Michael Hawke Peter Kwok

A Mini-Atlas of Ear-drum Pathology

SUMMARYThe authors provide a number of ear-drumpictures and identify and discuss diseasesaffecting the external ear canal, the tympanicmembrane and middle ear. They also dealwith the removal of foreign bodies from theexternal canal, perforation of the tympanicmembrane, and the use of an artificialventilation tube. (Can Fam Physician 1987;33:1501-1507.)

A N ACCURATE EXAMINATION of the external audi-tory canal and the tympanic membrane is the first step

in the management of any patient with symptoms sugges-tive of ear disease. The majority of diseases affecting the ex-ternal ear canal, and many of those affecting the tympanicmembrane and middle ear, can be diagnosed primarily onthe basis of their otoscopic appearance.These deeply recessed structures are best visualized if the

examiner uses one of the modern otoscopes which have aquartz halogen light source that is evenly distributedthrough a ring of glass fibres.

Figure 1External Canal Foreign BodyForeign bodies should be removed as safely and expedi-tiously as possible, while avoiding damage to the delicateskin of the external canal, tympanic membrane and ossi-cles. The method of removal depends on the type of foreignbody present and the level of patient co-operation. Manysmall foreign bodies can be flushed out with an ear syringe,whereas others may require special forceps. When a foreignbody is tightly impacted, or when the patient is unable totolerate manipulation, removal under general anesthetic isusually safer.

Figure 2External Canal ExostosesExostoses are areas of bony hypertrophy which develop asthe result of repeated stimulation (or irritation) by coldwater of the periosteum lining the tympanic bone. Such ac-tivities as swimming, surfing, and diving may cause thecondition. Exostoses appear as hard, round or oval excre-sences which are usually multiple and bilateral. Since mostexostoses are asymptomatic, they usually require no treat-ment. In some patients, however, huge exostoses may nar-row the external canal to such an extent that debris from theskin lining the canal accumulates and produces a conduc-

RESUMECet article presente plusieurs images du tympan etidentifie et discute les differentes pathologiesaffectant le conduit auditif externe, la membranetympanique et l'oreille moyenne. Les auteurspoursuivent la discussion sur l'extraction de corpsetrangers du conduit auditif exteme, la perforationde la membrane tympanique et l'usage d'un tube deventilation artificielle.

Key words: ear-drum pathology,management of ear problems

-V~2~22.V-22 42

CAN. FAM. PHYSICIAN Vol. 33: JUNE 1987 1501

;, "," -,.;.q -.i, .-,4 ", xA"Kolb

mm

tive hearing loss. This severe form of exostoses has beencalled 'surfers' ear'. In these patients, a trans-canal removalmay be necessary. Because exostoses are caused by coldwater, they may be prevented by the wearing of ear plugs.

Figure 3Extemal Canal FuruncleA furuncle is a small Staphylococcal abscess which arisesfrom the base of a hair follide. These extremely painful lo-calized swellings only occur in the outer cartilaginouscanal, as the skin of the deep canal is hairless. If the furun-cle is obviously pointing, it can be lanced with a 16-gaugesterile hypodermic needle, bringing relief from pain. If thepatient is seen at an earlier stage, analgesics and a fullcourse of an effective antistaphylococcal systemic antibiotic(e.g., cloxacillin or amoxicillin and clavulinic acid) are indi-cated.

Figure 4Acute Otitis ExternaAcute otitis extema (Swimmer's ear), is an acute and dif-fuse bacterial infection of the skin of the extemal ear canal.A gram-negative bacteria (Pseudomonas aeruginosa) is thecausative organism in most cases of acute otitis externa.Local trauma (e.g., from fingemails or bobby pins) and ex-posure of the skin to water (e.g., in swimmning, sweating orshowering) are the main predisposing factors in the devel-opment of this disease. The skin of the outer canal is dif-fusely swollen, extremely tender, and shiny in appearance.In some cases the ear is so inflamed that even the gentlestmovement of the pinna causes severe pain.Acute otitis externa is treated primarily by local or topical

medications. For this type of treatment to be effective, thecanal must be thoroughly cleaned. If the swelling of theskin lining the canal is severe enough to occdude the lumen,a cotton wick should be gently inserted in the lumen tocarry the medication into the canal. The frequent instilla-tion of an acid aluminum acetate solution (e.g., Burosol oticdrops) is usually all that is needed. If the ear is extremelypainful, systemic analgesics may be needed for one or twodays.

