Chronic suppurative otitis media is one of the most common ear infections in the world. Dr. M. DJamil hospital in padang, penulis, is the only hospital in the country that has a dedicated otis media unit. The department of ENT at the University of Andalas is the only one in the country to offer this service.
Chronic suppurative otitis media is one of the most common ear infections in the world. Dr. M. DJamil hospital in padang, penulis, is the only hospital in the country that has a dedicated otis media unit. The department of ENT at the University of Andalas is the only one in the country to offer this service.
Chronic suppurative otitis media is one of the most common ear infections in the world. Dr. M. DJamil hospital in padang, penulis, is the only hospital in the country that has a dedicated otis media unit. The department of ENT at the University of Andalas is the only one in the country to offer this service.
Shofi Faiza (1010312069) Mohd. Luthfi B (1010312024)
Preceptor : dr. Jacky Munilson, Sp.THT-KL
ENT HN DEPARTMENT DR. M. DJAMIL HOSPITAL PADANG FACULTY OF MEDICINE, UNIVERSITAS ANDALAS 2014 2
PREFACE Alhamdulillah, we extend our gratitude to Allah SWT, thanks to His grace and guidance so that we can finish this paper with the title "Chronic Suppurative Otiti Media". We say also successive greetings to Prophet Muhammad and his family, companions and followers. This paper is one of the requirements for their clinical follow ENT health sciences at the Faculty of Medicine, University of Andalas. We would like to thank our precept dr.Jacky Munilson, Sp.THT-KL as mentors who have provided input and guidance in the preparation of this paper, We are fully aware that this paper is still far from perfection, therefore we expect criticism and suggestions to improve this paper. Hopefully, this paper can be useful for us all to understand the importance of chronic suppurative otitis media.
Padang, June 2014 Penulis
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TABLE OF CONTENT PREFACE CHAPTER 1 FOREWORD 1.1.Introduction..................................................................................................... 4 1.2.Point of discussion............................................................................................5 1.3.Goals..............................................................................................................5 1.4.Method...........................................................................................................5 BAB II LITERATURE REVIEW 2.1.Anatomy ...6 2.2.Physiology....12 2.3.Definition.........................................................................................................12 2.4.Classification...13 2.5.Epidemiology..................................................................................................13 2.6.Etiology and Pathogenesis......................................................................... 14 2.7.Clinical Manifestation.....................................................................................15 2.8.Diagnosis..........................................................................................................15 2.9.Complication....................................................................................................16 2.10. Treatment .........................................................................................21 2.11. Differential diagnosis.......................................................................... 27 2.12. Prognosis....................................................................................................27 CHAPTER III CASE ILUSTRATION.............................................................29 CHAPTER IV DISCUSSION ... 33 REFERENCES ...34
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CHAPTER 1 FOREWORD
1. 1. Introduction Chronic suppurative otitis media (CSOM) is the result of an initial episode of acute otitis media and is characterized by a persistent discharge from the middle ear through a tympanic perforation. The chronic otitis media is defined as a permanent perforation of the drum membrane, which does not close by itself, and an inflammatory reaction in the mucosa (mucositis) of the middle ear. It is an important cause of preventable hearing loss, particularly in the developing world. The larger the tympanic membrane perforation, the more likely the patient is to develop CSOM. Some studies estimate the yearly incidence of CSOM to be 39 cases per 100,000 persons in children and adolescents aged 15 years and younger. In Britain, 0.9% of children and 0.5% of adults have CSOM. In Israel, only 0.039% of children are affected. 1,2 Microbial, immunological, and genetically determined factors, as well as Eustachian tube characteristics, are supposed to be involved in the pathogenesis of CSOM, many aspects of the pathogenesis of CSOM still need to be clarified. Optimal treatment strategy has not been established yet. The objective of this review is to present and evaluate the current state of knowledge of CSOM. 3 Two main forms of the chronic otitis media are distinct: the suppurative otitis media and the cholesteatoma. The suppurative otitis media is often accompanied by secretion into the external ear canal (otorrhoe), but "dry ears" are also common. Other frequent, but not obligatory symptoms are hearing impairment, tinnitus, and aural pain or pressure. Although genetically determined microbial and immunological factors, as well as Eustachian tube characteristics, are supposed to be involved in the pathogenesis of chronic suppurative otitis media, many aspects of the pathogenesis still need to be clarified. Ear microscopy will show the perforation in the drum membrane. Further diagnostic tools are audiometry, vestibular testing, radiological examination (high-resolution 5
computed tomography) and microbiological investigation. The curative treatment for chronic suppurative otitis media is surgery (tympanoplasty, i.e. closure of the perforation in the drum membrane and also--if necessary--the reconstruction of the ossicular chain), not conservative antimicrobial therapy. 3 To help identify the disease at an early stage without unduly increasing the number of unnecessary referrals to specialists, the questions that health workers should ask and the procedures for visualizing the eardrum must be refined, standardized, and validated. Before the management of any patient with CSOM one should take into account the fact that patients with intracranial or extracranial infections are more appropriately treated with surgery.Mastoidectomy with or without tympanoplasty eradicates mastoid infection in about 80% of patients and may be combined with surgical drainage of otogenic abscesses elsewhere. However, such treatment is costly and does not always lead to satisfactory hearing improvement, and is inaccessible in many developing countries. 1
1.2 Point of discussion This working paper dicusses about definition, epidemiology, etiology, pathogenesis, clinical manifestation, diagnoses, complication, treatment, and prognoses of chronic suppurative otitis media.
