Chronic Suppurative Otitis

Etiology

CSOM typically develops after untreated, inadequately treated, or recurrent acute otitis media, particularly when it results in a persistent tympanic membrane perforation, allowing ongoing microbial entry into the middle ear.[4] Tympanic membrane perforations leading to chronic suppurative otitis media may also result from trauma or iatrogenic factors, such as the placement of ventilation tubes or previous ear surgical procedures, including tympanoplasty. Otorrhea is a common sequela in children with tympanostomy tubes, although otorrhea does not necessarily indicate CSOM.[12]

The theories of the mechanics of CSOM include:

• Translocation through the tympanic membrane perforation
  • Bacteria from the external auditory canal pass through the tympanic membrane into the middle ear cleft
  • The pathogens cultured tend to be those predominantly present in the external ear canal
• Eustachian tube reflux (retrograde)
  • Pathogens travel backward up the eustachian tube from the throat to the middle ear cleft
  • Evidence remains inconclusive [13]

Microbiologically, CSOM is usually polymicrobial, with common pathogens including Pseudomonas aeruginosa, Staphylococcus aureus, Proteus spp, and various anaerobes. These organisms often form biofilms on the middle ear mucosa and within the tympanomastoid system, thereby enhancing resistance to host immune defenses and reducing antibiotic efficacy. Therapies targeting bacteria that evade the immune system may become part of the treatment approach for CSOM in the future.[14] Host-related factors such as eustachian tube dysfunction, which impairs middle ear ventilation and drainage, play a central role in disease persistence. Structural disease, such as cholesteatoma, can further perpetuate chronic infection through the accumulation of keratin debris and local tissue destruction.[15] Additional contributing factors for CSOM include immunocompromise, allergic rhinitis, and repeated upper respiratory tract infections, all of which impair mucosal immunity and promote chronic inflammation.[4]

CSOM is more prevalent in resource-limited settings, where overcrowding, poor sanitation, malnutrition, and limited access to primary health care increase the frequency and severity of early childhood ear infections and reduce timely treatment.[1] Socioeconomic deprivation and exposure to environmental risk factors such as secondhand smoke and recurrent upper respiratory tract infections further contribute to disease persistence. Additionally, other risk factors include frequent or untreated acute otitis media, inappropriate treatment of ear infections, genetic predisposition, malnutrition, and structural abnormalities such as cleft palate, Down syndrome, cri du chat syndrome, choanal atresia, DiGeorge syndrome, cleft lip, and microcephaly.[16] Additional factors that increase the likelihood of CSOM include frequent acute otitis media and parents with a history of CSOM.[17] Furthermore, allergies may be another risk factor because results from certain studies have identified allergens that obstruct both the eustachian tube and the nasal passages.[18]

Epidemiology

CSOM is a major global health concern and a leading cause of preventable hearing loss, with prevalence estimates of approximately 1% to 3% in high-income countries and up to 4% in resource-limited regions, where the disease burden is disproportionately concentrated. CSOM is estimated to affect 1 in 26 people globally, or more than 297 million people, including 64 million with bilateral disease and 184 million with associated hearing loss.[19] Hearing loss strongly correlates with both the size of the perforation and the likelihood of CSOM.[20] CSOM most commonly affects children, particularly in resource-limited countries, reflecting the high incidence of early-life upper respiratory tract infections, limited access to timely medical care, and reduced availability of appropriate antimicrobial therapy. CSOM is a major global disease, underscoring the need for heightened awareness, increased health resources, and public health approaches to combat it. Beyond its clinical impact, CSOM also carries economic implications through healthcare costs, chronic disability affecting employment, and education.

Epidemiologically, CSOM is strongly associated with socioeconomic deprivation, overcrowding, malnutrition, and inadequate sanitation, all of which increase the risk of recurrent acute otitis media and impede the resolution of middle ear infection. Environmental exposures such as secondhand tobacco smoke and poor indoor air quality further increase susceptibility. Disease persistence is influenced by underlying risk factors, including persistent tympanic membrane perforation, eustachian tube dysfunction, and structural middle ear disease such as cholesteatoma, which promote ongoing bacterial colonization and inflammation.

The burden of CSOM is also higher in populations with limited access to specialist otolaryngologic care and hearing rehabilitation services, leading to delayed diagnosis, prolonged disease duration, and increased risk of long-term complications, including permanent hearing loss. Populations at increased risk of CSOM include American Indian people, Eskimo populations, and children from Guam, Hong Kong, South Africa, and the Solomon Islands.[21] Prevalence does not appear to differ by sex. 