Figure 5Otomycosis of theExternal CanalAspergillous niger and Candida albicans are two fungiwhich may infect the external canal. Otomycosis may pres-ent either as acute or as chronic otitis externa. Aspergillousniger can usually be diagnosed by otoscopy, whereas can-didal infections have no characteristic features and areusually diagnosed by culture. The finding in the canal ofthe white fluffy hyphae or the tiny brown or black conidio-phores (fruiting heads) of aspergillus niger are diagnostic.The underlying skin is often inflamed and granular becauseof the invasion of the skin by the fungal mycelia. The cor-nerstone of treatment is thorough deaning of the canal bysuction, dry mopping or synnging (if the tympanic mem-brane is intact). Cotrimazole lotion (Canestin) is highly ef-fective in treating both aspergillus and candida.

CAN. FAM. PHYSICIAN Vol. 33: JUNE 19671502

Figure 6Bullous MyringitisBullous myringitis is an unusual form of viral or mycoplas-mal infection of the epithelium lining the tympanic mem-brane and deep canal skin which is characterized by serousor hemorragic blebs. Patients with this disease frequentlyexperience severe earache which may be followed, 12 to 20hours later, by a sero-sanguinous otorrhea. The tympanicmembrane is covered by relatively large blebs filled with a 41;

yellow serous or serosanguinous fluid. In some cases it maybe difficult to distinguish this condition from a severe acuteotitis media. As this is a self-limiting condition, and asthere is no specific treatment for the causative organisms,therapy is directed to providing adequate analgesia for oneor two days and preventing the development of a secon-dary infection (bacterial otitis externa) by keeping the eardry.

Figure 7Normal Tympanic MembraneThe normal tympanic membrane appears as a pale grey,ovoid, semi-transparent membrane which is obliquely setat the medial end of the bony external auditory canal. Theposterior margin of the drum is closer (more lateral) thanthe anterior border. The handle of the malleus can be seenextending downwards and backwards ending at the umbo.The triangular reflected "cone of light" can be seen extend-ing antero-inferiorly from the umbo. Note the small whitebony protuberance on the upper end of the malleus (the lat-eral process of the malleus). The long process of the incusand its articulation with the head of the stapes and thechorda tympani nerve passing between the handle of themalleus and the long process of the incus, may frequentlybe seen through the postero-superior quadrant of the parstensa of a thin tympanic membrane.

Figure 8Acute Otitis MediaAcute otitis media (AOM) is an acute bacterial infection ofthe mucoperiosteal linirig of the middle-ear cleft (the eusta-chian tube, tympanic cavity, and mastoid air cells) that isprimarily, but not exclusively, a disease of children. Thecommon causative organisms include Staphyloccocusaureus, hemophilus influenzae, Pneumoccocus and Strep-tococcus. Clinically, AOM is characterized by pain in the in-volved ear associated with the constitutional signs of infec-tion (fever, malaise, and, in children, gastrointestinalsymptoms).

Otoscopically the manubrial and circumferential vesselssupplying the tympanic membrane dilate, and the entiretympanic membrane eventually becomes uniformly fieryred in colour. The pressure of the creamy white mucopuru-lent exudate which accumulates within the middle earcauses the tympic membrane to bulge outwards.

1503CAN. FAM. PHYSICIAN Vol. 33: JUNE 1987

11111

Figure 9Advanced Acute Otitis MediaIf the infection progresses, the tympanic membrane mayrupture, releasing the purulent middle-ear exudate into theexternal canal.As AOM is a bacterial infection, systemic antibiotics effec-

tive against the causative organisms (amoxicillin or amoxi-cillin combined with clavulinic acid) are the mainstay oftreatment.

