal cells in the overlying perichondrium, with these chondroblasts forming new cartilage in seven to ten days which results in 'cauliflower ear' deformity.

• This occurs almost exclusively on the anterior surface of the auricle where the skin is tightly adherent to the underlying perichondrium

• shearing forces applied to the ear separate the perichondrium from the cartilage.

• On the posterior surface, intervening areolar tissue allows the skin to glide over the perichondrium.

• Rarely, a tear through the cartilage can allow haematomas to collect under the perichondrium on both sides of the cartilage.

CLINICAL PICTURE• history of trauma, often sports-related;

• wrestling and rugby scrumming classically producing these shearing injuries.

• Schuller et al demonstrated that in wrestlers, protective headgear provides only partial protection (26 percent chance of haematoma versus 52 percent unprotected) and that non-use is widespread.

• The haematoma is painless and inflammation is minimal.

Complication

• If left untreated-deformity of the pinna and the classic 'cauliflower' or 'wrestler's' ear

• More rarely, supervening infection can lead to perichondritis and cartilage necrosis - particularly if the cause or the subsequent treatment breach the skin barrier.

• Or coexisting diabetes mellitus(uncontrolled) or immunocompromised state

MANAGEMENT• The haematoma requires evacuation

observing strict asepsis.

• either aspiration with a thick bore needle or, if this is inadequate, an incision.

• Such an incision can be hidden on the anterior surface by placement parallel to natural contours.

• Alternatively, a posterior incision with removal of a small 'window' of cartilage has been advocated

• Aspiration alone, however, results in a very high incidence of re-collection until the perichondium is again firmly adherent (about seven days).

• In order to prevent this, the following options have been devised.

• The use of moulded pressure bandages or splints of various materials applied on both sides of the pinna.

• Keeping them in place long enough to effectively prevent re-collection can be difficult.

• A drain left in the incision site• A posterior incision, with excision of a disc of

cartilage and placement of a suction drain.• Through-and-through 'mattress' or 'quilting'

suturesto apply compression, with or without materials to distribute the compression more evenly

• While perichondritis and pressure necrosis are theoretical considerations,

• aseptic techniques, antibiotic prophylaxis and appropriate suture tension make these rare.

• The advantage of using a thick transparent silicone sheeting 'sandwich‘ is the visibility it provides to exclude excessive tension of the mattress suture and fluid reaccumulation

• After seven to ten days, aspiration is ineffective

• surgery for removal of the organizing haematoma and newly formed cartilage with/withoutoverlying perichondrium is necessary.

• Whether to do so should logically be based on the amount of residual

• Giffin describes doing this through incisions parallel to the helix or antihelix.

Perichondritis of the external ear• The term correctly refers to infection or

inflammation involving the perichondrium of the external ear: auricle and external auditory canal.

• it is commonly used to describe a continuum of conditions of the external ear,

• from erysipelas (infection of the overlying skin), through

• cellulitis (infection of the soft tissue), and true perichondritis to chondritis (infection involving the cartilage itself).

AETIOLOGY• The thin skin, minimal subcutaneous tissue and vulnerable

anatomical position make conchal cartilage particularly susceptible to trauma with subsequent infection.

• Trauma--– laceration of the auricle– surgery to the external ear– frostbite– Burns– chemical injury– infection of a haematoma of the pinna– aspiration or incision of a haematoma and– 'high' piercing of the( cartilaginous) portion of the auricle for the

insertion of earrings.• Superficial infections of the skin (erysipelas) or subcutaneous tissue

(cellulitis) of the external auditory meatus or pinna may spread deeply to involve the perichondium (perichondritis) or cartilage (chondritis).

organisms

• most commonly isolated are Pseudomonas aeruginosa and Staphylococcus aureus (with culture rates quoted as up to 75-90 percent and 50 percent respectively).

• Other organisms cultured include Gram negatives (proteus and Escherichia coli).

• Streptococcal infection has also been reported.

PATHOLOGY• Martin et al. describe hyperplasia of the

dermal layers,thickened subcutaneous tissue, intense infiltration with polymorphonuclear leukocytes, thickening of the perichondium and destruction of the cartilage by phagocytes.

Perichondritis: Symptoms

• Pain over auricle and deep in canal

• Pruritus

Perichondritis: Signs

• Tender auricle• Induration• Edema• Advanced cases

– Crusting & weeping– Involvement of soft

tissues

DIAGNOSIS• dull pain increasing in severity• classical signs of inflammation involving

thecartilaginous pinna • The lobule, whichcontains no cartilage, is

spared.• The severity of the pain and swelling of

the pinna are indicators for true perichondritis as opposed to the more superficial conditions of erysipelas and cellulitis.