1.3 Goal This working paper has goal to improve knowledge about Chronic Suppurative Otitis Media 1.4 Method Method of this working paper by using literature review and clinical study.
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CHAPTER 2 LITERATURE REVIEW 2.1 Anatomy External Ear
Figure 2.1 The external or outer ear is that portion of the ear that is lateral to the tympanic membrane. It consists of the external auditory canal as well as the auricle and cartilaginous portion of the ear. The auricle is a semicircular plate of elastic cartilage characterized by a number of ridges or grooves. The major ridges of the auricle are the helix and antihelix, the tragus and antitragus, which surround the concha, (figure 1.1) which is the scaphoid depression posterior to the external auditory meatus. 9 7
Figure 2.2 The cartilage of the external auditory meatus is continuous with that of the outer portion of the ear canal and auricle. The external auditory canal is made up of a cartilaginous extension of the auricle in its outer half and the mastoid and tympanic portion of the TB in its medial half. Tympanic membrane circular and concave when viewed from the direction of the ear canal and seen obliquely to the axis of the ear canal. The upper part is called the pars flaccida (shrapnell membrane), while the lower part is called the pars Tensa (membrane propria). Pars flaccida consists of two layers, namely the outer ear canal is skin epithelium and the inside is lined with ciliated cube cells, such as airway mucosal epithelium. Pars Tensa has one more layer is the middle layer consisting of collagen fibers and elastin fibers that little run radier on the outside and circular on the inside.
Figure 2.3 8
Shadow protrusion malleus on the bottom of the tympanic membrane called the umbo. From the umbo there will be light reflex (cone of light) toward the bottom is at 7 o'clock for the left ear and right ear at 5 oclock. 10
Medial ear
Figure 2.4 The middle ear is an air-filled cavity called the tympanic cavity (tympanum). The walls of the cavity are formed from the temporal bone and the cavity is lined with mucous membrane tissue. The overall volume of the middle ear is approximately 2 cm 3 (0.12 in 3 ). 3 The lateral wall of the middle ear contains the tympanic membrane (previously described), and the medial wall is formed by a bony wall that separates the middle ear from the inner ear. This wall contains two membranous windows, called the oval and round windows, which act to anatomically and physiologically connect the middle ear with the inner ear. The air in the middle ear cavity remains just below atmospheric pressure due to the connection between the tympanic cavity and the upper part of throat (nasopharynx) by a narrow duct called the Eustachian tube (auditory tube). 9
Within the middle ear cavity are three small bones called the malleus (hammer), incus (anvil), and stapes (stirrup). These bones are collectively called the ossicles and form a chain called ossicular chain that connects the tympanic membrane with the oval window. The chain is suspended inside the cavity by middle ear ligaments and two middle ear muscles: the tensor tympani and the stapedius. 13
Figure 2.5 Inner Ear The inner ear is the final and the most complex part of the ear. It occupies a small bony cavity called the bony labyrinth (osseous labyrinth) that is located directly behind the medial wall of the middle ear. The inner ear consists of three main anatomical elements: the semicircular canals, the vestibule, and the cochlea. The structure and main elements of the inner ear are shown in Figure 8-10. The bony labyrinth of the inner ear has a volume of approximately 2 cm and is lined by the membranous labyrinth that closely follows the shape of the bony labyrinth. 5 The blood supply to the membranous labyrinth is provided by various small blood vessels extending from the labyrinthine artery. The space between the bony labyrinth and the membranous labyrinth is filled with incompressible body 10
fluid called perilymph. The perilymph is high in sodium but low in potassium resembling in its chemical composition in the blood and the cerebrospinal fluid surrounding the brain. The space inside the membranous labyrinth is filled with another incompressible body fluid called endolymph. Endolymph is low in sodium but high in potassium and chemically resembles the intercellular fluid found inside cells in the body. The differences in the chemical composition of the perilymph and endolymph create an electric potential difference that like a battery, sustains the physiological activities of the sensory organs located in the inner ear. 12
Figure 2.6 Cochlea The cochlea is a coiled structure that resembles the snail and extends anteriolaterally from the vestibule. Its structural base is the bony spiral lamina, which makes 2 to 2 turns around the bony core of the cochlea called the modiolus. The external diameter of the cochlea varies from approximately 9 mm (0.35 in) at its base to approximately 5 mm (0.20 in) at its apex (top) and its uncoiled length is 32 to 35 mm (1.25 to 1.38 in). The cochlea is divided along its 11
length into three parallel channels: the scala vestibuli, scala media, and scala tympani. The scala vestibuli and scala tympani are parts of the bony labyrinth whereas the scala media is a part of the membranous labyrinth. The scala vestibuli and scala tympani are connected at the apex (top) of the cochlea through a small opening called the helicotrema. At the base of the cochlea, the scala vestibuli joins the vestibule. The scala vestibule is terminated at its base by the oval window, the fenestra ovalis, while scala media terminates at the round window, the fenestra rotunda. The membrane of the oval window has a surface area of 3.2 to 3.5 mm2, is completely covered by the footplate of the stapes, and is sealed in the bony opening by the annular ligament. The round window has a surface area of approximately 2 mm 2 and is located inferior and anterior to the oval window in the wall between the middle ear and inner ear and serves as a pressure valve between the two scalae. When an acoustic stimulus causes mechanical vibration of the stapes footplate this movement is translated to the membrane of the oval window. The membrane pushes back and forth on the perilymph of the scala vestibuli and through the helicotrema, the perilymph of the scala tympani. This motion results in alternating outward and inward movement of the membrane of the round window. The membrane bulges outward as the fluid moves from the scala vestibuli to the scala tympani and bulges inward as the fluid moves from the scala tympani to the scala vestibule. 