Intratympanic Steroid Injection

Anatomy and Physiology

Tympanic Membrane

The tympanic membrane is a thin, semitransparent membrane approximately 1 cm in diameter that separates the external auditory canal from the middle ear cavity. The tympanic membrane consists of the larger, fibrous pars tensa and the smaller, more compliant pars flaccida. The handle of the malleus is embedded within the pars tensa and serves as an important landmark during otoscopic examination. Intratympanic injections are typically performed through the pars tensa, most commonly in the posteroinferior quadrant, to minimize the risk of injury to the ossicular chain, chorda tympani nerve, and adjacent vascular structures while facilitating corticosteroid delivery into the middle ear.

Middle Ear

The middle ear is an air-filled cavity within the petrous temporal bone that contains the auditory ossicles, including the malleus, incus, and stapes, which transmit sound from the tympanic membrane to the oval window of the cochlea. The middle ear communicates anteriorly with the nasopharynx through the eustachian tube and posteriorly with the mastoid air cell system. For intratympanic drug delivery, the most clinically relevant structures are the round window niche and oval window, which provide pathways for medication to enter the inner ear. After injection, patients are typically positioned with the treated ear upward for 15 to 30 minutes to maximize contact between the corticosteroid solution and the round window membrane and minimize drainage through the eustachian tube.

Internal Ear

The inner ear comprises the cochlea, vestibule, and semicircular canals housed within the bony labyrinth. The membranous labyrinth, suspended within the bony labyrinth, contains endolymph and is surrounded by perilymph. The cochlea converts mechanical energy into neural signals through inner and outer hair cells located within the organ of Corti. Two membrane-covered openings communicate with the middle ear: the oval window, occupied by the stapes footplate, and the round window, which functions as a pressure-release membrane during sound transmission. The round window membrane also serves as the principal route for diffusion of intratympanically administered medications into the cochlear perilymph. Additionally, the blood-labyrinth barrier regulates exchange between the systemic circulation and the fluids of the inner ear. Similar to the blood-brain barrier, the blood-labyrinth barrier restricts penetration of many circulating medications into cochlear tissues, limiting the effectiveness of systemic drug delivery and providing the rationale for local intratympanic therapy.[8]

Physiology of Intratympanic Drug Delivery

The cochlea is one of the most challenging organs to treat pharmacologically because systemic medications must cross the blood-labyrinth barrier to reach therapeutic concentrations within the inner ear.[9][10] Intratympanic administration bypasses this limitation by delivering corticosteroids directly into the middle ear, where they diffuse primarily across the semipermeable round window membrane and, to a lesser extent, through the oval window annular ligament into the perilymph.[8][10] Results from numerous experimental and clinical studies demonstrated that intratympanic corticosteroid administration produces substantially higher perilymph corticosteroid concentrations than systemic administration while maintaining significantly lower plasma drug levels.[11][12][13][14] Drug distribution within the cochlea follows a basal-to-apical concentration gradient, with the highest concentrations occurring near the round window. Medication absorption may be influenced by factors such as the integrity and thickness of the round window membrane, the presence of mucosal folds or fibrous adhesions within the round window niche, corticosteroid formulation, molecular weight, dwell time within the middle ear, and eustachian tube function.[8][13][15]

Mechanism of Action

Although the precise mechanisms responsible for many inner ear disorders remain incompletely understood, inflammation, oxidative stress, immune dysregulation, vascular compromise, and altered cochlear ion homeostasis may contribute to cochlear injury in susceptible patients.[16] Corticosteroids exert multiple therapeutic effects by suppressing proinflammatory cytokine production, reducing oxidative injury, stabilizing cellular membranes, regulating ion transport within the stria vascularis, and preserving cochlear homeostasis.[13][17] Local intratympanic administration achieves high intracochlear drug concentrations while minimizing systemic adverse effects, making this treatment particularly valuable for patients who cannot tolerate systemic corticosteroids or who require salvage therapy after an incomplete response to oral treatment.