• The diagnosis is clinical history of underlying trauma to the external ear should be sought.

Differential diagnosis• Relapsing polychondritis

• differentiated on the basis of the systemic nature of the condition. This manifests in the involvement of cartilaginous structures at multiple sites, possibly ocular conditions(scleritis, iritis and keratitis) and, occasionally, vasculitis.

• Rare cases of extranodal non-Hodgkin's lymphoma of the pinna, both with4 and without5 the presence of human immunodeficiency virus

COMPLICATION• If untreated, a subperichondrial abscess

may develop,• leading to avascular necrosis of the

underlying cartilage and marked deformity of the pinna.

• The infection may spread to the cartilage itself.

• Rare complications of perichondritis include fatal septicaemia secondary to streptococcal infection, subacute bacterial endocarditis and necrotizing fasciitis of the neck.

MANAGEMENT-Prevention• Careful placement of ear piercings away from

the cartilaginous pinna.• Surgery in and around the ear should avoid

trauma to cartilage and tight head bandages.• Haematomas of the auricle should be drained

promptly and using careful aseptic techniques• The meticulous management of burn injuries to

the ears should include the use of prophylactic antibiotics against Gram-negative bacteria

• local care including daily dressings and the removal of eschars and crusts.

First-line management• mildest forms--topical and oral antibiotics.

• discharge or an abscess needs draining, a pus swab should be sent for culture and sensitivity

• antibiotic treatment should not be delayed.

• broad-spectrum antibiotic at a high dose, possibly intravenously, should be designed to cover common organisms and, in particular, P. aeruginosa.

• Subperichondrial abscesses require incision and drainage,

• only when definite fluctuation is present, as premature incision may result in further spread of the infection.

Resistant cases• Nonresponse to the above treatment,

accompanied by persistent pain, suppuration and extensive signs of inflammation, necessitates further intervention.

• Stroud and, subsequently, Dowling advocate aggressive excision of necrosed cartilage including the overlying skin and subcutaneous tissue.

• it is difficult to decide how much cartilage to excise, and repeated debridement may be required.

• this procedure usually results in deformity, especially if the peripheral cartilagenous framework has to be removed.

• In severe cases, where the entire area is involved total chondrectomy via an incision in the helical margin, the ear being split in bivalve fashion,

• the necrotic cartilage resected, and a layer of fine mesh gauze placed between the flaps and changed daily.

• Stevenson, Apfelberg et al. and, subsequently,Bassiouny advocate a system of continuous drainage and irrigation with an antibiotic and steroid solution as an alternative in order to preserve the structure and form of the auricle.

• Fenestrated polyethylene tubes are placed in subperiosteal tunnels on either side of the cartilage, and aminoglycoside/cortisone solution used to irrigate these twice daily

Other forms of management• Iontophoresis,effective local antibiotic

delivery without systemic absorption.

• Rapperport et al.and Macaluso and Kennedy demonstrated experimentally the effectiveness of iontophoresis in delivering high levels of penicillin and gentamycin, respectively, to burn injured rat and rabbit ears (animal evidence).

• Low-dose radiation has been used, based on the lethal effect of such radiation on microorganisms. GovrinYehudain et al. advocate three or four sessions of approximately 0.8 Gy of radiation over a period of two days, and they report a significant response from perichondritis that was resistant to antibiotic treatment

• Lele, in 1964,employed ultraviolet radiation

Relapsing polychondritis• rare disease of episodic inflammation and

degeneration involving multiple cartilaginous structures, usually those of the upper respiratory tract, as well as connective tissue at various other sites.

• first described in 1923 byJacksh-Wartenhorst, who called it polychondropathis.

• Other names have included polychondropathy, systemic chondromalacia and chronic atrophic polychondritis.

• Pearson et al coined the term relapsing polychondritis.

PATHOLOGY• All types of cartilage may be involved.

• Histology shows an initial neutrophil infiltration,

• strikingly early loss of the normal basophilia of cartilage, and later infiltration by histiocytes, plasma cells and lymphocytes.

• Eventually,atrophic cartilage is seen with cystic spaces containing gelatinous materiaL

• Other proteoglycan -rich structures, such as the eyes and the cardiovascular system, may also undergo similar inflammation and degeneration.

• McAdam et aI point to a high incidence (56 percent) of vasculitis.

AETIOLOGY• uncertain • thought to be autoimmune.• Dolan et aI. demonstrated immunofluorescent

deposits of immunoglobulins • Foidert et al. and Terato et al. serum antibodies

to type II collagen in the acute phase • Associations with other vasculitides and

connective tissue,and autoimmune conditions occur in approximately 30 percent of cases.