Pathophysiology

Chronic suppurative otitis media (CSOM) is characterized by persistent infection and inflammation of the middle ear cleft, resulting from unresolved acute otitis media, ongoing eustachian tube dysfunction, or structural middle ear disease. The condition is sustained by a cycle of impaired ventilation, chronic infection, and mucosal damage that prevents normal healing and promotes long-term disease. CSOM pathophysiology includes the following components:

• Eustachian tube dysfunction and middle ear hypoventilation
  • Impaired eustachian tube function leads to negative middle ear pressure, fluid stasis, and mucosal edema.
  • The resulting middle ear environment facilitates recurrent infection and prevents the resolution of acute inflammation.
• Tympanic membrane perforation
  • A persistent perforation eliminates the protective barrier between the external canal and middle ear, allowing continuous contamination with bacteria, water, and debris.
  • Persistent contamination perpetuates chronic infection and inhibits normal mucosal healing.
• Microbial colonization and biofilm formation
  • CSOM is commonly polymicrobial, with organisms such as Pseudomonas aeruginosa, Staphylococcus aureus, Proteus species, Klebsiella pneumoniae, and diphtheroids.
  • These bacteria form biofilms that enhance survival, increase antibiotic resistance, and allow persistent or recurrent otorrhea despite treatment.
  • Anaerobes and fungi may grow concurrently with the aerobes in a symbiotic relationship.[22]
• Chronic mucosal inflammation and impaired clearance
  • Ongoing infection triggers sustained inflammatory responses, leading to mucosal thickening, granulation tissue formation, and disruption of normal mucociliary clearance mechanisms within the middle ear.
  • No evident association exists between the course of the disease and granulation tissue formation. T-cell–mediated cellular immunity is involved in granulation tissue formation in CSOM.[23]
• Ossicular and tissue destruction
  • Prolonged inflammation and enzymatic activity can erode ossicles and adjacent structures, resulting in progressive conductive hearing loss.
• Disease extension and complications
  • Infection may extend into the mastoid air cells (mastoiditis) or, in severe cases, particularly with cholesteatoma, cause bone erosion and intracranial complications such as abscess or meningitis.

Histopathology

Chronic suppurative otitis media (CSOM) is associated with persistent polymicrobial infection, most commonly involving Pseudomonas aeruginosa, Staphylococcus aureus, and anaerobic organisms. Ongoing infection and inflammation produce characteristic histopathologic changes within the middle ear mucosa, reflecting a transition from acute inflammatory injury to chronic reparative and remodeling processes. These include:

• Granulation tissue formation
  • The hallmark of active CSOM is fibrovascular granulation tissue composed of proliferating capillaries, fibroblasts, and a dense inflammatory infiltrate of lymphocytes, plasma cells, and macrophages, reflecting a chronic reparative response.
• Epithelial metaplasia and hyperplasia
  • Chronic irritation leads to the transformation of pseudostratified ciliated columnar epithelium into stratified squamous epithelium, reducing mucociliary function and increasing susceptibility to persistent infection.
  • Epithelial transformation is particularly prominent in long-standing disease and cholesteatoma.
• Aural polyp formation
  • Aural polyps consist of edematous granulation tissue covered by epithelium and arise from chronic mucosal inflammation.
  • Histologic evaluation may be necessary to exclude neoplastic processes in atypical presentations.
• Glandular and goblet cell hyperplasia
  • Increased mucous gland activity and goblet cell proliferation contribute to excessive mucus production and persistent otorrhea.
• Chronic inflammatory infiltration and fibrosis
  • Long-standing disease demonstrates persistent lymphoplasmacytic infiltration with progressive subepithelial fibrosis, leading to irreversible structural changes and conductive hearing loss.[24]

Toxicokinetics

Quinolone ear drops are the preferred treatment for chronic suppurative otitis media because of their broad-spectrum antimicrobial activity and favorable safety profile. Notably, quinolone ear drops do not cause ototoxicity, even when the tympanic membrane is perforated. Conversely, topical aminoglycoside preparations are effective and less expensive but carry a known risk of ototoxicity, particularly with prolonged or repeated use. This ototoxicity can lead to cochlear damage, resulting in sensorineural hearing loss, and, less commonly, vestibular dysfunction. Consequently, aminoglycosides are typically reserved for specific cases in which alternative treatments are unavailable or contraindicated.[25]