Idiopathic Sudden Sensorineural Hearing Loss

Idiopathic sudden sensorineural hearing loss (ISSNHL) is considered an otologic emergency characterized by sensorineural hearing loss of 30 dB or greater across 3 consecutive frequencies occurring within 72 hours without an identifiable cause.[4][5] Although its pathophysiology remains uncertain, proposed mechanisms include viral infection, vascular insufficiency, autoimmune injury, inflammatory responses, and metabolic dysfunction. Intratympanic corticosteroid therapy may be used as primary treatment when systemic corticosteroids are contraindicated or as salvage therapy for patients with incomplete recovery after initial systemic treatment, consistent with current clinical practice guidelines.[6]

Ménière Disease

Ménière disease is characterized by recurrent episodes of spontaneous vertigo, fluctuating low-frequency sensorineural hearing loss, tinnitus, and aural fullness. The disorder is strongly associated with endolymphatic hydrops, although its underlying pathophysiology is likely multifactorial, involving abnormalities of endolymph regulation, immune function, genetic susceptibility, and inflammatory pathways.[7][15][18] Most patients achieve satisfactory symptom control with dietary modification and medical therapy; however, patients with persistent or refractory symptoms may benefit from intratympanic therapy. Intratympanic corticosteroid injection may control vertigo while preserving vestibular and cochlear function and is generally preferred over ablative treatments in patients with serviceable hearing. Intratympanic gentamicin remains an effective option for refractory disease but carries a greater risk of permanent vestibular hypofunction and hearing deterioration.[15][18]

Indications

Idiopathic sudden sensorineural hearing loss (ISSNHL) is the most common indication for intratympanic corticosteroid administration. Treatment should be initiated promptly after the diagnosis has been confirmed and appropriate evaluation has excluded an identifiable cause of hearing loss.

Primary Treatment

Corticosteroids may be offered as initial therapy within 2 weeks of symptom onset. Intratympanic corticosteroid injection may be selected as primary treatment when systemic corticosteroids are contraindicated, poorly tolerated, or considered clinically undesirable because of conditions such as poorly controlled diabetes mellitus, severe hypertension, significant psychiatric disease, or a history of serious systemic corticosteroid–related adverse effects.[6]

Intratympanic treatment may also be considered after shared decision-making when the patient prefers localized therapy. Results from comparative studies suggested that intratympanic corticosteroids may provide hearing outcomes similar to those achieved with systemic corticosteroids when used as primary therapy. However, the available evidence is heterogeneous and generally of low or very low certainty, and intratympanic treatment has not been shown consistently to be superior to systemic therapy.[19][20] 

Salvage Treatment

Intratympanic corticosteroid therapy should be offered to patients with incomplete hearing recovery after initial treatment for ISSNHL. Current clinical practice guidelines recommend offering salvage intratympanic corticosteroid therapy approximately 2 to 6 weeks after symptom onset.[6] The likelihood of meaningful recovery generally decreases with increasing time between symptom onset and treatment. Therefore, patients with persistent hearing loss should undergo prompt repeat audiometric assessment and timely referral for salvage treatment rather than prolonged observation. Results from studies showed improved hearing in a subset of patients treated with intratympanic corticosteroids after an inadequate response to systemic therapy, although reported response rates vary with the treatment protocol, the definition of hearing recovery, initial severity, and the timing of therapy.[1][11][21]

Combined Treatment

Intratympanic corticosteroids may be administered concurrently with systemic corticosteroids as combined initial therapy. Results from some studies suggested that combined treatment may produce a small additional hearing benefit, particularly in patients with severe or profound hearing loss. Conversely, results from other studies found no clinically meaningful advantage over systemic or intratympanic therapy alone.[20][22][23] Because the evidence remains inconsistent, combined treatment should not be considered universally superior. The decision should account for the severity of hearing loss, time since onset, medical contraindications, patient preferences, treatment burden, and the potential adverse effects of systemic corticosteroids.

Ménière Disease

Intratympanic corticosteroid injection may be offered to patients with active Ménière disease who continue to experience disabling vertigo despite appropriate noninvasive treatment. Noninvasive management may include patient education, dietary and lifestyle modification, treatment of associated conditions, and maintenance pharmacotherapy when appropriate.[7] Intratympanic corticosteroids are nonablative and are intended to reduce vertigo while preserving residual cochlear and vestibular function. Therefore, clinicians commonly consider intratympanic corticosteroids before intratympanic gentamicin or ablative surgical procedures in patients with serviceable hearing. Treatment may be delivered as a defined series of injections or repeated according to symptom recurrence and clinical response.

Results from clinical trials and systematic reviews suggested that some patients experience meaningful reductions in the frequency of vertigo after intratympanic corticosteroid treatment. However, estimates of benefit vary, and the certainty of evidence is limited by differences in diagnostic criteria, corticosteroid preparations, dosing schedules, follow-up periods, and outcome definitions.[15][24] Patients should be counseled that treatment may reduce vertigo attacks but may not prevent progressive hearing loss, tinnitus, or aural fullness. Intratympanic gentamicin generally provides more definitive vestibular ablation and may offer greater vertigo control in selected patients, but this treatment carries a higher risk of permanent vestibular hypofunction and hearing deterioration. Intratympanic corticosteroids remain an appropriate hearing-preserving option when noninvasive treatment has not provided adequate symptom control.