DIAGNOSIS• the multi-system nature• Mc ADAM’S SIGNS• recurrent chondritis of both auricles;• nonerosive inflammatory polyarthritis;• chondritis of nasal cartilages;• ocular inflammation including conjunctivitis,keratitis, scleritis/ episcleritis and/or uveitis;• chondritis of the respiratory tract involving

laryngeal and/ or tracheal cartilage;• cochlear and/or vestibular damage manifested byneurosensory hearing loss, tinnitus and/or vertigo

These were modified by Damiani and Levines to the following criteria:

• three or more of McAdam's signs - histologic

confirmation not necessary;

• one or more of McAdam's signs with positive

histologic confirmation;

• involvement of two or more separate anatomic

locations with response to steroids and/or dapsone.

• Moloney's 1978 review provides a good clinical overview.

• fever in the acute phase.• The cartilages involved include those of one or

both pinnae in 89 percent of patients.• This is the presenting symptom in one-third of

cases• Initial inflammation gives way to cartilaginous

resorption and floppy pinnae• The nasal chondritis presents with pain, a feeling

of fullness, inflammation or sudden painless saddle deformity

• The inflammation and later resorption of laryngeal and tracheal cartilages present with hoarseness, tenderness, airway obstruction and softening to palpation.

• Critical stenosis and collapse of tracheal and bronchial cartilages may lead to airway compromise.

• Costochondral cartilages may be involved.• Involvement of the Eustachian tube may lead to

otitis media with effusion.• Peripheral joints may display a seronegative,

nondeforming, nonerosive poly- or oligoarthritis.• Noncartilaginous structures may also be

involved

• Ocular inflammation is common, and can affect almost any part of the eye

• Inner ear symptoms (hearing loss and dysequilibrium) are attributed to possible vasculitis.

• Various vascular and cardiovascular consequences have been reported.

• Skin lesions are often vasculitic in nature.• There are no specific diagnostic tests and

the diagnosis rests on the clinical picture, perhaps supported by histology.

Differential diagnosis• Initial lesions might be mistaken for local

inflammatory conditions of the pinna (perichondritis), nose or larynx.

• The systemic inflammatory 'granulomatosis' diseases(Wegener's granulomatosis, T-cell lymphomas, tuberculosis,sarcoidosis, etc.) should be considered

OUTCOMES• follow a course of acute exacerbations and

remissions.

• Long-term consequences are largely the result of cartilaginous destruction.

• Otological consequences include deformity of the pinna, conductive hearing loss, sensorineural hearing loss and vertigo.

• Saddle-nose deformity is common.

• Laryngeal and tracheobronchial collapse can lead to critical airway compromise.

MANAGEMENT OPTIONS• High doses (30-60 mg prednisone daily)

may be required to induce remission, and maintenance (5-10 mg daily) to suppress recurrences.

• Immunosuppressants have been utilized in an attempt to reduce steroid doses, particularly azathioprine or methotrexate.

• Dapsone has been advocated by some

• suggested that nonsteroidal antiinflammatories and colchicinemay control mild episodes.

• The use of anti-CD4 monoclonal antibody and oral minocycline have recently been reported.

• Surgical treatment is limited to the essential maintenance of an airway, by tracheostomy or possibly expandable stents.

Effects on outcome

• All series report that steroids seem to induce remissions in a significant proportion of, but not all, cases.

• Relapse is likely, especially if steroids are withdrawn.

Osteoradionecrosis of the temporal bone

• defined as exposure and necrosis of a variable portion of previously irradiated petrous temporal bone which fails to heal over a period of three months.

AETIOLOGY AND PATHOGENESIS• Because of its density, bone absorbs a

greater proportion of radiation than soft tissues.

• Osteoradionecrosis and chondroradionecrosis may occur in various sites in the head and neck following high-dose radiotherapy, despite the relative radioresistance of bone and cartilage

• This occurs far more commonly in the mandible than in the petrous temporal bone.

• Also chondronecrosis of the larynx, and osteonecrosis of the maxilla and nasal bone, nasopharynx, zygoma, palate, clavicle and hyoid

• Osteoradionecrosis of the petrous temporal bone occurs as a result of high -dose radiotherapy administered to and around the petrous temporal bone for malignancies of the parotid gland, external auditory canal, middle ear, maxilla, nasopharynx and pituitary.

• The radiation causes inhibition of mitosis and the capacity for tissue repair, and a vasculitis leading to obliteration of blood vessels and avascular necrosis.

• Marx et aI characterized the tissue as hypoxic,hypo cellular and hypovascular.

