Tympanic membrane perforation (TMP) is a condition as old as the human species.
The tympanic membrane, also called the eardrum (or just the drum), is a stiff (but flexible), translucent, diaphragmlike structure. The eardrum moves synchronously in response to variations in air pressures, which constitute sound waves. The drum’s vibrations are transmitted through the ossicular chain to the cochlea. In the cochlea, vibratory mechanical energy changes to electrochemical energy and streams via the eighth cranial nerve to the brain. The tympanic membrane and its attached ossicles thus act as a transducer, changing one form of energy into another form.
Tympanic membrane (TM) as continuation of the upper wall of external auditory canal (EAC) with angle of incline up to 45 degrees on the border between middle ear and the EAC.
Tympanic membrane perforations (TMPs) can result from disease (particularly infection), trauma, or medical care. Perforations can be temporary or persistent. Effect varies with size, location on the drum surface, and associated pathologic condition.
Incidence of TMP in the general population is unknown. One survey found that that 4% of a population of Native American children had TMP. Another study found that 3% of children treated with ventilation tubes had the condition.
However, the incidence in the general population has not been studied. Even the exact number of surgical TMP repairs performed each year is unknown. Analysis of government statistics indicates that perhaps 150,000 tympanoplasties are performed per year in a population of 280 million.
Infection is the principal cause of TMP. Acute infection of the middle ear may cause a relative ischemia in the drum concurrent with increased pressure in the middle ear space. This leads to a tear or rupture of the eardrum that is usually preceded by severe pain. If the perforation does not heal, it leaves a residual TMP.
A prominent school of thought now advocates less aggressive use of antibiotics. Those who hold this position recognize that many episodes of otitis media are caused by viruses, so they resolve spontaneously; advocates of this position desire to slow emergence of antibiotic-resistant bacterial strains. Evidence is emerging that an increased incidence of acute mastoiditis is resulting from reduced use of antibiotics. Time will tell whether increased incidence of perforation and other complications of otitis media, such as brain abscess, meningitis, and septic sigmoid sinus thrombosis, also occur.
Ear canal infections rarely cause TMP. When this occurs, it is often associated with infection by Aspergillus niger.
Traumatic perforations may result from blows to the ear (eg, being struck with the flat of the hand; falling from water skis with the head hitting the water surface, ear down). Exposure to severe atmospheric overpressure from an explosion can tear the drum.
TMP from water pressure occurs in scuba divers, usually in a drum with atrophy from previous disease. Objects used to clean the ear canal can perforate the drum.
Inexpertly performed irrigation of the ear canal for wax can lead to perforation. In some settings, when irrigation for cerumen is relegated to medical assistants, otolaryngologists may see 10-20 patients per year with this injury. Evidence exists that such perforations are less likely to heal spontaneously. TMP is intentionally created whenever a surgeon makes an incision in the eardrum (myringotomy). When pressure-equalizing tubes (ventilating tubes) are placed, the TMP purposely is held open. Failure of surgically created openings to heal when the tube extrudes results in chronic TMP.
The eardrum tends to heal itself. Even eardrums that have been perforated multiple times often remain intact. At times, a perforation heals with a thin membrane consisting only of mucosal and squamous epithelial layers without a fibrous middle layer. Such a neomembrane may be so thin that it can be mistaken for a perforation instead of a healed perforation. Neomembranes may retract deeply into the middle ear, sometimes making them more difficult to distinguish from actual perforations. Examination under the operating microscope resolves ambiguity. Deep retraction, especially in the posterior superior quadrant of the drum, may presage formation of cholesteatoma.
The presence of perforation renders the ear more susceptible to infection if water enters the ear canal. If bacteria-contaminated water passes through the perforation, infection can result. Water surface tension may protect the ear from penetration through a very small perforation. This explains higher infection rates from hair washing than from swimming activities (ie, soap lowers surface tension so water can enter the middle ear). Presence of perforation is an absolute contraindication to irrigation for cerumen removal. History of perforation is also an absolute contraindication unless personal knowledge derived from prior examination indicates an intact drum.
Perforation symptoms may include audible whistling sounds during sneezing and nose blowing, decreased hearing, and a tendency to infection during colds and when water enters the ear canal. Copious purulent drainage, which may be sanguineous in both acute and chronic perforation, confirms both perforation and infection. Ear canal infections also can cause purulent drainage, but usually in lesser amounts. Perforations uncomplicated by infection or cholesteatoma are never painful. Presence of pain should alert the physician to a concurrent disease process. Perforations accompanied by otorrhea or cholesteatoma are usually not painful.
Many persons live their lives with TMP that are entirely without symptoms. Repair of such lesions is usually not indicated. Perforations may be associated with recurrent infection when exposed to water. In swimmers, divers, and other water sports enthusiasts, repair may be indicated as a quality-of-life issue. Hearing loss may be present, especially with larger perforations, and may be a reason for repair. Because a risk to residual hearing exists with every operation on the ear drum, a risk-benefit analysis in which the patient participates is mandatory. For example, question whether the person may be helped just as much with use of a hearing aid.