Figure 10Mucoid Otitis MediaMucoid otitis media (MOM) is primarily a disease of chil-dren. It is characterized by the presence of thick mucoidnon-purulent fluid in the middle-ear cleft. While the causeof MOM has not yet been clearly delineated, it currently ap-pears that the mucoid effusion arises from the mucoperios-teal lining of the middle-ear cleft in response to a viralupper respiratory infection as the result of an incompletelyresolved episode of AOM.MOM is a relatively silent disease characterized clinically

by a conductive hearing loss (because of the presence of thethick fluid in the middle ear). Otoscopically, the tympanicmembrane may have a subtle discolouration (greyish, whi-teish or yellowish), and the radial blood vessels may haveincreased prominence. The turbidity of the effusion pre-vents the examiner from seeing the long process of theincus and the medial wall of the middle ear. The tympanicmembrane is immobile to the pneumatic otoscope. As thereis, unfortunately, no truly effective medical treatment forthis condition, the physician should wait for an appropriateperiod of time (two to three months) to see if spontaneousresolution will occur (as it does in 90% of cases).

Figure 11Serous Otitis MediaSerous otitis media (soM), unlike MOM, is primarily a dis-ease of adults (with the exception of children who have acleft palate deformity). Serous otitis media is characterizedby the presence of a non-purulent clear, thin, watery,golden-yellow fluid in the middle-ear cleft. SOM is the re-sult of a blockage of the eustachian tube (most commonlyfrom a viral URI, and in rare instances from a carcinoma ofthe nasopharynx).The presence of the thin serous effusion within the mid-

dle ear generally gives the tympanic membrane a yellowishor orangish discolouration. The transparent nature of thefluid (unlike that of MOM) allows the examiner to lookthrough the transudate and to see clearly the long processof the incus and the medial wall of the middle ear. If theeustachian tube obstruction is incomplete, air bubbles or anair-fluid level may be present. The tympanic membrane isfrequently retracted (pulled medially) by negative pressurein the middle ear.As in MOM, "tincture of time" is the most effective treat-

ment. The performance of Valsalva's manoeuvre (auto-inflation) by having the patient blow into the nose whileholding the nostrils closed is often an effective method of

CAN. FAM. PHYSICIAN Vol. 33: JUNE 1987

ommmmmmmom

1504

re-aerating the middle ear. If these measures are ineffec-tive, a myringotomy may be necessary. Because a non-re-solving or recurrent episode of serous otitis media in anadult may signify the presence of an underlying carcinomaof the nasopharynx, a thorough examination of the naso-pharynx with indirect mirror, nasopharyngoscope and, ifnecessary, directly under general anesthesia, is necessaryin these patients.

Figure 12Artificial Ventilation Tube

The aim of treatment in non-resolving cases of mucoid orserous otitis media is to drain the fluid from the middle earand restore normal ventilation. This can be accomplishedby incising the tympanic membrane and aspirating the fluid(myringotomy). Myringotomy incisions usually close (heal)within seven days. In some patients it is desirable to keepthe opening in the tympanic membrane patent. This can beaccomplished by the insertion of an artificial ventilationtube into the myringotomy incision (myringotomy and tubeinsertion).

Figure 13Adhesive Otitis MediaAdhesive otitis media is a condition that develops in somepatients (as the result of recurring episodes of middle-earinfection or inflammation that have been severe enough todamage the mucosal lining of the middle ear) in which thetympanic membrane has become pulled or "stuck" onto themedial wall of the middle ear by fibrous adhesions. Thiscondition is not medically treatable. It usually produces aconductive hearing loss of varying severity. In this patient,the long process of the incus has been resorbed, and thetympanic membrane is lying directly on top of the head ofthe stapes. This is called a 'natural myringostapediopexy.'

Figure 14Tympanic Membrane Perforation

Tympanic membrane perforations may result from trauma(traumatic perforations) or as a complication of an acute at-tack of otitis media. Perforations of the drum are usuallyclassified according to their location as either central or mar-ginal. Central perforations are often termed "safe", as theyare not usually associated with cholesteatoma, whereas bythe same reasoning, marginal perforations are frequentlytermed "unsafe". Note how the medial wall of the middleear can be seen through this large kidney-shaped perfora-tion.

CAN. FAM. PHYSICIAN Vol. 33: JUNE 1987 1505

Figure 15Chronic Otitis MediaPatients with perforated tympanic membranes may de-velop middle-ear infections during upper respiratory infec-tions or from contaminated water passing through the per-foration into the middle ear. Unlike acute otitis media,these infections are usually painless, and the prime symp-tom is the development of a foul-smelling otorrhea. Thecausative bacteria are usually of the gram-negative variety(pseudomonas, proteus or E. coli). The most effective treat-ment is the application of an appropriate topical antibioticear drop and the avoidance of water.