12 Organ Corti Organ of Corti lies in the width of the basilar membrane in the basal part of 0:12 mm and up to 0.5 mm wide at the apex, shaped like a spiral. Some of the important components of the organ of Corti is the hair cells inside, the outer hair cells, supporting Deiters cells, Hensen's, Claudiu's, tektoria membrane and reticular lamina. Hair cells are arranged in four rows, which consists of 3 lines of the outer hair cells are located lateral to the tunnel formed by the pillars of Corti, and a line of hair cells located in the medial to the tunnel. Hair cells in the amounts to about 3500 and the number of outer hair cells play a role in changing 12
the 12000 sound conduction in the form of mechanical energy into electrical energy. 9
Figure 2.7 2.2 Physiology Scheme of the hearing process begins with the arrest of sound energy by the outer ear and vibrate the tympanic membrane into the middle ear and passed through a series of bone loss that would amplify the vibrations through the ossicular leverage and multiplication ratio of the tympanic membrane and the oval aperture. Vibrating energy that has been amplified is passed to the inner ear and are projected on the basilar membrane, so that will cause relative motion between the basilar membrane and membrane tektoria. This process is mechanical stimuli that cause deflection stereosilia hair cells, so that the ion channels open and the release of electrically charged ions from the cell body. This situation raises the hair cell depolarization, thus releasing neurotransmitters into the synapse that would give rise to an action potential in the auditory nerve, and then proceed to the auditory nucleus to the auditory cortex. 9 2.3 Definition A unifying definition of the term chronic otitis media is any structural change in the middle ear system associated with a permanent defect in the 13
tympanic membrane (TM). 1 Chronic supurative otitis media (CSOM) is chronic infection in middle ear with tymphanic membrane perforation and with secretions that come out continuously or intermittent. 2 The condition is considered chronic if the TM defect is present for a period greater than 3 months. 1 Generally, patients with tympanic perforations which continue to discharge mucoid material for periods of from 6 weeks to 3 months, despite medical treatment, are recognized as CSOM cases. The WHO definition requires only 2 weeks of otorrhoea, but otolaryngologists tend to adopt a longer duration, e.g. more than 3 months of active disease. 1
2.5 Classification CSOM can be divided into 2 type in general : 10 a. Safety type CSOM (benigna) The process of inflammation is confined to the mucosa only and usually not on the bone. Perforations located in the central part. Generally safety type CSOM rarely cause dangerous complications and no cholesteatoma. b. Danger type CSOM (maligna) In this danger type is usually accompanied by cholesteatoma. This CSOM is also known by bone type. Perforation of this type located in marginal or in attic. Most of these danger type are accompanied with danger and fatal complications.
Based on the known activity of secretions known active and inactive type CSOM. Active type CSOM is secretions out of the tympanic cavity is actively while inactive type is a state when tympanic membrane looks wet or dry and the secretions not active. 10
Other classification devided into 2 groups : CSOM with cholesteatoma or CSOM without cholesteatoma. 2.6 Epidemiology 14
Prevalence survey by WHO show that global burden oh illness from CSOM involves 65-330 million indviduals with draining ears, 60% oh whom (36-200 million) suffer from significant hearing impairment. CSOM accounts for 28.000 deaths and a disease burden over 2 million DALYs. Over 90% of the burden is borne by countries in the South-east Asia and Western Pacific regions, Africa and several ethnic minorities in the Pacific rim. 6 Some studies estimate the yearly incidence of CSOM to be 39 cases per 100,000 persons in children and adolescents aged 15 years and younger. In Britain, 0.9% of children and 0.5% of adults have CSOM. In Israel, only 0.039% of children are affected. 7 Other populations at increased risk include children from Guam, Hong Kong, South Africa, and the Solomon Islands. The prevalence of CSOM appears to be distributed equally between males and females.Exact prevalence in different age groups is unknown; however, some studies estimate the yearly incidence of CSOM to be 39 cases per 100,000 in children and adolescents aged 15 years and younger. 14 2.7 Etiology and Pathogenesis The diagnosis of CSOM requires a perforated tympanic membrane. These perforations may arise traumatically, iatrogenically with tube placement, or after an episode of acute otitis media, which decompresses through a tympanic perforation. Most of the CSOM develop from acute otitis media (AOM), with condition : late therapy, non-adequate therapy, high virulence bacterial, lack of immunity or bad hygiene. 10 In CSOM the bacteria may be aerobic (Pseudomonas aeruginosa, Escheria coli, S.aureus, streptococcus pyogenes, proteus mirabilis, Klabsiela species) or anaerobic (Bacteroides, Peptostreptococcus, Proprionibacterium). These bacteria are infrequently found in the skin of the external canal, but may proliferate in the presence of trauma, inflammation, lacerations or high humidity. 1 There are several risk factor which cause CSOM : a. Chronis inflammation due to persisten Eustachian tube dysfunction. 15