• The compact, rather than cancellous, nature of the petrous temporal bone, and poor blood supply of the tympanic ring, may increase susceptibility.

• The occurrence of osteoradionecrosis may be increased in patients with microvascular disease (atherosclerotics and diabetics), and as a result of trauma after radiotherapy

• classically dental extractions in the case of the mandible.

• High local doses of brachytherapy may give an increased incidence.

PATHOLOGY• The tissues affected include bone, overlying

subcutaneous tissues and skin. • Auricular cartilage is seldom affected due to the

low superficial radiotherapy dose received in all but irradiation of skin tumours.

• The histological changes in bone include death of osteocytes and osteoblasts resulting in empty lacunae,

• preponderance of osteoclasts, demineralization, osteolysis, loss of marrow substance, reparative fibrosis and often secondary infection.

• Soft tissue histological changes include epithelial hyperplasia, atrophy of dermal structures, dermal fibrosis and soft tissue necrosis with replacement by fibrosis.

• Macroscopically, there is loss of skin and soft tissue exposing bone, bony sequestration and frequently the complication of secondary infection.

• Of the parts of the temporal bone, the tympanic ring appears particularly susceptible.

CLINICAL PICTURE• The time interval between radiotherapy and

clinically evident osteoradionecrosis can vary considerably – from less than 12 months to 23 years.

• Ramsden et al usefully divided cases into localized and diffuse (extensive) forms.

• The localized form presents mild otalgia and otorrhoea, with small areas of exposed bone in the external auditory canal .

• It generally occurs when the petrous bone was in the periphery of the irradiated field.

• Computed tomography (CT) scanning shows only small areas of sequestration.

• This type can heal if managed conservatively.

• The diffuse or extensive form occurs generally when irradiation is directed at the petrous temporal bone, and has more severe symptoms of pain and otorrhea

• CT imaging shows widespread bony destruction.• Erosion of the facial canal and extension to the

inner ear can occur, as well as intracranial complications, brain abscesses, meningitis and death.

• Radical surgical debridement and repair is often necessary to prevent complications and effect healing.

MANAGEMENT OPTIONS• The likelihood of osteoradionecrosis

should be reduced by careful planning of the radiotherapy, by the scheduling of any surgical intervention prior to radiotherapy, and by waiting for full wound healing before irradiation.

• In an established case, the first step should be to exclude an underlying recurrence of malignancy.

• Thereafter,the severity of the problem guides management .

LOCALIZED NECROSIS• Such cases, which may just leave an area

of exposed dead bone in the floor of the external auditory canal, can successfully be managed conservatively, with toilet, careful removal of sequestra, local antibiotics and analgesics,

• although healing may take up to four years.

• Hill et al. describe the use of a local rotational flap from postauricular skin to cover small exposed areas of bone in the external auditory canal

DIFFUSE NECROSIS

• Conservative management is inadequate

• However, the poorly vascularized irradiated field is less than ideal for surgery.

• In Ramsden et al.'s and Thornley et al.'s series, radical surgical debridement required revision in half the cases.

• For this reason, subsequent authors recommend bringing in a vascularized soft tissue flap at the time of debridement, and careful placement of incisions in order to optimize blood supply.

• Marx et aI.demonstrated the effectiveness of hyperbaric oxygen and its superiority over penicillin in preventing osteoradionecrosis of the mandible in previously irradiated patients undergoing dental extraction

Foreign bodies in the ear• The foreign bodies found most commonly

in the ear are, in order, cotton wool, insects, beads, paper, small toys and erasers.

• Seventy-two percent of otolaryngology referrals from failed attempts by nonspecialists consist of firm, rounded objects such as beads or beans.

CLINICAL PICTURE• Foreign bodies in the external auditory meatus

are most commonly seen in children who have inserted them into their own ears.

• Children may present asymptomatically, or with pain or a· discharge caused by otitis externa.

• Adults are often seen with cotton wool or broken matchsticks which have been used to clean or scratch the ear canal.

• Live insects in the ear, commonly small cockroaches, are annoying due to discomfort created by loud noise and movement.

MANAGEMENT OPTIONS• Removal can vary from being simple to

being very challenging and frustrating.

• Emergency or primary care physicians are successful at removing about two-thirds of foreign bodies under direct vision.

• In 82 percent of cases~these are irregularly shaped objects with soft, graspable parts.

• As a result, ear, nose and throat (ENT) departments see the problem cases these practitioners could not solve.

• Prior to embarking upon removal, it may be useful to consider three aspects of the situation:

• 1. the nature of the foreign body;

• 2. the precise location of the foreign body;

• 3. the patient.