Figure 16TympanosclerosisThese chalky white patches seen on the tympanic mem-brane actually consist of plaques of hyalinized collagenwhich have been deposited beneath the mucosal lining onthe medial surface of the drum. Current research suggeststhat these deposits are the result of an autoimmune reac-tion which has occurred during an episode of otitis media.These tympanosclerotic plaques are assymptomatic, haveno prognostic significance (although they stand as evidenceof a previous middle-ear infection), and can be safely ig-nored.

Figure 17CholesteatomaA cholesteatoma is a cystic collection of keratin debriswhich is enclosed by a sac of stratified squamous keratiniz-ing epithelium which has "invaded" the middle-ear cleft.The mouth of the sac is filled with a characteristic pearlydebris (the keratin squames). Note how the sac can be seenas a white mass deep in the drum and descending behindthe malleus. As the slowly enlarging sac of a cholesteatomacan erode not only the ossicle but also the bone of the mas-toid, surgical removal is usually necessary to prevent se-vere damage to the structure of the middle ear or even tothe adjacent intracranial structures.

CAN. FAM. PHYSICIAN Vol. 33: JUNE 19871506

Figure 18Glomus Jugulare TumourThis slowly enlarging and locally invasive vascular tumourarises from chemoreceptor tissue (the glomus bodies)within the middle ear. The usual symptom is that of a pul-satile tinnitus in the affected ear. Note the red vascular tu-mour behind the tympanic membrane. Glomus tumoursfrequently have a visible arterial pulsation. Small to me-dium-sized glomus tumours can usually be surgically re-moved (after embolization to reduce their vascularity),while large tumours which have extended intracraniallymay be treated by local irradiation.

Dr. Hawke, chief of Otolaryngology at St. Joseph'sHealth Centre, Toronto, has a special interest in diseasesof the ear. Dr. Kwok practised otolaryngology in HongKong before becoming a research fellow at St. Joseph'sHealth Centre, Toronto. Requests for reprints to: Dr.Michael Hawke, Ste. 10, 1849 Yonge St., Toronto, Ont.M4S 1Y2Colour printing sponsored by Beecham Laboratories Inc.

(ranitidine HCI)

Prescribing InformationZantac Tablets (ranitidine hydrochloride)Pharmacological Classification Histamine H2-receptor antagonistIndications and Clinical use-Zantac Tablets are indicated for the treatment of allconditions where a controlled reduction of gastric secretion is required for the rapid relief ofpain and/or ulcer healing. These include duodenal ulcer, benign gastric ulcer and refluxoesophagitis.Contraindications-Zantac is contraindicated for patients known to have hypersensitivity tothe drug.Warnings-Gastric ulcer -Treatment with a histamine H2-antagonist may mask symp-toms associated with carcinoma of the stomach and therefore may delay diagnosis of thecondition. Accordingly, where gastric ulcer is suspected the possibility of malignancy shouldbe excluded before therapy with Zantac Tablets is instituted.Precautions- Use In pregnancy and nursing mothers -The safety of Zantac in thetreatment of conditions where a controlled reduction of gastric secretion is required duringpregnancy has not been established. Reproduction studies performed in rats and rabbits haverevealed no evidence of impaired fertility or harm to the foetus due to Zantac. If theadministration of Zantac is considered to be necessary, its use requires that the potentialbenefits be weighed against possible hazards to the patient and to the foetus. Ranitidine issecreted in breast milk in lactating mothers but the clinical significance of this has not beenfully evaluated.Use In Impaired renal function - Ranitidine is excreted via the kidney and in the presenceof severe renal impairment, plasma levels of ranitidine are increased and prolonged.Accordingly, in the presence of severe renal impairment, clinicians may wish to reduce thedose to a half of the usual dose taken twice daily.Children - Experience with Zantac Tablets in children is limited and such use has not beenfully evaluated in clinical studies. It has however been used successfully in children aged 8-18years in doses up to 150 mg twice daily without adverse effect.Interactions with other drugs -Although ranitidine has been reported to bind weakly tocytochrome P450 in vitro, recommended doses of the drug do not inhibit the action of thecytochrome P450-linked oxygenase in the liver. There are conflicting reports in the literatureabout possible interactions between ranitidine and several drugs; the clinical significance ofthese reports has not been substantiated. Amongst the drugs studied were warfarin,diazepam, metoprolol and nifedipine.Adverse Reactions-Headache, rash, dizziness, constipation, diarrhoea and nadsea havebeen reported in a very small proportion of drug-treated patients but these also occurred inpatients receiving placebo. A few patients on re-challenge with Zantac have had a recurrenceof skin rash, headache or dizziness. Some increases in serum transaminases and gamma-glu-tamyl transpeptidase have been reported which have returned to normal either on continuedtreatment or on stopping Zantac. In placebo controlled studies involving nearly 2,500patients, there was no difference between the incidence of elevations of SGOT and/or SGPTvalues in the Zantac-treated or placebo-treated groups. Rare cases of hepatitis have beenreported but have been transient and no causal relationship has been established.