b. Genetic and constitutional factor that affect healing capacity and resistance of the mucosa c. Special anatomic characteristic s oh the middle ear spaces such as pneumatization and relative size. d. The nature, pathogenicity, virulence, and resistance oh the infecting organ. The presence of perforation tympanic membrane cause infection from the ear canal. 1 And also cause cholesteatoma. Cholesteatoma is epiterial cyst containing epithelial desquamation (cheratine). It formed by the entry of the ear canal skin from the side of a perforated tympanic membrane or ear canal into the middle or occur as a result of the tympanic cavity mucous metaplasia due to infection that lasts a long time. Cholesteatoma is a good medium for the growth of germs (infection). The most frequent is proteus and pseudomonas aeruginosa. And these infections can lead to local immune response resulting in the production of various inflammatory mediators and cytokines. These inflammatory mediators stimulate cells cholesteatoma keratinocytes are hyperproliferative, destructive and stimulate angiogenesis. This will suppress the cholesteatoma mass and surrounding organs and urgent cause necrosis of the bone. The process was intensified by necrosis of the bone due to the formation of acid reaction by bacterial decay. This facilitates the process of bone necrosis onset of complications such as labyrinthitis, meningitis and brain abscess. 1,6,9 2.8 Clinical manifestation CSOM safety type usually present initially with chronic otorrhea, generally a mucopurulent discharge. After the secret clear the patient few or no ther symptoms other than a variable degree oh hearing loss. For acute exacerbations inflammation usually present pain in several patient. 1 CSOM danger type present abses or retroauriculer fistel, polyp, or granulation tissue in outer ear canal. And also present mucopurulent secret and characteristic odor. 1 2.9. Diagnosis 16
1. Anamnesis History-taking should be carried out to elicit the symptoms of ear pain, ear discharge, ear tugging or crying when the ear is touched, all of which suggest an ear problem. 1 A history of previous ear discharge, especially when accompanied by episodes of colds, sore throat, cough or some other symptom of upper respiratory infection, should raise the suspicion of CSOM. A history of vigorous ear cleaning, itching or swimming that could traumatize the external ear canal suggests acute otitis externa (AOE), and not usually CSOM. A history of ear pain suggests AOE or AOM, not usually CSOM 4 . In the case of AOM, the ear is only painful until the eardrum perforates, relieving the pressure. Thus, if the main symptom is painless otorrhoea, the duration of otorrhoea will help distinguish AOM from CSOM. Reliable history-taking depends on good recall on the part of the patient or carer, an infrequent trait since neither parents nor teachers of children with otitis media have been shown to reliably estimate the number of otitis media episodes, the degree of hearing loss, or the possible impact of the condition 5 . The exact duration of otorrhoea that distinguishes CSOM from AOM is controversial, but this is only crucial in the absence of actual visualization of the eardrum. The size of the perforation, character of discharge, and the appearance of the middle ear mucosa on otoscopy can confirm the presence of CSOM more than patient anamnesis.
2. Physical Examination 1
Otoscopy The diagnosis of CSOM rests on the verification of a discharging tympanic perforation. This is only possible by removing any obstructing wax, ear discharge, debris or masses in the external auditory canal and visualizing the whole expanse of the eardrum and, if possible, the middle ear through the perforation. Such an examination requires adequate illumination through a head mirror, head light, otoscope or otomicroscope, suction apparatus and small instruments. 17
Not all draining ears are CSOM. Acute otitis externa and acute otitis media can produce both ear pain and ear discharge. However, tragal pain is found in otitis externa, mastoid pain in otitis media. The discharge in otitis externa is less profuse and foul-smelling and there is no mucus, as can be tested with a cotton mop by the tendency to form mucus threads. Fever is also higher in otitis media than in otitis externa. 4 CSOM produces painless mucoid otorrhoea without fever, unless accompanied by otitis externa or complicated by an extracranial or intracranial infection.
Figure 2.8 central perforation
The diagnostic value of bacterial cultures In places where bacterial cultures are available, can they be used to aid in diagnosing CSOM ? . Bacterial cultures may not be needed to establish the diagnosis of CSOM since exhaustive studies have established that 90100% of chronic draining ears yield two or more isolates consisting of both aerobic and anaerobic bacteria. Also, treatment may eradicate middle ear bacteria but this does not guarantee non-recurrence of otorrhoea or complete resolution of the CSOM. Leiberman et al. reported recovering Pseudomonas aeruginosa from draining ears in the pre-treatment and in the recurrent stage. Some would argue that perforated drums might develop discharge from time to time even without the presence of bacteria and that this does not constitute CSOM which must be treated. In practice, however, patients with draining ears do expect some treatment regardless of culture results. Since topical treatment is often effective and seldom 18
harmful, most experts would start with a wide-spectrum antibiotic on an empiric basis and make a request for cultures if drug resistance is suspected.
2.10. Complication In the present era of antibiotics, complications from CSOM are rarely seen because of early antibiotic intervention. However, surgery does play an important role in managing CSOM with or without cholesteatoma. CSOM without prompt, proper treatment can progress to a variety of mild to life-threatening complications that can be separated into 2 subgroups: intratemporal and intracranial.