Autoimmune Inner Ear Disease

Systemic corticosteroids remain the usual initial treatment for suspected autoimmune inner ear disease. Intratympanic corticosteroid therapy may be considered as an adjunct or alternative for patients who respond incompletely to systemic therapy, experience recurrent hearing deterioration during corticosteroid tapering, or have contraindications to prolonged systemic corticosteroid exposure.[25] Evidence supporting intratympanic treatment for autoimmune ear disease is derived primarily from small observational studies and heterogeneous case series. Treatment should therefore be individualized and coordinated with an otologist or neurotologist and, when systemic autoimmune disease is suspected, a rheumatologist. Serial pure-tone and speech audiometry should be used to document treatment response and identify continued progression.

Other and Investigational Uses

Intratympanic corticosteroids have been investigated for acute acoustic trauma, tinnitus, and other inflammatory or immune-mediated cochleovestibular disorders. Evidence for these uses remains limited and inconsistent. Intratympanic corticosteroid injection should not be routinely recommended for chronic isolated tinnitus because a reproducible and clinically meaningful benefit has not been established. Treatment may occasionally be considered in carefully selected patients with acute tinnitus associated with recent sensorineural hearing loss or acoustic injury, but therapy should be directed toward the underlying cochlear disorder rather than tinnitus alone. Patients should be counseled regarding the uncertain benefit and the procedural risks before treatment.

Contraindications

Because intratympanic corticosteroid injection is minimally invasive and generally well tolerated, absolute contraindications are uncommon. Most contraindications are relative and can be addressed before treatment.

Absolute Contraindications

• A patient who is unable to remain still during the procedure despite appropriate counseling or anxiolysis because sudden patient movement may result in injury to the external auditory canal, tympanic membrane, or middle ear structures.
• Known hypersensitivity to the corticosteroid preparation or any component of the formulation.

Relative Contraindications

• Acute otitis externa or acute otitis media, which should be treated before elective intratympanic injection to minimize the risk of spreading infection.
• Suspected tympanic membrane, middle ear, or external auditory canal neoplasm, or a vascular lesion such as a glomus tumor, until appropriate evaluation has been completed.
• Inability to adequately visualize the tympanic membrane because of cerumen impaction, canal stenosis, inflammation, or anatomic distortion. Visualization should be optimized before proceeding.
• Significant anatomic abnormalities of the external auditory canal or tympanic membrane that prevent safe needle placement.
• Persistent tympanic membrane perforation when the planned technique requires an intact membrane, although medication may be administered through an existing perforation or tympanostomy tube when clinically appropriate.

Special Considerations

The presence of a functioning tympanostomy tube is not a contraindication to intratympanic corticosteroid therapy. Corticosteroids may instead be instilled directly through the tube into the middle ear, avoiding the need for additional tympanic membrane puncture.

Equipment

The equipment required for intratympanic corticosteroid injection is readily available in most outpatient otolaryngology clinics.

• Binocular operating microscope or high-definition otologic endoscope for visualization of the tympanic membrane.
• Appropriately sized sterile ear speculum.
• Microsuction equipment for removal of cerumen or debris when necessary.
• Sterile 1-mL syringe fitted with a 25- to 27-gauge spinal or long injection needle to facilitate controlled delivery through the tympanic membrane.
• Topical or local anesthetic. Common options include topical phenol, topical lidocaine (eg, 10% lidocaine spray or viscous lidocaine), eutectic lidocaine-prilocaine (EMLA) cream applied to the tympanic membrane, or infiltrative local anesthesia when indicated. No anesthetic technique has consistently demonstrated superiority over another, and selection is generally based on clinician preference and patient tolerance.[26][27]
• Corticosteroid preparation: The most commonly used agents are dexamethasone, typically 10 to 24 mg/mL, and methylprednisolone, typically 30 to 62.5 mg/mL. Although no standardized dosing regimen exists, both medications have demonstrated clinical efficacy for the treatment of inner ear disorders.[28][29][30]
• Sterile cotton-tipped applicators and suction for anesthetic application and removal of excess medication.
• Personal protective equipment, including sterile gloves and protective eyewear, in accordance with institutional infection control practices.