Anaphylactoid reactions (anaphylaxis, urticaria, angioneurotic oedema, bronchospasm)have been seen rarely following the parenteral and oral administration of Zantac. Thesereactions have occasionally occurred after a single dose.

Decreases in white blood cell count and platelet count have occurred in a few patients.Other haematological and renal laboratory tests have not revealed any drug related abnormalities.

No clinically significant interference with endocrine or gonadal function has been reported.Symptoms and Treatment of Overdosage - No particular problems are expectedfollowing overdosage with Zantac. Symptomatic and supportive therapy should be given asappropriate. If need be, the drug may be removed from the plasma by haemodialysis.Dosage and Administration -Adults: Duodenal ulcer and benign gastric ulcer: 300 mgonce daily, at bedtime. It is not necessary to time the dose in relation to meals. In most casesof duodenal ulcer and benign gastric ulcer, healing will occur in four weeks. In the smallnumber of patients whose ulcers may not have fully healed, these are likely to respond to afurther course of treatment.

Patients who have responded to this short term therapy, particularly those with a historyof recurrent ulcer, may usefully have extended maintenance treatment at a reduced dosage ofone 150 mg tablet at bedtime.

To help in the management of reflux oesophagitis, the recommended course oftreatment is one 150 mg tablet twice daily for up to 8 weeks.

Experience with Zantac in children is limited and it has not been fully evaluated in clinicalstudies-see Precautions.Availability-Zantac Tablets are available as white film-coated tablets engravedZANTAC 150 on one face and GLAXO on the other, containing 150 mg ranitidine (as thehydrochloride), in packs of 28 and 56 tablets.Zantac Tablets are also available as white, capsule shaped, film-coated tablets engravedZANTAC 300 on one face and GLAXO on the-other, containing 300 mg ranitidine (as thehydrochloride) packed in cartons containing 28 tablets.

Zantac Injection is available as 2 mL ampoules each containing 50 mg ranitidine (as thehydrochloride) in 2 mL solution for intravenous or intramuscular administration. Packages of10 ampoules.References:1. Gledhill T. et al: Single nocturnal dose of an H2-receptor antagonist for thetreatment ofduodenal ulcer GUT 1983, 24:904-908. 2. Dragstedt L.R. & Owens, F.M.: Supradiaphrag-matic section of the vagus nerves in treatment of duodenal ulcer. Proc. Soc. Exp. Biol. (NY)1943, 53:152-154. 3. Colin-Jones D.G.: Comparison of ranitidine, 150 mg twice daily, withranitidine 300 mg in one evening dose, in the treatment of duodenal ulcer. In Misiewicz J.J. &Wood J.R. (eds) Ranitidine Therapeutic Advances, Excerpta Medica 1984, 140-153. * SeeAppendix at end of chapter for physicians collaborating in this study. 4. Dammann H.G. etal: Affects of histamine H,-receptor antagonists and other agents on Intragastric Acidity andAcid Secretion. In Misiewicz J.J. & Wood J.R. (eds) Ranitidine Therapeutic Advances,Excerpta Medica 1984,126-139.

GlaxroGlaxo LaboratoriesA Glaxo Canada Limited Company PMBToronto, Ontario Montreal, Quebec ICCPP

CAN. FAM. PHYSICIAN Vol. 33: JUNE 1987 1507