Intratemporal complications include petrositis, facial paralysis, and labyrinthitis. Intracranial complications include lateral sinus thrombophlebitis, meningitis, and intracranial abscess. Sequelae include hearing loss, acquired cholesteatoma, and tympanosclerosis. 4
Petrositis Petrositis occurs when the infection extends beyond the confines of the middle ear and mastoid into the petrous apex. Patients may present with Gradenigo syndrome (ie, retro-orbital pain, aural discharge, and abducens palsy). A CT scan of the head and temporal bone helps define the extent of the disease, diagnose any intracranial spread, and plan a surgical approach. Treatment includes systemic culture-directed antibiotics with petrous apicectomy in cases that do not respond to medical therapy. Facial paralysis Facial paralysis may occur in the setting of CSOM with or without cholesteatoma. Surgical exploration with removal of diseased mucosa, granulation tissue, and inspissated pus (usually by mastoidectomy) should be undertaken promptly in the setting of cholesteatoma or chronic otitis media. Labyrinthitis 19
Labyrinthitis occurs when the infection spreads to the inner ear. This may happen emergently or over an extended period. The infection gains access to the inner ear through the round and oval windows or through one of the semicircular canals exposed by bony erosion. The 4 categories of labyrinthitis have been recognized as acute serous, acute suppurative, chronic, and labyrinthine sclerosis. The symptoms of acute serous labyrinthitis are acute onset of vertigo and hearing loss. Early surgical exploration to remove the infection may reduce damage to the labyrinth. Patients with acute suppurative labyrinthitis present with profound hearing loss, tinnitus, and vertigo with associated nausea and vomiting. Patients initially demonstrate nystagmus with the rapid component directed toward the affected ear; they later demonstrate nystagmus away from the affected ear after destruction of the membranous labyrinth. Treatment includes aggressive surgical debridement (including labyrinthectomy) to prevent the possibly lethal intracranial complications of meningitis or encephalitis. Administration of broad-spectrum antibiotics with cerebrospinal fluid penetration is also necessary. Culture and sensitivities should direct any changes in the antibiotic regimen. Chronic labyrinthitis is characterized by the gradual onset of vertigo, tinnitus, and hearing loss. Most commonly, the infection reaches the labyrinth through the lateral canal. Treatment involves mastoidectomy, culture, and appropriate medical therapy. Labyrinthine sclerosis occurs as the inflammation in the labyrinth causes the body to replace it with fibrous tissue and new bone. Lateral sinus thrombophlebitis Lateral sinus thrombophlebitis occurs as the infection extends through the mastoid bone into the sigmoid sinus. The infected thrombus may release septic emboli, causing distal infarcts. Patients may present with altered mental status, headaches, retroauricular pain, postauricular edema, and fever. Mastoidectomy with incision and drainage of perisinus purulence is indicated in patients who do not respond to systemic antibiotics. Removal of the entire thrombus until bleeding 20
is visualized is not necessary and may result in additional complications, including intracranial hemorrhage. Ligation of the internal jugular vein is rarely required for patients with progressive septic emboli who do not respond to systemic therapy. Culture-directed antimicrobial treatment is the first step in the management of sinus thrombophlebitis. Debate still exists on the necessity of anticoagulation and its efficacy in establishing recanalization of the sinus. 5
Meningitis Meningitis develops as a consequence of direct or hematogenous spread of the infection. If meningitis is suspected, a lumbar puncture should be performed to recover the causative organism for culture and sensitivity prior to the initiation of empiric broad-spectrum antibiotic therapy. When stable, patients are taken to the operating room for surgical removal of the cholesteatoma or middle ear infection. Intracranial abscesses The various intracranial abscesses that may occur can be extradural, subdural, or parenchymal. A patient with an extradural abscess may present with meningitic signs and symptoms or may be asymptomatic. Regardless of the presentation, imaging to define the abscess should be acquired, and the abscess should be drained with the assistance of neurosurgeons as needed. Patients with subdural abscesses are very ill and exhibit meningeal signs, possible seizures, and hemiplegia. Prompt neurosurgical consultation, adequate imaging, drainage, and antibiotics are the appropriate treatment. Otologic surgery to remove the nidus of infection is necessary once the patient has stabilized. Parenchymal abscesses occur as the infection spreads through the tegmen tympani or tegmen mastoideum to the temporal lobe or the cerebellum. Their presentation may be indolent, as this disease initially grows in "silent" areas of the brain. However, if the clinician suspects intracranial involvement, the previous plan of imaging, neurosurgical drainage, and antibiotic therapy is the standard of care. 6
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Middle ear complications Conductive hearing loss as a consequence of CSOM may result from the perforated tympanic membrane, a disruption in the ossicular chain, or both. Surgical removal of the infection and cholesteatoma with ossicular chain reconstruction mitigates morbidity associated with decreased hearing. 2.11. Treatment 2.11.1 Medical management 9 The treatment of CSOM generally begins with local care of the ear and outpatient medical management. For medical management to be successful, aural toilet is imperative. This intervention requires repeat microscopic examination of thebear and diligent suctioning. The main goal is to remove debris from the external auditory canal (EAC) overlying the TM and middle ear cleft so that topical antimicrobial agents can successfullybpenetrate to the middle ear mucosa. 9 Topical medications may include antibiotics, antifungals, antiseptics, and corticosteroid preparations alone or in combination with other medications. The use of neomycin in ototopical preparations continues to be extremely widespread owing to long-standing prescribing habits and low cost, despite the fact that almost no strains of Pseudomonas remain sensitive to this medication. In addition, there is a fairly high incidence of localized and diffuse allergic reactions to the topical use of neomycin. For these reasons, preparations containing neomycin should eventually fade from the ototopical armamentarium. More recently, fluoroquinolone antibiotic drops such as ciprofloxacin and ofloxacin have gained popularity because of their antipseudomonal properties, minimal bacterial resistance, and lack of ototoxicity. If otorrhea is profuse, it may be helpful to have the patient irrigate the ear daily with a body temperature half-strength solution of acetic acid (50% white vinegar diluted with warm water) prior to the application of otic drops. 9 The use of systemic antibiotics in COM is limited by several factors. Antibiotic penetration into the middle ear may be hampered by mucosal edema. 22
