Chronic suppurative otitis media (CSOM) is one of the most common preventable causes of acquired hearing loss in children and is more prevalent in developing nations, where suppurative complications have a significant impact on childhood mortality. As such CSOM contributes to a significant global health burden. The definition of CSOM is chronic inflammation of the middle ear cleft (MEC), in the presence of a non-intact tympanic membrane that leads to frequent and recurrent otorrhea from the ear [1]. There has been a lack of consensus regarding the duration of symptoms. The World Health Organization (WHO) definition is a discharging ear that persists beyond 2 weeks but many otolaryngologists would say that acute otitis media (AOM) transitions to CSOM after at least 6 weeks of otorrhea and despite medical treatment [2–4]. In addition, certain specialists will refer to active and inactive disease. The term active CSOM is used to refer to perforation associated with infection whereas a chronic perforation in the absence of infection is termed inactive disease [5]. The ear can subsequently become reinfected by reflux of bacteria from the nasopharynx or from the introduction of pathogens from the external ear canal.

True prevalence and incidence of CSOM is difficult to establish given the wide range of definitions for the condition. The WHO estimates the global burden of illness as a result of CSOM to include 65–330 million people worldwide. Approximately 60 % of these individuals suffer significant hearing impairment and 28,000 die, usually as a complication of the disease. Ninety percent of CSOM occurs in South East Asia and the Western Pacific as well as certain parts of Africa [1]. A 4 % prevalence rate of CSOM is considered to be indicative of a major public health issue [6]. Indigenous populations such as Inuit from Alaska, Canada and Greenland, American Indians and Australian Aboriginals are considered especially high risk. Among Australian Aboriginals, as many as 50 % of the children suffer from CSOM [7]. These startlingly high prevalence rates are thought to be multifactorial in etiology but environmental factors are likely to be most strongly implicated. Young Aboriginal children have been shown to suffer early exposure to OM pathogens, persistent bacterial colonization, and chronic mucosal disease [8]. CSOM is generally thought to occur secondary to an episode of AOM in childhood but may also occur as a sequel of otitis media with effusion (OME) [5]. Risk factors for AOM are most likely implicated in the prognosis and development of CSOM: age, race, frequent upper respiratory tract infection, poor access to health care, crowded living conditions, poor hygiene and nutrition, attendance at day care centers, bottle-feeding [9], exposure to passive smoking [10], and family history of OM. CSOM is least prevalent in developed nations such as the USA and European countries and when it occurs it is usually linked to tympanostomy tube (TT) insertion [11]. Placement of TTs can be associated with CSOM. One meta-analysis showed the rate of chronic otorrhea in intubated ears was 3.8 %, recurrent otorrhea was 7.4 %, and both of these sequelae were associated with longer-term TTs [12].

Even though the genetics of CSOM is poorly understood there are several studies looking at the genetics of AOM and COME. These include epidemiological studies of various methodologies as well as genetic studies [13–15]. Candidate gene studies have identified a handful of genes contributing to OM susceptibility, including several immune genes, such as IL10 and TNF, as well as FBXO11 , which have been significantly associated with OM in three independent cohorts [16–18]. The first genome-wide association study looking at the OM phenotype has identified CAPN14 and GALNT14 on chromosome 2p23.1 and the BPIFA gene cluster on chromosome 20q11.21 as novel candidate genes which warrant further analysis [19].

OM occurs when viruses and bacteria evade the host mucociliary and immune responses establishing inflammation within the middle ear (ME) [20]. Chronic infection is often polymicrobial in nature with Pseudomonas aeruginosa and Staphylococcus aureus being the most common organisms isolated. Other isolates include Staphylococcus epidermis, Proteus species, beta-hemolytic Streptococcus, Haemophilus influenza, and enteric Gram-negative bacilli [21–23]. In recent years, the importance of the role of bacterial biofilm has come to light in the pathogenesis of CSOM, particularly in relation to the placement of TTs. Van Leeuwenhoek first described bacterial biofilm in the seventeenth century when he examined the “animalcules” on the surface of his own teeth. Costerton and his colleagues put the modern theory of biofilm predominance forward in 1978 [24]. This theory has subsequently been refined to a community of bacteria irreversibly adherent to a surface, embedded in a self-produced matrix of extracellular polymeric substance, and exhibits altered phenotype with respect to the growth rate and gene transcription [25]. Biofilm and intracellular infection have been demonstrated on ME mucosa of children with CSOM, recurrent AOM, and chronic OME, and are mechanisms of bacterial persistence in the ME causing recalcitrance to treatment and disease recurrence [26–28]. Similarly, a number of studies have shown that TTs are highly subject to biofilm build up [29] which leads to refractory otorrhea and TT occlusion. Systemic antibiotics are known to have poor ME biofilm penetration. Krause et al. investigated the concentrations of a number of antimicrobial agents in ME fluid. For all agents it was shown that ME concentrations were significantly lower than serum concentrations [30]. A number of studies have been conducted looking at the use of TTs with resistance to biofilm formation with some promise. Phosphorylcholine-coated fluoroplastic TTs have been demonstrated to inhibit biofilm formation by both P. aeruginosa and S. aureus [31].