The nature of the foreign body

• Living insects should first be killed by instilling oil into the meatus to drown them before removal.

• Irregular/soft graspable non-living objects(dead insects, cotton wool, paper, small toys) may be removed with a pair of crocodile forceps.

• Organic objects (beans, etc.), which may absorb water, swell and cause pain, should not be syringed.

• Button batteries should not be syringed as they may leak on exposure to water.

• They should be removed urgently .

• Inorganic round/smooth non-graspable (beads,erasers).

• Smooth, firm, rounded objects, such as beads or toy gun pellets, are difficult to grasp and can easily be wedged deeper into the meatus

• Syringing is safe and is often successful, but may fail with tightly impacted foreign bodies

• any smooth, hard, rounded foreign body or any patient where prior removal attempts have failed should be referred directly to an otorhinolaryngologist. These objects are best removed using microscopic vision and a blunt ear hook, or by syringing in the uncooperative patient.

• It is useful to look carefully for a space between the foreign body and the canal wall, which can be used for the introduction of water (as in syringing) or the wax hook.

• Nineteen percent of patients referred to an otolaryngologist will require general anaesthesia for removal.

• An alternative method for removing beads is using a cyanoacrylate glue-impregnated cotton bud to adhere to the object and pull it out

Location of the foreign body• The easier access, wider diameter, elastic

nature and lesser sensitivity of the lateral canal make the removal of laterallying foreign bodies easier.

• Space between the foreign body and the canal wall allows access for water or an instrument through for removaL

• Firmly impacted foreign bodies medial to the isthmus,particularly when failed removal attempts have caused trauma and swelling of the canal skin, may require surgical removaL

• A post -auricular approach and widening of the canal by bone drilling is advised

Patient considerations• Younger, uncooperative children require

special handling.

• Prior unsuccessful attempts at removal may have caused pain and trauma and the child may be unhappy and uncooperative.

• Time spent gaining the child's confidence is a worthwhile investment.

• Syringing is often useful in children as it is better tolerated, and the risk of causing trauma is low.

• Once the foreign body has been removed it is advisable to check the ears for underlying pathology as the child may have put in the foreign body due to itch, pain or otorrhoea.

COMPLICATIONS• caused by the action of introducing the

foreign body or the foreign body itself.

• In general, these are limited to lacerations of the canal skin and otitis externa.

• Rarely, facial nerve palsy may occur secondary to leakage of alkaline material from a button battery and necrosis of the surrounding tissue.

• Damage and perforation of the tympanic membrane

• ossicular chain dislocation or fracture may occur.

• Multiple attempts at removal and the use of multiple instruments are associated with complications.

• It has been suggested that referral to an otorhinolaryngologist be considered by emergency department doctors if more than one attempt has been made, or more than one instrument has been used in attempted removal.

Herpes zoster oticusDEFINITION

• Herpes zoster oticus is defined as a herpetic vesicular rash on the concha, external auditory canal or pinna with a lower motor neuron palsy of the ipsilateral facial nerve.

NOMENCLATURE

• Herpes zoster oticus is commonly known as Ramsay Hunt syndrome following the first description of 60 cases by John Ramsay Hunt in 1907.

• To be more accurate,herpes zoster oticus should actually be called Ramsay Hunt syndrome type 1 as Hunt actually described three neurological syndromes

PATHOLOGY• The disease is a reactivated varicella

zoster infection from dormant viral particles resident in the geniculate ganglion of the facial nerve and the spiral and vestibular ganglia of the VIIIth nerve.

• Recent work looking for varicella,zoster in the geniculate zone of the concha using polymerase chain reaction (PCR) showed the virus to be present in 100 percent of patients with vesicles and in 71 percent of individuals with no initial skin lesions, but who developed vesicles within a week.

DIAGNOSIS• The diagnosis is essentially still a clinical

one

• magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis having been shown to have no role in establishing either diagnosis or prognosis

• In the acute phase, MRI can actually be confusing as the inflammation of the nerve in the internal auditory canal can occasionally be mistaken for a small vestibular schwannoma

• The VIIIth nerve may be involved to a variable degree,resulting in hearing loss, tinnitus and/or vertigo

• Detailed audiological studies have shown that almost all patients with herpes zoster oticus have abnormalities of the auditory pathway at several different locations from the cochlea to the brainstem, even though subjective hearing loss may not be present.

• Subjective hearing loss occurs in 25 percent of children and 50 percent of adults.

• Auricular pain is often the first symptom and other cranial nerves are frequently involved.

• In 14 percent of patients, the rash is not present initially but develops several days after the onset of pain and facial palsy.