The tympanic membrane has two distinct zones. The larger of the two zones is the pars tensa. This zone consists of a tough and resilient fibrous layer with a diaphanous mucosal layer inside and squamous epithelium outside. The smaller zone is the pars flaccida, which lies superior to the suspensory ligaments of the malleus and lacks a fibrous layer. Perforations of this area often are described as more frequently associated with complications. This is true if the definition of TMP includes depressions of the drum into the middle ear, forming saclike structures (retraction pockets). Clearly, such pockets are more often associated with cholesteatoma formation. Behind (or medial to) the drum is the middle ear. In front of the drum (or lateral or exterior) is the ear canal. The drum lies at an angle to the bore of the ear canal, creating a vestibule, which can retain cerumen or debris. The malleus is invested by the fibrous layer of the tympanic membrane, securely incorporating it within the drum.
TMP may be unilateral or bilateral. Select the worse-hearing ear first when performing bilateral TMP repair. If increased hearing loss complications ensue, the better-hearing ear remains uninjured. For the same reason, if TMP is present in a patient’s single hearing-capable ear, only incipient life-threatening complications justify repair attempts.
Radiography and MRI are of no value unless the clinical picture suggests ossicular destruction and/or cholesteatoma. Asymptomatic perforations, especially if hearing is near normal, require no imaging studies.
- Most tympanic membrane perforations (TMPs) are diagnosed using routine otoscopy
- Small perforations may require otomicroscopy for identification
- Some hearing screening programs include middle ear impedance testing
- Screening tympanometry may reveal abnormalities consistent with perforation. Confirmation still requires examination
- Always perform audiometry upon initial TMP diagnosis and again before any repair attempt, whether in the office or in the operating room
- Preoperative and postoperative audiography should always be performed. A major conductive loss not only alerts the surgeon to the possible existence of ossicular lesions, but documentation of a preexisting sensorineural hearing loss may protect the surgeon from later allegations that the surgery caused the hearing loss
- Audiometry often reveals normal hearing. The presence of mild conductive hearing loss is consistent with perforation, and a conductive component of at least 30 dB indicates possible ossicular discontinuity or a pathologic condition
In rare cases, otomicroscopy and impedance studies still leave the TMP diagnosis questionable. To provide evidence of perforation (in the form of a stream of bubbles), fill the ear canal with sufficient distilled water or sterile saline to cover the tympanic membrane and have the patient perform the Valsalva maneuver. A negative test result is suggestive but not definitive. A positive test result is caused only by TMP.
In chronic TMP, squamous epithelium is found adjacent to middle ear mucosa and creates a perforation edge with no raw surface. Such healing of the perforation edge is undoubtedly a contributing factor to perforation persistence.
Medical therapy for perforations is directed at controlling otorrhea. Take into account ototoxicity risk from topically applied eardrops when treating ear infections concurrent with TMP. Infection alone occasionally can cause sensorineural hearing loss. Clinical toxicity from eardrops in the presence of ear infection has not been demonstrated unequivocally, although experiments in animals clearly demonstrate a correlation. Legal implications of administration of ototoxic eardrops preceding sensorineural hearing loss are clear. For this reason, avoid eardrops containing gentamicin, neomycin sulfate, or tobramycin in the presence of TMP. When they are used, substitute a less toxic alternative as soon as drainage and mucosal edema begin to subside. Avoiding contamination of the middle ear space with water via the TMP is critical in minimizing otorrhea from a perforation.
Systemic antibiotics are occasionally used when controlling otorrhea from a TMP. Antibiotics (eg, trimethoprim-sulfamethoxazole, amoxicillin) directed at typical respiratory flora suffice in most cases. Overgrowth with Pseudomonas aeruginosa or resistant Staphylococcus aureus may occur. Failure of drainage to clear after several days’ therapy may require alteration of therapy following culture and sensitivity tests. A tendency of the ear canal to pseudomonad overgrowth indicates that the most accurate testing can be obtained by suctioning a culture specimen (under microscopic control) directly from the middle ear through the perforation.
Under routine circumstances, the surface tension of water may prevent it from entering the middle ear through a small perforation. The addition of soap reduces the water tension. The ear is therefore at greater risk of infection during hair-washing or bathing than from plain water.
Treatment of TMP falls into 3 categories. No treatment is necessary for nonswimming patients with minimal hearing loss and no history of recurrent ear infection. A hearing aid may prove the only necessary treatment for patients with symptomatic hearing loss but no infection or swimming history.
Two options exist for patients who are not in either category.
The first option is to perform one of the available office treatments. Such treatments have the best chance of working when the perforation is small and involves neither the umbo nor the annulus.
Several methods apply:
The simplest, but least effective, method is to cauterize the edges of the TMP with a caustic, such as trichloroacetic acid (10% solution), and then apply a small patch of cigarette paper. This technique was developed in the 1800s; it presumably remains in the repertoire because it sometimes works. Mechanical stripping of the perforation margin (with topical anesthetic or without) before applying the patch slightly increases the success rate.