The management of CSOM has two principal aims: First, to eradicate infection and hence reduce morbidity and mortality, second, to close the tympanic membrane perforation to reduce hearing loss and risk of reinfection of the ME [1]. Recognition of those cases that are better managed surgically should be prompt to avoid delayed treatment and reduce morbidity. In some cases, this means instituting treatment to stop discharge from the ear before it can be established whether the patient has either active mucosal chronic otitis media (COM) or active squamous COM (cholesteatoma) both of which require surgical intervention [32].

Medical management of CSOM is appropriate in the absence of cholesteatomatous disease, attico-antral disease, or suppurative complications of OM. There is a general lack of consensus among physicians regarding the optimal medical management of CSOM. A number of Cochrane review studies have examined the benefits of aural toilet, topical antiseptics, topical antimicrobials, systemic antimicrobials (oral and parenteral), and topical and systemic steroids. Presently, aural toilet combined with topical antibiotics is the mainstay therapy [1]. Quinolone antibiotics are the most commonly used topical agents but there are not many studies comparing agents. One randomized controlled trial (RCT) compared topical ciprofloxacin (CIP) with topical framycetin-gramicidin-dexamethasone (FGD) for the treatment of CSOM in Australian Aboriginal children . The study showed similar rates of improvement for both treatment arms (70 % CIP vs. 72 % FGD; CI-20–16) [33]. Topical quinolones are generally favored over nonquinolones because of the lack of safety data for the latter. The above trial did not show any significant difference in conductive hearing loss for CIP versus FGD, nor did it show the development of sensorineural loss, but ototoxicity was not an outcome that was directly measured in the study. Topical quinolones have been shown to be more effective than systemic quinolones in treating ear discharge at 1–2 weeks [34]. A Cochrane review has shown that topical antibiotics alone are better than systemic antibiotics in terms of resolution of otorrhea and eradication of ME bacteria [1]. A similar review in 2009 looked at whether combined topical and systemic antibiotics are better than topical antibiotics alone [34]. It found no trials showing statistically significant benefit from the addition of systemic antibiotics to topical treatment despite an increase in the cost of treatment and adverse effects of oral therapy. Leach et al. investigated the benefit of prophylactic antibiotics in relation to AOM and CSOM. They concluded that there is still uncertainty about the impact of prophylactic antibiotics on episodic AOM with perforation and CSOM [35].

For some patients otorrhea will persist despite aggressive aural toilet and prolonged courses of topical antibiotics. For these patients a long-term course (6–8 weeks) of parenteral antimicrobial therapy should be considered. Appropriate agents depend on culture results but generally include penicillin with anti-Pseudomonal cover such as piperacillin or a third-generation cephalosporin such as ceftazidime. Many of these patients will require tympanomastoid surgery.

Surgery is indicated in cases of CSOM that are refractory to maximal medical therapy. There are several aims of surgery but the most important by far is to achieve a safe and dry ear [36]. Secondary considerations include stopping the discharge, healing the tympanic membrane, and restoring function to the ear [32]. Tympanoplasty , with or without mastoidectomy, is the primary procedure performed. Tympanoplasty is an operation to eradicate disease in the ME and reconstruct the hearing mechanism with or without using a graft to recreate the tympanic membrane [37]. Many materials have been used as graft material, the most popular of which is temporalis fascia, first described in the 1960s, [38] because it is easily harvested at the time of surgery and closely resembles the innate structure. Other grafts used include perichondrium, cartilage (tragus or conchal bowl), fat, vein, periosteum, and even Alloderm [39]. Three approaches are used in tympanoplasty: transcanal, endaural, or postauricular. The decision to use a particular approach is based on the size and location of the perforation, individual patient anatomy, and surgeon preference. Grafts may be placed medial or lateral to the tympanic membrane remnant depending on the location of the perforation and also the technical skills of the surgeon.