• In some cases, the vesicular rash may in fact present on the tongue or pharyngeal mucosa and never present in the ear.,

• Spread from the facial nerve to the VIIlth and/or other cranial nerves is thought to occur via the vasa nervorum

• although there are also numerous neurological anastomoses between the lower cranial nerves within the skull base which allow for easy viral transmission.

• A facial palsy, without a cutaneous or mucosal rash, may still be due to varicella zoster.

• A rise in serological titres or the presence of zoster DNA in the skin confirms the viral aetiology.

• This condition is known as zoster sine herpeteand may be the cause in up to 3 percent of cases of facial palsy.

• In one prospective study of 1507 patients, evaluated consecutively for facial palsy between 1966 and 1976,

• 185 cases (12 percent) were diagnosed as Ramsay Hunt syndrome.

• In 25 percent, the diagnosis of herpes zoster was confirmed by acute and convalescent serum titres for varicella-zoster virus.

• In 75 percent, the diagnosis was based on the characteristic clinical presentation of the Ramsay Hunt syndrome.ll

• In children, up to 18 percent of cases with facial palsy may be due to herpes zoster.

• This makes herpes zoster oticus the second commonest cause of unilateral facial palsy after idiopathic Bell's

OUTCOMES• In untreated patients, over 60 percent develop a

complete facial paralysis within a week • even higher in individuals over the age of 50.• If the palsy is complete,only 10 percent will get a

full return of normal function if facial nerve studies reveal the absence of neural activity ten days later.

• Even those that recover are likely to have residual synkinesis.

• If the palsy is incomplete, 66 percent will recover completely.

• Overall, approximately 50 percent of adults and 80 percent of children will achieve full recovery to House-Brackmann grade

MANAGEMENT OPTIONS• In a retrospective study of 80 patients, improved

outcomes were obtained if individuals were commenced on acyclovir and prednisolone within three days of the onset of symptoms.

• Seventyfive percent had a complete recovery with early treatment, compared to only 30 percent when treatment was started on or after day 8.

• There was no difference between the group treated with intravenous antivirals when compared to the group given oral therapy.

• In another nonrandomized trial, treatment of intravenous acyclovir plus steroids produced a 90 percent recovery to grade 1,compared to 64 percent if only steroid was given.

• The early treatment of herpes zoster infections with antiviral agents is also known to significantly reduce the prevalence of post-herpetic neuralgia.

• Cost-benefit studies also support the use of aggressive early antiviral treatment in suspected herpes zoster oticus

BASAL CELL CARCINOMA• Jacob first described the characteristics of

a basal cell carcinoma (BCC) as a rodent ulcer as early as 1827.

• The BCC arises from pluripotential cells within the epidermis or hair follicles.

• Clinically, these tumours are usually slow growing following an indolent course and may take years to develop into a significant size

• BCC are found most commonly in sun-exposed areas

• The common sites-helix,tragus

• Men >50yrs

• Presents as a nodule with central crust,removal results in bleeding

• Ulcer has a raised/beaded edge

• Extends cicumferentially into skin,may penetrate deeper involving cartilage or bone

• LN METS usually do not occur

• Rarely arise from meatus-diag by biopsy

• The risk of developing one or more lesions after a primary BCC or squamous cell carcinoma (SCC) is 35 percent at three years and 50 percent at five years.

• The estimated risk of metastasis from BCC is less than 0.1 percent

• lymphatic and blood-borne spread both reported.

Risk factors• The risks of developing a BCC can be

divided into

• Genetic Predispositions

• Environmental exposure

• Premalignant conditions

GENETIC PREDISPOSITIONSkin type• Sun-exposed skin is the main anatomical

site for BCC and SCC.• The susceptibility of the skin to sun

damage is directly related to the amount of melanin.

• This skin phenotype classified by Fitzpatrick divides the skin into

• six types according to the melanin content, pigmentation and sensitivity to sunlight

Fair skin that always burns is at a higher risk of developing a BCC or SCC than Africo-Caribbean skin.

Syndromes• Xeroderma pigmentosum: An autosomal recessive

condition resulting in the inability of the body to repair ultraviolet (UV)-induced skin damage. Develop multiple BCC and SCC early, poor prognosis.

• Gorlins' syndrome: An autosomal dominant condition characterized by a number of features including multiple BCC. Genetic analysis has found the disease to be located at a tumour suppressor gene on the long arm of chromosome 9.

• Epidermodysplasia verruciformis: A viral and partially inherited disorder resulting in the inability to resist human papilloma virus(type 3 and 5) leading to degeneration of the lesion into a BCC.

ENVIRONMENTAL EXPOSURESun exposure• total time spent in the sun and the number of

sun burns plays a cumulative risk of developing skin cancer.

