Tympanic Membrane Perforation: Traumatic, Infectious
Rupal S. Jain
Dunia Abdul-Aziz
THE CLINICAL CHALLENGE
The tympanic membrane (TM) is a thin, three-layered tissue that divides the external auditory canal from the middle ear. The TM functions to amplify and transmit sound vibration to the ossicles, which in turn transmit that acoustic stimulation to the inner ear (cochlea). Perforations of the TM therefore lead to varying degrees of predominantly conductive, or mechanical, hearing loss, depending on their sizes and locations. Although most perforations heal spontaneously within 4 weeks, morbidity associated with TM perforations is reduced with early identification, treatment of underlying infection or disease, recognition of more complicated/severe cases, and appropriate referral.
TM perforation occurs most commonly as a complication of a middle ear infection, but it can also occur owing to rapid changes in pressure (barotrauma), blunt and penetrating trauma, acoustic trauma, and middle ear disease (eg, cholesteatoma). The diagnosis of TM perforation is mainly clinical, relying on history and physical examination findings. Clinicians must have a high index of suspicion in children with acute otitis media (AOM) with drainage and in adult patients with trauma. Complete visualization of the TM may not always be possible with a limited otoscopic examination. Certain features of the history may suggest perforation, such as symptoms of AOM, followed by aural purulence or blood, which relieves the pain. Direct visualization of the TM is important to distinguish otorrhea caused by otitis externa (OE) from otorrhea caused by otitis media (OM) with perforation, because management differs. Certain topical antibiotics containing gentamicin, neomycin, or tobramycin are ototoxic and cause sensorineural hearing loss; these should be avoided in the setting of perforation. Although most cases of TM perforation have a favorable prognosis, ENT follow-up is required to ensure healing, recovery of hearing, and intervention for progressive and destructive cases that may necessitate surgical intervention.
PATHOPHYSIOLOGY
Traumatic Perforation
Traumatic TM perforation or rupture often presents with acute pain in response to an exposure. Examples include barotrauma (eg, scuba diving or rapid changes in pressure during air travel), acoustic trauma (eg, loud blast), blunt trauma (eg, open-handed slap across the ear), penetrating
trauma (eg, cotton swabs), chemical and thermal burns (eg, slag injuries), and iatrogenic injury (eg, during cerumen/foreign body removal).1 Any of these forces transmitted to the less-than-onemillimeter-thick TM can cause either a partial tear or a complete rupture, impeding conduction of sound vibrations. Studies have suggested that larger-sized perforations, perforations in the posterior or anterior quadrants, and perforations that contact the manubrium of the malleus portend more severe hearing loss.2
trauma (eg, cotton swabs), chemical and thermal burns (eg, slag injuries), and iatrogenic injury (eg, during cerumen/foreign body removal).1 Any of these forces transmitted to the less-than-onemillimeter-thick TM can cause either a partial tear or a complete rupture, impeding conduction of sound vibrations. Studies have suggested that larger-sized perforations, perforations in the posterior or anterior quadrants, and perforations that contact the manubrium of the malleus portend more severe hearing loss.2
Infectious Perforation
Infectious TM perforations most commonly result from an acute middle ear infection, or AOM. They can also result from OE, which may be bacterial and/or fungal (otomycosis), as well as superinfection of chronic middle ear disease (chronic OM, cholesteatoma). In AOM, which is defined by a suppurative process of short-term or sudden onset with infected fluid in the middle ear and associated inflammation of the middle ear mucosa, the increased pressure from middle ear infection results in spontaneous rupture through the TM. The most common infectious pathogen associated with AOM with TM perforation is nontypeable Haemophilus influenzae (approximately 50% of cases) followed by Streptococcus pneumoniae and Moraxella catarrhalis.3 Viral infection can cause TM perforation, either as the primary infectious agent or as a coinfection with a bacterium. Severe outer ear infections, usually fungal, can also result in TM perforation, with Aspergillus niger and then Candida being the most common culprits in these cases.4
Risk factors for developing TM perforation in the setting of infection include severity of infection, duration of infection, recurrent infections, underlying otologic disease (eg, cholesteatoma) and prior surgery or trauma to the TM and middle ear (eg, tympanostomy tube placement). These factors can be gathered in the history and increase the suspicion for perforation.
APPROACH/THE FOCUSED EXAM
TM perforation is a clinical diagnosis defined by the presence of a hole in the TM (Figure 8.1A and B). The exam should note the size and location of the perforation. Size should be described as a percentage relative to the entire TM. Location should be described relative to the manubrium of the malleus. On pneumatic otoscopy, the perforated TM is immobile, because a pressure seal cannot be formed. A 512 Hz tuning fork can help distinguish the conductive versus sensorineural nature of the hearing loss; with a TM perforation, a conductive hearing loss pattern (Weber lateralizes to the affected ear, Rinne negative [bone conduction louder than air conduction] in severe cases) is expected. Details of the tuning fork exam are more completely described in Chapter 2.