Systemic aminoglycosides carry a risk of ototoxicity and require parenteral administration with monitoring of serum levels. Oral ciprofloxacin has proven to be a safe and effective treatment for adults with COM; however, safety in patients under 18 years of age has not been established. 9 For patients with otorrhea secondary to cholesteatoma, the hope is to minimize granulation tissue and perhaps achieve a dry ear prior to surgical intervention. Before addressing the granulation tissue with topical cautery, one must be reasonably convinced that the critical landmarks are properly identified and that there is no dural defect with an encephalocele present. 9 Medical management of COM may be difficult for both the patient and the physician. Multiple office visits are often required for adequate aural toilet. Patients are asked to comply with a regimen that may include not only daily irrigation but also multiple administrations of otic drops throughout the day. Medical treatment usually requires 14 to 21 days. Most often, it is appropriate to proceed to operation if the ear does not respond to microscopic dbridement and ototopical management. 9
2.11.2 Surgical Management 9 The primary goal of surgery for COM is to eradicate disease and obtain a dry, safe ear. Restoration of hearing is by necessity a secondary consideration because any attempt at middle ear reconstruction will fail in the setting of persistent inflammation and otorrhea. Absolute indications for surgical intervention include impending or established intratemporal or intracranial complications. Various pathologic conditions within the middle ear, such as cholesteatoma and chronic fibrotic granulation tissue, are irreversible and require elective surgical attention. In addition, patients with otorrhea failing to respond to medical treatment are surgical candidates, as well as those who respond but are left with a correctable conductive hearing loss or a TM perforation. 9
Tympanoplasty The goal of tympanoplasty is to repair the TM with a connective tissue graft in the hope that squamous cell epithelium will proliferate over the graft and 23
seal the perforation. Various grafting materials are available. Autogenous temporalis fascia is used most often because it is readily available through a postauricular incision and is extremely effective. Other alternatives include tragal perichondrium, periosteum, and vein. 9
Preserved homograft materials such as cadaveric TM, dura, and heart valve have limited application because of concern for disease transmission. The two most common approaches are the transcanal tympanomeatal flap and the postauricular approach with creation of a vascular strip. The two classic types of tympanoplasty are the lateral and the medial technique, which define the final relationship of the graft to the fibrous layer of the TM remnant and the anulus tympanicus. 9
In both techniques, the graft is placed medial to the handle of the malleus. The lateral technique is more technically demanding but provides more reliable results when repairing large anterior or pantympanic perforations. It is useful when ear canal anatomy is unfavorable and extensive removal of bone from the anterior canal wall (canalplasty) is necessary. The canalplasty improves access to the anterior half of the TM. The lateral technique may be complicated by displacement of the graft laterally during healing and formation of cholesteatoma between the graft and the remnant of the TM. 9
If, in the canalplasty, the soft tissue of the temporomandibular joint is violated, the posterior aspect of the joint can be eroded, allowing the condyle of the mandible to prolapse into the ear canal. This feared complication is difficult to correct and should be assiduously avoided. The medial technique is easier and less time consuming, and postoperative care is less compared with the lateral technique. Ultimately, the technique chosen will depend on the location of the perforation, the bony anatomy of the EAC, and the surgeons experience. 9
Myringoplasty , which the lightest kind of tympanoplasty type. Reconstruction is only performed on the tympanic membrane , performed on CSOM benign type and quite phase, with only mild hearing loss caused by perforation of the tympanic membrane .
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Ossicular Chain Reconstruction 9
The numerous techniques and middle ear prostheses available to the otologic surgeon lend credence to the claim that ossicular chain reconstruction remains to be perfected. Reconstruction should achieve closure of the airbone gap to within 20 dB in two-thirds of patients with an intact stapes arch and one half of patients missing the stapes superstructure. Autograft ossicles are removed from the patient and sculpted to serve as inter-position grafts. The incus is used most often. Immediate availability, obvious biocompatibility, and a low extrusion rate have made autograft ossiculoplasty very popular. However, extensive bone erosion caused by middle ear disease may limit availability.
Cortical Mastoidectomy 9
Tympanoplasty failures occur in eustachian tube dysfunction and persistent inflammatory disease. For this reason, a cortical mastoidectomy is often recommended as an adjuvant to tympanoplasty. The goal is to eliminate all irreversible mucosal disease, improve mastoid ventilation, and increase the buffering action of the mastoid cavity by enlarging its volume. Intact Canal Wall Tympanoplasty with Mastoidectomy 9
In an attempt to expose and eradicate middle ear disease better while preserving normal anatomic relationships for improved sound conduction, the posterior tympanotomy approach was introduced. This technique allows access from a cortical mastoidectomy defect into the posterior mesotympanum by removal of the bony wall bound by the fossa incudis, the second genu of the facial nerve, and the chorda tympani. Since the access point into the middle ear is the facial recess of the posterior part of the tympanum, this operation is often referred to as a facial recess approach. The major advantage of the intact canal wall (ICW) tympanoplasty with mastoidectomy is the avoidance of a mastoid bowl that requires lifelong cleaning. However, this advantage comes with a higher risk of residual and recurrent disease because preservation of the posterior canal wall limits visualization and access to the middle ear. Because an ICW tympanoplasty with mastoidectomy 25
does not address the problem of negative pressure within the middle ear, ideal candidates are individuals with large pneumatized mastoids and wellaerated middle ear clefts. As a result of the high rate of recidivism, most surgeons advocate a second-stage procedure when treating cholesteatoma in this manner.