• The UV spectrum is the only significant wavelength in the pathogenesis of skin cancer

• UVA potentiating the direct effects that UVB has on skin cell DNA.

Ionizing radiation• Total accumulated dose. • It is recognized as an occupational hazard in

radiology, mining, airline pilots and occurs in patients treated with radiotherapy.

Chemicals• Certain chemicals act by direct toxic effects or

potentiating the effects of UV radiation• Polycyclic aromatic hydrocarbons, psoralens

and arsenic exposure.

Immune suppression• Inability of the host to detect and repair

damaged cells is a feature of immune suppression.

• predisposes to the spontaneous development of malignant cells

• 30 percent of skin cancers that develop are highly aggressive.

PREMALIGNANT LESIONS

• Sebaceous naevus of Jadassohn usually presents at birth as a yellow plaque, with approximately 10 percent undergoing malignant change

Types of BCC• There are several types of BCC.• Nodular: The most common type, usually

arising in the head and neck. Slow-growing, fleshy or pearly coloured nodule.

• Superficial: These lesions often develop on the trunk in multiple patches, contained within the epidermis with no dermal invasion, may have shallow ulcer,atrophic scar or crusting.

• Pigmented: Lesion contains melanin causing confusion with melanomas.

• Morphoeic: These lesions are usually indurated, with irregular borders, behave aggressively and are frequently misdiagnosed and incompletely excised.

Treatment of BCC of external ear• Superficial lesions irradiated,cosmetic

deformity avoided

• Lesion involving cartilage may require surgical excision

• In EAC-wide surgical excision+post op RT

SQUAMOUS CELL CARCINOMA• arises from the basal layer in the epidermis. • accounts for 25 percent of nonmelanoma skin

cancer• poorer prognosis than BCC due to its aggressive

local invasion of tissues and metastatic potential. • develops within altered skin, previously sun-

damaged areas such as within an actinic keratosis,or malignant change in a chronic sinus or ulcer

• It arises most commonly in sun-exposed areas with 70-80 percent found in the head and neck.

• Overall,the risk of metastatic spread, usually via lymphatics,is 2-5 percent.

• Site of prediliction-helix• Males in 50s,fair skinned• Painless nodule or ulcr with raised everted

edge,indurated base• Cases in EAC-in cases of long standing

ear discharge• May arise primarily from meatus,or sec.

extension frm ME Ca• Sympt-blood staining of hitherto

mucopurulent or purulent discharge,sev earache

• Exmn.-ulcerated area in the meatus/ bleeding polypoid mass/ granulation

• Facial N may be paralysed because of local extnsn thru post. Meatal wall or its spred into ME

• Regional LN-pre,post auricular,upper deep cervical may be involved

Risk factors for SCCGENETIC PREDISPOSITION• Skin types-as for BCCSyndromes• Xeroderma pigmentosum: as for BCC• Albinism: an autosomal recessive condition,

resulting in an increased risk of see due to the absence of melanin.

• Epidermolysis bullosa: Variable genetic penetrance characterized by recurrent blistering of the skin predisposing to SCC with a poor prognosis.

• Porokeratosis: An autosomal dominant condition resulting in abnormal keratinisation, 13 percent undergo malignant change.

ENVIRONMENTAL EXPOSURE• Similar environmental risks for BCC

• exposure to ultraviolet light,

• ionizing radiation,

• chemical exposure

• immune suppression

PREMALIGNANT CONDITION

• Actinic keratosis (synonyms: solar keratosis, senile keratosis),

• caused by sun damage, is a premalignant lesion with a malignant transformation rate of 10-l3 percent.

Types of SCC• There are no different types of scc• Graded histologically to indicate the aggressive

nature of the individual tumour.• Markers include the depth of tumour,• degree of cell differentiation (poorly

differentiating equals poor prognosis)• mitotic index (high mitotic index equals poor

prognosis). • Occasionally, the use of immunohistochemistry

and specific dermal antibodies is needed to differentiate a poorly differentiated see from melanoma

Treatment • Small lesions with no nodal mets- excised

locally with 1cm of healthy area around it

• Larger lesions of pinna/within1 cm of EAC and those with nodal mets-total amputation of pinna,often with en bloc rem of parotid gland ,cervical LN

• SCC of EAC-en bloc wide surgical excision+post op RT

MALIGNANT MELANOMA• Melanoma comes from the Greek word melanos

meaning black. • Unpredictable nature and variable response to

conventional treatment modalities • In the USA, melanoma accounts for 3 percent of

all cancer diagnoses and 1.2 percent of deaths.• It differs from the other skin cancers(SCC and

BCC) in that although it is primarily a disease of fair skin, it occurs in all races and is not limited to sunexposed areas.