A fat-plug tympanoplasty can be performed. Obtain a small plug of fat from the postauricular sulcus with the patient under local anesthesia. Prepare the TMP by anesthetizing its margins with carefully applied phenol solution. Next, mechanically débride the edges with microcup forceps. The fat is then tucked into the perforation, extending both into the canal and into the middle ear space. The paper-patch method has a reported success rate of 67%; the fat-plug tympanoplasty of 87%.
Another successful office treatment, which has the major disadvantage of requiring 6-10 weekly postsurgical office visits, is the irritant oil method.
In this method, freshen the perforation by stripping the margin using microcup forceps. Performed carefully, this can often be accomplished without anesthetic. If necessary, use a small amount of phenol solution for anesthesia. Apply a cotton ball that is 1-2 mm larger than the diameter of the perforation to the TMP. The patient then instills a solution of irritative and aromatic oils daily into the ear.
The solution is dispensed in 30-mL dropper bottles and is formulated by the pharmacy (all substances United States Pharmacopoeia [USP] grade) as 2 mL eucalyptol, 1.10 mL methyl salicylate, 0.39 g thymol, 0.455 g menthol, 1.20 mL oil of orange, 20.25 g sifted powdered sodium borate, 20.25 g powdered boric acid, 60 mL of 90% ethyl alcohol, saffron to suit for color, and water in a sufficient quantity to make 5000 mL. Change the cotton weekly. Repeat edge freshening if no progress is seen.
This nonsurgical method was initially reported to have a 70% success rate, and this author has obtained similar results using it as the sole therapy for perforations occupying less than 25% of the drum area.
Other recently reported forms of office treatment use fibrin glue or a patch composed of a hyaluronic acid ester and a dressing component. The use of basic fibroblast growth factor with a proprietary patch that consists of a silicone layer and atelocollagen has been described. Excellent success has been reported, but with very small numbers of patients. Time will tell if these new techniques will prove useful additions to treatment options.
The second option is to perform tympanoplasty with the patient under local or general anesthesia. An incision may be made behind the ear or entirely through the ear canal, depending on the location and size of the TMP. Repair requires preparation of a suitable bed for placement of a graft. By far, the most commonly used grafting material is postauricular fascia. Allograft tympanic membranes obtained from cadavers, once abandoned because of fear of transmitting viral pathogens, are again being used. Other substances, such as the urinary bladder matrix, are being evaluated.
Grafts may be placed medially or laterally to the perforation, or in a combined position. Surgeon preference plays a part in these decisions and in decisions concerning the technical problems associated with size and location of the perforation and the shape, angle, and bore of the ear canal.
Tympanoplasty successfully closes the TMP in 90-95% of patients. Fortunately, second and third operations succeed in more than 90% of the remaining patients. Consequently, fewer than 1 per 1000 persons still has TMP after three operations.
Preoperative preparation of the ear for surgery consists of eliminating infection whenever possible. Preoperative preparation of the patient includes convincing the smoker to stop during the immediate postoperative period.
The first known incident of tympanoplasty performed on the wrong ear occurred in 2004. Surgeons are therefore advised to adopt methods similar to those used in other fields, and mark the ear to be operated upon with ink while the patient is awake and able to confirm the accuracy of the selection.
Postoperative care is identical for office treatment and operating room repair techniques. Instruct patients to keep water out of their ears. When incisions and ear canal packing are present, use protective dressings, which are commercially available. Otherwise, silicone rubber plugs (also commercially available) or cotton balls waterproofed with a little petroleum jelly suffice.
Risk of cholesteatoma formation, either through the natural course of the disease or from squamous epithelium trapped during treatment, requires regular follow-up care for all patients postoperatively. Several annual visits should be the minimum once TMP healing is verified. Untreated TMP may not require regular follow-up care if a patient can be relied upon to seek medical advice if hearing changes or persistent drainage from the ear is noted. Location of the TMP informs the timing and frequency of follow-up care. Perforations in the pars tensa (stiff portion of the drum) rarely lead to complications.
The exceptions are pars tensa perforations located at the annulus or rim of the tympanic membrane. TMPs in this location are at risk of developing middle ear cholesteatoma from migration of surface epithelium into the middle ear. Perforations in the pars flaccida (the portion without a fibrous center layer) are more frequently associated with complications and require more frequent follow-up care.
Each operation carries a risk of exacerbating hearing loss. Exact incidence of such hearing loss is unclear, with reported rates varying widely in the medical literature. In one series, approximately 1 per 500 operations resulted in much worse hearing. In another, the rate was nearly 2% for some degree of loss. Of 1000 patients, expect one to experience a perforation and 4 to endure lost hearing. In a small group of patients, persistent eustachian tube dysfunction leads to late complications, such as cholesteatoma, reperforation, or middle ear effusion. When the underlay technique of tympanoplasty is used, incidence of intratympanic cholesteatoma is less than 1%. These complications each require unique treatment.
Outcome and Prognosis
Uncomplicated TMP requires no treatment. Perforations remain stable, and prognosis for absence of morbidity is good. Repaired drums reperforate in as many as 10% of patients. Potential for late perforation and the potential for formation of cholesteatoma mandate regular follow-up care for many years after apparently successful surgery.