Modified Radical Mastoidectomy 9
Today, the classic Bondy modified radical mastoidectomy is used infrequently since it only addresses the rare instance when one is treating isolated atticoantral cholesteatoma with disease lateral and posterior to the ossicles. Modifications have been made to the original approach to explore the middle ear and correct the conductive hearing loss that often results in the setting of cholesteatoma. This combination of the open mastoidectomy and tympanoplasty with or without ossicular chain reconstruction is what most surgeons mean today when they use the term modified radical mastoidectomy. An alternate, less ambiguous term for this operation is tympanoplasty with canal wall down (CWD) mastoidectomy. A small, sclerotic mastoid, a low-lying middle cranial fossa dura, and an anteriorly positioned sigmoid sinus will limit surgical exposure and often necessitate the removal of the canal wall. Other indications include operating on extensive cholesteatoma in the only hearing ear, presence of a large labyrinthine fistula, recurrent retraction cholesteatoma in the epitympanum, and significant destruction of the scutum or posterior canal wall. The major disadvantage of this approach is the need for periodic mastoid bowl cleaning. Success of a CWD mastoidectomy and long-term care of the mastoid cavity depend on key operative techniques, including opening air cells at the sinodural angle, along the tegmen and in the perilabyrinthine region; lowering the facial ridge to leave a thin layer of bone over the facial nerve; exenterating the mastoid tip cells and amputating the tip; saucerizing, by wide beveling, the cavity to form smooth walls; and creating a meatoplasty by resecting a crescent of conchal cartilage. Open cavities take 6 to 10 weeks to heal. During this period, the patient is seen every 2 to 3 weeks for dbridement of the cavity and management of 26
granulation tissue. Early granulation tissue is suctioned away, and the base is cauterized. Early neomembrane formation is disrupted. Ototopical drops with an antibiotic and corticosteroid should be continued until there is no granulation tissue and the cavity is lined with skin.
Radical Mastoidectomy 9
Radical mastoidectomy entails exteriorization of the entire middle ear and mastoid by combining a CWD mastoidectomy with removal of the TM and the ossicles (with the exception of the stapes if present). In doing so, the mastoid, middle ear, and EAC become one common cavity. There is no attempt at middle ear reconstruction, and patients are left with a substantial conductive hearing loss. Given this significant functional deficit, radical mastoidectomy is considered a last resort, usually after previous surgical attempts have failed or when it is not possible to remove mesotympanic cholesteatoma. Radical mastoidectomy is also indicated if middle ear ventilation is impossible owing to complete inadequacy of eustachian tube function.
Mastoid Cavity Obliteration 9
The mastoid cavity created by a radical or modified radical mastoidectomy is at risk for chronic infection and persistent drainage. In the setting of a potentially large cavity, some surgeons elect to perform a mastoid obliteration procedure using materials such as bone pate, cartilage, acrylic, and HA cement. Alternatives include free abdominal fat grafts and regional soft tissue flaps. The major disadvantage associated with obliteration of the mastoid is that recurrent disease can remain hidden within the cavity. A CT scan may be required to evaluate patients for recurrent disease.
2. 12 Differential Diagnosis 1 Difference between CSOM and other forms of chronic otitis media 27
Several systems of nomenclature have been developed to distinguish between different types of otitis media, reflecting the lack of complete understanding of the processes responsible for the inflammation and healing of the middle ear. For the purpose of this report, the presence of a persistent tympanic perforation and middle ear discharge differentiates CSOM from other chronic forms of otitis media. CSOM is also called chronic active mucosal otitis media, chronic oto-mastoiditis, and chronic tympanomastoiditis. A subset of CSOM may have cholesteatomas or other suppurative complications. The non- CSOM group includes such entities as chronic non-suppurative otitis media, chronic otitis media with effusion (COME), chronic secretory otitis media, chronic seromucous otitis media, chronic middle ear catarrh, chronic serous otitis media, chronic mucoid otitis media, otitis media with persistent effusions, and glue ear. All these are recurrent or persistent effusions in the middle ear behind an intact tympanic membrane in which the principal symptom, if present at all, is deafness and not ear discharge. 1
2.13. Prognosis Patients with chronic suppurative otitis media (CSOM) respond more frequently to topical therapy than to systemic therapy. Successful topical therapy consists of 3 important components: selection of an appropriate antibiotic drop, regular aggressive aural toilet, and control of granulation tissue. Inpatient care is rarely necessary for the patient with CSOM. In patients for whom the otolaryngologist chooses systemic parenteral antibiotics, inpatient hospitalization may be required. Otherwise, excluding complications, this disease can be treated effectively in the outpatient setting. Patients who present with suspected intracranial complications to hospitals that function without CT scanning capabilities or neurosurgical care should be transferred as soon as possible to an institution with such capabilities. Antibiotic therapy should be started prior to transfer. 28
Failures of topical antimicrobial therapy are almost always failures of delivery. Specifically, failure of delivery describes the inability of an appropriate topical antibiotic to reach the specific site of infection within the middle ear. Various elements may obstruct the delivery of the medication, including infectious debris, granulation tissue, cholesteatoma, neoplasia, cerumen, and others. When topical therapy fails, the patient needs a thorough evaluation for anatomic obstruction, including microscopic examination and radiologic studies as needed. Additionally, a clear understanding of the very high concentration of the antibiotic within topical preparations must be kept in mind. Surgical Prognosis Tympanoplasty provides most patients with a healed, dry ear. In patients with cholesteatoma, a staged procedure may be beneficial to ensure complete eradication of cholesteatoma. The ossicular chain can be reconstructed with autologous tissue (cartilage, bone) or with prosthetic implants at the second surgery. These patients require diligent surveillance as recurrence of the original disease process is not uncommon. The general and most desirable outcome for a patient who has undergone a tympanomastoidectomy is a dry, nondischarging, healthy ear. Long-term follow- up care of these patients is essential to detect the recurrence of cholesteatoma at its earliest onset. In such cases, another procedure may be necessary. The likelihood of hearing preservation depends on the extent of the disease and the involvement of the ossicles, which varies widely.