History and Physical

Chronic suppurative otitis media (CSOM) typically presents with a history of chronic or recurrent ear disease marked by persistent otorrhea and variable hearing impairment. Symptoms often follow an episode of acute otitis media or recurrent upper respiratory tract infections, particularly in patients with underlying eustachian tube dysfunction or socioeconomic risk factors. Key findings include:

History

• Chronic or intermittent otorrhea: Persistent or recurrent, often mucopurulent, and may be foul-smelling; classically lasting more than 6 weeks.
• Hearing loss: Usually conductive and progressive, though often noticed in children as delayed speech development or inattentiveness.
• Aural fullness or discomfort: Typically mild; severe otalgia is less common unless an acute exacerbation is present.
• History of recurrent ear infections: Often begins in childhood with multiple prior episodes of acute otitis media.
• Water exposure worsens symptoms: Patients may report increased drainage after bathing or swimming.
• Occasional complications symptoms (advanced disease): Vertigo, facial weakness, or severe headache may indicate labyrinthine or intracranial extension.

Physical Examination 

• Otoscopic examination: Tympanic membrane perforation (central or marginal, depending on subtype), with visible mucopurulent discharge in the external auditory canal.
• Middle ear mucosal changes: Inflamed, edematous mucosa; granulation tissue may be present.
• Aural polyp: Red, friable polypoid tissue may protrude through the perforation or external canal.
• Hearing assessment:  Conductive hearing loss on tuning fork testing (Rinne test results are negative, and Weber test lateralizes to the affected ear) and pure-tone audiometry.
• Signs of complications (if present): Mastoid tenderness or swelling, postauricular erythema, facial nerve weakness, nystagmus, or neurological deficits.

Evaluation

The diagnosis of CSOM is primarily clinical, based on characteristic history and otoscopic findings; however, laboratory and imaging studies may be required in selected cases to guide antimicrobial therapy, evaluate complications, or plan surgical intervention. National and international guidelines (including recommendations from otolaryngology societies such as the American Academy of Otolaryngology–Head and Neck Surgery and the World Health Organization [WHO] guidance on chronic ear disease) emphasize clinical diagnosis with selective use of adjunct testing rather than routine, extensive investigations.

Laboratory Evaluation

• Aural discharge culture and sensitivity (when indicated): Recommended in cases of refractory, recurrent, or complicated CSOM, or when empiric therapy fails. Common isolates include Pseudomonas aeruginosa and Staphylococcus aureus, and results help guide targeted antibiotic therapy.
• Complete blood count (rarely required): May be considered in suspected systemic infection or intracranial complications, but is not routinely indicated.
• Inflammatory markers (erythrocyte sedimentation rate and C-reactive protein): Occasionally used in suspected mastoiditis or intracranial spread but lack specificity for CSOM itself.

Radiographic Imaging

• High-resolution computed tomography (HRCT) of the temporal bone is the preferred imaging modality for evaluating complications or planning a surgical procedure, including assessment of the following:
  • Extent of mastoid air cell disease
  • Ossicular chain erosion
  • Presence of cholesteatoma
  • Bony destruction suggesting advanced disease
• Magnetic resonance imaging (MRI) is indicated when there is suspicion of intracranial extension or cholesteatoma. Diffusion-weighted imaging is particularly useful for identifying cholesteatoma and distinguishing it from granulation tissue.

Audiologic Testing

• Pure tone audiometry: Essential to quantify the degree and type of hearing loss, typically demonstrating conductive hearing loss.
• Tympanometry: Often shows a flat (Type B) tracing consistent with tympanic membrane perforation or middle ear effusion.
• Tuning fork tests: Useful bedside assessments supporting conductive hearing loss (Weber test lateralization and Rinne test results that are negative on the affected side).

International guidelines, including recommendations from the World Health Organization (WHO) regarding chronic otitis media and advice from specialty societies, advocate for a stepwise approach to diagnosis and treatment.[WHO. Chronic Suppurative Otitis Media] Diagnosis begins clinically and is followed by targeted microbiological testing for patients who do not respond to initial treatment. Imaging should be reserved for cases in which complications are suspected or for preoperative evaluation. Routine imaging or laboratory tests are not recommended for uncomplicated chronic suppurative otitis media (CSOM).