• Melanoma is less common than BCC or SCC

• Different to the SCC, malignant melanoma (MM) of the ear has a better prognosis than the face, which is still better than the scalp and neck.

• If there is spread from an MM of the ear, it usually involves the parotid gland, which should be removed when a neck dissection is performed.

• Anywhere in the auricle

• Men of light complexion,exposed to sun

• Mets in 16-50% cases

• Rare in EAC

prognostic factors• Six major prognostic factors have been

identified, of which tumour thickness and ulceration are the most important.

1. Tumour thickness: Tumour thickness is the most important determinant of survival;

2. Ulceration: Ulceration is associatedwith an aggressive tumour and worseprognosis irrespective of depth andsize.

3. Anatomical site: The survival curves are equal for the trunk. compared to the head and neck, but there is poor prognosis with the scalp versus facial MM.

4. Sex: There is better prognosis in women, possibly due to common site and lower incidence of ulceration.

5. Level of invasion (Clark's level):Survival is inversely related to level of invasion.

6. Surgical treatment.

Risk factors• Genetic predisposition

• environmental exposure

• Premalignant conditions

GENETIC PREDISPOSITIONSkin type• white individuals,having a greater than ten-fold incidence

compared to Africo-Caribbean peoples.Syndrome• Atypical mole syndrome: Atypical mole syndrome is an

autosomal dominant condition. It is diagnosed in a patient with more than 100 naevi, where one or more have dysplastic features and are greater than 8 mm. The patient has a 10 percent chance ofMM.

• Giant hairy naevus: Giant hairy naevus occurs in a patient with a naevus > 20 cm, or more than 5 percent of the body surface area at birth. The estimated malignant transformation ranges from 3.8 to 18 percent.

ENVIRONMENTAL EXPOSURE• Sun exposure, especially the total

accumulated dose and also the number of sun burns

• the trunk predominating in men and the legs in women.

PREMALIGNANT CONDITIONS• Dysplastic naevus is thought by some to

be a melanoma in situ, as an estimated 40 percent transform into a superficial spreading melanoma.

• Lentigo maligna (synonym Hutchinson's freckle, senile freckle) is a precursor of lentigo malignant melanoma

Types of MMThere are four types of MM:1. superficial spreading;2. nodular;3. acral lentiginous;4. lentigo malignant melanoma.• Two phases of growth occur, the first

confined to the epidermis, called the horizontal phase

• Vertical phase is associated with an increased risk of metastasis.

Treatment • Superficial melanoma,<1cm in

diameter,over the helix,is managed by wedge resection and primary closure.

• Superficial melanoma.>1cm,infiltrative melanomas,melanoma of post. Auricular surface or concha and all recurrent melanoma—resection of pinna, parotidectomy,radical neck dissection

Adenocarcinoma

• Papillary or cystic growth in EAC

• Obstruction of EAC

• Pain in adenocystic Ca

• Treatment-wide excision of EAC+ surr bone,extended radical mastoidectomy,total petrosectomy in extensive cases

Sebaceous cell carcinoma

• Extremely rare tumour

• Occ in any part of the body

• Commonly seen in head & neck—concha of ear and ext nose

• Confirmed by biopsy

• Treatment- excision

Benign tumours• PA sinus/cyst• Sebaceous cyst –post. Auricular sulcus or

below and behind the ear lobule.Rx- total surgical excision

• Dermoid cyst-rounded mass over upper part of mastoid behind pinna

• Papilloma (wart) – tufted growth/ flat grey plaque.rough to feel.viral in origin.Rx-surgical excision or curettage with cauterisation of base

• Cutaneous horn- form of papilloma with heaping up of keratin,horn shaped tumour..at rim of helix in elderly..Rx surgical excision

• Keratoacanthoma – raised nodule with central crater.initially grows rapidly but slowly regresses leaving a scar..Rx- excision biopsy

• Neurofibroma – nontender,firm swelling,ass with von recklinghausen’s dis..Rx surg excision if occluding ear

• Haemangioma – congenital tumour seen in childhood.2 types

• Capillary hemangioma- mass of capillary-sized blood vessel.present as port-wine stain.does not regress spontaneously

• Cavernous hemangioma- (strawberry tumour) endothelial lined spaces filled with blood.increases rapidly during 1st yr..regresses thereafter..may completely disappear by 5th yr

• Keloid- follows trauma-piercing ear/surgical incision..genetic susceptibility+,black race

• Pedunculated tumour.Rx surgical excision with triamcinolone inj into surgical site or immediate post-op radiation of 300 rads

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