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CHAPTER 3 CASE ILUSTRATION PATIENT IDENTITY Name : Mr. M Age : 37 y.o Sex : Male
Anamnesis : Man, 37 y.o, came to ENT-HN Department of Dr. M.Djamil Hospital on June 2 nd , 2014 with Chief complaint : Discharge flew from right ear in a month ago. Clinical course : Patient got discharge in right ear for a month ago Discharge in right ear was looked like clear then yellowish and no smell Symptom increased when cough and cold, History discharge in left ear is negative Patient has right nasal obstruction Patient ever happened pain at the right fore ear history lump behind the left ear negative, negative wry face, dizziness negative spin, nausea vomiting (-) history of loss of consciousness (-) ringing in the ears (+) Past medical history : history sneezing more than 5 ti mes if exposed to dust and cold (-) long history of cough (-) fever (-) Patient clean the ears by his self Smoking (+) , drinking alcohol (-) 30
Patient ever went to see doctor since 6 months ago, then getting cured at that time, but now symptom re-appear and was suggested for operation History of familial disease Atopi (-) history of the same disease Physical examination Vital Sign General state : Good Pulse rate : 84x/ minutes Awareness : CMC Respiratory rate : 20x/minutes Cyanosis : negative Temperature : 36,5 C Edema : negative Icterus : negative
ENT Local Status Examination Abnormality Dextra Sinistra Auricular Congenital abnormality Trauma Metabolic abnormality Retraction pain Tragus pain - - - - - - - - - - Wall and Canal Ear wide enough (N) Narrow Hyperemic Edema Mass + - - - - + - - - - Secrete and cerumen - - Timpani membrane Intact Central perforated Mastoid - - Tuning fork Test Rinne Swabach Weber + Same with examiner No lateralitation - Prolong No lateralitation Paranasal sinus and nasal Congenital abnormalities (-) Outer part No deformity Inner part Vestibulum Nasal cavity Medial concha Inferior concha Septal Secret Mass Vibrae (+) Wide hypertrophy hypertrophy Deviasi (+) - - Vibrae (+) Wide Eutrophy Eutrophy Deviasi(-) - -
Nasopharynx Choana Mucose Tube orifice Open Pink Open Open Pink Open Adenoid - Post nasal drip + Mass - Oropharynx and mouth Pharyngeal arch Palatum Pharyngeal wall Symmetrical Still and uvula in the middle Posterior still Palatine tonsil Size T1 T1 Color Pink Pink Crypt Normo Normo Detritus - - 32
Peritonsil Normal Normal Mass - Teeth Caries + + Tongue Normal Larynx and hypopharynx Epiglotis Aritenoid Pseudo plica vocalis Plica vocalis Subglotis Trachea Mass Still Still Moving symmetrically Moving symmetrically Open Still - Lymphadenopathy -
Imaging findings : Impression: right mastoiditis, no bone destruction, thickening sphenoidalis sinus mucosal and bilateral maxillary sinus, especially at left side. Diagnosis : Chronic Suppurative Otitis Media Auricula Dextra Susp. Benign type, quite Phase Treatment : - Local myringoplasty
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CHAPTER 4 DISCUSSION A male patient , aged 37 years , present with watery right ear at 1 month ago . The fluid that came out initially and then colored clear turned yellowish and odorless . Patients also experienced right ear buzzing with diminished hearing . Complaints increased when patients cough and cold , with a runny nose until thick yellowish translucent color . While the history of the left ear has not discharge and hearing loss. The patient also had experienced pain in the front of the ear . Patients also experience nasal congestion in the nasal cavity of the right. Patients have a habit of picking his own ears and smoking . At 6 months ago the patient had experienced similar complaints , then went to the ENT specialist and experienced recovery, but the complaint re-appeared and advised patients for surgery . In localist ENT status , obtained the right ear canal is quite roomy , central tympanic membrane perforation right , on the right ear, we found Rinne test - , Weber test lateralized to the right , extending swabach test . Results for anterior rinoscopy, nasal cavum quite large, medial concha hypertrophy , inferior concha hypertrophy , septal deviation + ( crest ) , secretions - . Based on history and physical examination , the diagnosis can be established that chronic suppurative otitis media type safe quiet phase . For the definitive management of these patients is myringoplasty , which the lightest kind of tympanoplasty type. Reconstruction is only performed on the tympanic membrane , performed on CSOM benign type and quite phase, with only mild hearing loss caused by perforation of the tympanic membrane . 34
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