Treatment / Management

Management of CSOM aims to eradicate infection, control otorrhea, preserve or improve hearing, and prevent complications. National and international guidelines, including recommendations from the WHO and otolaryngology specialty societies such as the American Academy of Otolaryngology–Head and Neck Surgery (AAO-HNS), emphasize a stepwise approach that begins with medical therapy. Goals include regular, aggressive aural toilet, selection of the most appropriate topical antibiotic drop, and control of granulation tissue. Surgery is typically reserved for refractory or complicated disease.

Medical Management

• Topical antibiotic therapy (first-line treatment)[26][27]
  • Fluoroquinolone ear drops (eg, ciprofloxacin or ofloxacin) are recommended as first-line therapy because of their effectiveness against common pathogens (eg, Pseudomonas aeruginosa, Staphylococcus aureus) and their lack of ototoxicity when a tympanic membrane perforation is present.[28][29]
  • Neomycin and polymyxin B
  • Gentamicin, dexamethasone, and tobramycin (off-label)
  • Aminoglycosides have potential hearing and vestibular toxicity
• Aural toilet, also known as ear cleaning, involves mechanically removing debris and discharge to enhance antibiotic effectiveness. Aural toilet is highly recommended as a standard part of ear care. A commonly used solution for aural irrigation is a mixture of 50% acetic acid and 50% sterile water. Otolaryngologists typically use otomicroscopy, suction, and microinstruments for this procedure.
• Topical antiseptics may be used when access to antibiotics is limited, consistent with WHO guidance for resource-constrained settings. Systemic antibiotics are typically reserved for cases involving systemic infection, complications, or failure of topical treatments.
• Control of granulation tissue includes the use of topical antimicrobial drops, topical corticosteroids, and, in some cases, either micropolar cautery or chemical cautery with silver nitrate.[30]

Surgery

• Indications: 
  • Otorrhea that persists for 4 to 6 weeks despite medical management
  • Tympanic membrane perforation that does not heal
  • Cholesteatoma
  • Conductive hearing loss
  • Coalescent mastoiditis
  • Possible contraindications to surgical procedures include procedures involving the only hearing ear, poor general health, high anesthesia risk, or severe complications such as a brain abscess.
• Tympanoplasty: Performed to repair tympanic membrane perforation, restore middle ear function, and reduce recurrent infection.
• Mastoidectomy: Indicated in cases of chronic mastoid disease, cholesteatoma, or persistent infection not responsive to medical therapy.
• Cholesteatoma surgical procedure (canal wall up or down procedures): Required for complete removal of keratinizing epithelium to prevent progression and complications.

Hearing Rehabilitation and Supportive Care

• Hearing aids: Air-conduction or bone-conduction devices may be used when hearing loss persists or when surgical procedure is not feasible.
• Patient education: Avoiding water exposure to the ear and adhering to treatment are important for reducing recurrence.

Guideline-Based Principles

• WHO guidance: Prioritizes topical antibiotics and aural toilet as first-line therapy, especially in resource-limited settings, with an emphasis on preventing complications and hearing loss.
• American Academy of Otolaryngology-Head and Neck Surgery and other Otolaryngology guidelines: Support topical fluoroquinolones as first-line therapy, discourage routine use of ototoxic aminoglycosides in perforated ears, and recommend surgery for persistent disease or cholesteatoma.[AAO–HNS. Clinical Guidelines]

Overall, contemporary guidelines support a medical-first, surgical-second approach, tailored to disease severity, response to therapy, and presence of complications.

Differential Diagnosis

Careful otoscopic evaluation is essential to confirm a tympanic membrane perforation consistent with CSOM. The absence of perforation should prompt consideration of external ear pathology, while atypical features such as severe otalgia, bleeding, cranial neuropathies, vertigo, or failure to respond to standard therapy warrant further evaluation with imaging and, when indicated, biopsy to exclude alternative diagnoses or complications. Accurate diagnosis requires integration of clinical history, otoscopic findings, audiometry, and selective use of microbiologic testing and imaging. Several conditions may present with chronic otorrhea, tympanic membrane abnormalities, or conductive hearing loss and may be mistaken for CSOM, including the following:

• Cholesteatoma:  Keratinizing squamous epithelial lesion of the middle ear or mastoid that may coexist with or mimic CSOM. Cholesteatoma presents with chronic, foul-smelling otorrhea, progressive conductive hearing loss, and marginal or attic tympanic membrane retraction or perforation. Cholesteatoma is more destructive than uncomplicated CSOM and requires surgical treatment.
• Otitis externa (including malignant otitis externa): External canal infection causing otorrhea and pain, typically with an intact tympanic membrane. Malignant otitis externa occurs in patients with diabetes or immunocompromise and may present with severe pain and cranial neuropathies.
• Acute otitis media with perforation: Sudden onset of otorrhea following acute infection; symptoms are typically self-limited and resolve with treatment.
• Otitis media with effusion (glue ear): Middle ear effusion without infection or tympanic membrane perforation, presenting with hearing loss but no purulent discharge.
• Tuberculous otitis media: Rare cause of chronic otorrhea, often with multiple tympanic membrane perforations, granulation tissue, and disproportionate hearing loss; systemic symptoms may be absent.
• Granulomatous and inflammatory disease (eg, granulomatosis with polyangiitis [formerly Wegener granulomatosis] and sarcoidosis): May involve the middle ear and mimic chronic infection, often with systemic manifestations.
• Neoplasms (eg, squamous cell carcinoma of the external or middle ear): Present with chronic non-healing otorrhea, bleeding, or friable granulation tissue; should be suspected in refractory or atypical cases.
• Foreign body or chronic canal irritation: Particularly in children, retained foreign material or chronic manipulation may cause persistent unilateral otorrhea.

Intracranial and extracranial complications of otitis media are rare but clinically important considerations when evaluating suspected CSOM, particularly in severe, atypical, or refractory cases. These complications may overlap clinically with CSOM or arise from disease extension and should be considered when patients present with systemic symptoms, neurologic deficits, severe pain, vertigo, or treatment failure. Complications include the following:

Intracranial Complications

• Meningitis
• Brain abscess
• Sigmoid sinus thrombosis
• Petrositis
• Labyrinthitis
• Gradenigo syndrome, a rare complication of acute otitis media in children, is characterized by suppurative otitis media, unilateral facial pain, and ipsilateral abducens nerve palsy [31] 

Extracranial Complications

• Mastoiditis
• Facial nerve paralysis
• Bezold abscess is a rare deep neck abscess and an intratemporal complication of coalescent mastoiditis, caused by direct extension into the perimastoid tissues [32] 

Toxicity and Adverse Effect Management

Quinolone drops are preferred for CSOM because of their safety and efficacy; aminoglycoside antibiotic drops may be less expensive but carry a risk of ototoxicity, which can lead to sensorineural hearing loss and vestibular dysfunction.[25]

Prognosis

The prognosis of CSOM is generally favorable, although prognosis may vary depending on disease duration, the presence of complications, and access to appropriate medical and surgical care. Untreated CSOM is often associated with persistent otorrhea, progressive conductive hearing loss, and a risk of recurrent or chronic infection, with potential long-term structural damage to the middle ear. With appropriate treatment, including topical fluoroquinolone antibiotics and aural toilet (professional ear cleaning), many patients experience resolution of otorrhea and clinical improvement.

However, recurrence is common, and a persistent tympanic membrane perforation may persist, predisposing patients to future episodes of infection and ongoing hearing impairment. In cases requiring surgical procedures, tympanoplasty with or without mastoidectomy can provide durable disease control, restore tympanic membrane integrity, and improve hearing outcomes. Surgical procedures are particularly effective for refractory disease, cholesteatoma, or cases with complications, although hearing restoration may vary depending on the extent of ossicular damage. Overall, early recognition and timely treatment are key determinants of prognosis, with significantly improved outcomes when intervention occurs before advanced middle ear or intracranial complications develop.

Complications

Chronic suppurative otitis media can lead to significant health issues due to both local and systemic complications, especially when diagnosis is delayed or treatment is inadequate. Although uncommon, intracranial complications are the most serious. These include meningitis, brain abscess, lateral (sigmoid) sinus thrombosis, and other types of intracranial suppuration, all of which can be life-threatening and require urgent interdisciplinary treatment.

Extracranial complications arise from the local spread of infection and may include mastoiditis, postauricular abscess formation, and facial nerve paralysis. Each of these conditions is associated with increased disease severity and a higher risk of long-term functional impairment. Chronic infection can also commonly result in conductive hearing loss due to perforation of the tympanic membrane and damage to the ossicles. In advanced stages of the disease, prolonged inflammation or labyrinthine involvement may lead to sensorineural hearing loss. The presence of these complications significantly worsens the prognosis and often requires urgent escalation of care, which may include systemic antimicrobial therapy and surgical procedures such as tympanomastoidectomy or tympanoplasty. Therefore, early recognition and treatment are crucial in reducing morbidity and preventing permanent complications.