Many clinicians allow the corticosteroid solution to reach room or body temperature before injection to reduce patient discomfort and minimize vestibular stimulation, although evidence supporting routine warming is limited.[31]

Personnel

Intratympanic corticosteroid injection is typically performed by an otolaryngologist or another clinician with appropriate training in otologic procedures and familiarity with middle ear anatomy. Competency in otomicroscopy or endoscopic ear examination, patient selection, sterile technique, and the recognition and management of procedural complications is essential for safe and effective treatment. Additionally, a trained nurse or medical assistant can improve procedural efficiency by preparing the equipment and medication, assisting with patient positioning, maintaining aseptic technique, monitoring patient comfort, and providing postprocedure instructions. Audiologists play an important role in establishing baseline hearing, performing serial audiometric assessments, and monitoring treatment response. Coordination among otolaryngologists, audiologists, nursing staff, and primary care clinicians facilitates timely diagnosis, appropriate referral, treatment, and longitudinal monitoring, particularly for patients with idiopathic sudden sensorineural hearing loss and Ménière disease.

Preparation

Before performing an intratympanic corticosteroid injection, the clinician should confirm the indication for treatment, review recent audiometric findings, discuss the expected benefits and limitations of therapy, and obtain informed consent. Patients should be counseled regarding potential complications, including transient dizziness or vertigo, injection site discomfort, persistent tympanic membrane perforation, otitis media, transient tinnitus, and, rarely, worsening hearing loss. Additionally, patients should be advised that transient vertigo or imbalance may occur immediately after the procedure. Although most symptoms resolve within minutes, patients should be encouraged to arrange transportation home if they are concerned about driving or anticipate significant vestibular symptoms.

The patient is positioned comfortably in the supine or semireclined position with the treated ear facing upward and the head rotated approximately 30° to 45° toward the contralateral side. This position facilitates visualization of the tympanic membrane and promotes prolonged contact between the corticosteroid solution and the round window membrane following injection. The external auditory canal should be examined under an operating microscope or high-definition otologic endoscope using an appropriately sized ear speculum. Cerumen, debris, or desquamated epithelium should be removed to ensure unobstructed visualization of the entire tympanic membrane and relevant anatomic landmarks.

Topical anesthesia is commonly achieved with phenol, topical lidocaine (eg, 10% lidocaine spray or viscous lidocaine), or EMLA cream applied directly to the intended injection site. Alternatively, infiltrative local anesthesia may be used in selected patients. No single anesthetic technique has demonstrated consistent superiority, and the choice is generally based on clinician preference, patient comfort, and institutional practice.[26][27] The corticosteroid solution should be prepared immediately before the procedure and inspected for particulate matter or discoloration. Many clinicians allow the solution to reach room or body temperature before administration to improve patient comfort and minimize vestibular stimulation, although supporting evidence is limited.

Technique or Treatment

Preparation

Before performing an intratympanic corticosteroid injection, the clinician should confirm the indication for treatment, review recent audiometric findings, and ensure that no contraindications to the procedure are present. The expected benefits, alternative treatment options, and potential risks, including transient vertigo, pain, persistent tympanic membrane perforation, otitis media, tinnitus, and the rare possibility of worsening hearing loss, should be discussed with the patient, and informed consent should be obtained. The patient is positioned comfortably in the supine or semireclined position with the treated ear facing upward and the head rotated approximately 30° to 45° toward the contralateral side. The external auditory canal is examined under an operating microscope or high-definition otologic endoscope, and cerumen or debris is removed as needed to provide unobstructed visualization of the tympanic membrane.

Topical anesthesia is applied to the intended injection site using the clinician's preferred method, such as topical phenol, 10% lidocaine spray, viscous lidocaine, or EMLA cream. Alternatively, infiltrative local anesthesia may be used. No single anesthetic technique has demonstrated consistent superiority over another.[26][27]

The corticosteroid solution is prepared immediately before administration. Dexamethasone (typically 10 to 24 mg/mL) or methylprednisolone (typically 30 to 62.5 mg/mL) is most commonly used. Many clinicians allow the solution to reach room or body temperature before injection to improve patient comfort and minimize vestibular stimulation, although evidence supporting this practice is limited.[28][29][30][31][32]

Technique

After adequate anesthesia is achieved, the tympanic membrane is visualized under the operating microscope or with an otologic endoscope. Using a sterile 1-mL syringe fitted with a 25- to 27-gauge spinal or long injection needle, the clinician punctures the pars tensa, typically in the posteroinferior or anteroinferior quadrant, while avoiding the ossicular chain, chorda tympani nerve, and areas of tympanosclerosis whenever possible. Approximately 0.3 to 0.8 mL of dexamethasone or methylprednisolone is injected slowly into the middle ear cavity until the round window niche is adequately bathed or the middle ear space is nearly filled. The exact volume depends on the size of the middle ear, patient tolerance, and evidence of reflux through the injection site. Slow injection minimizes discomfort and reduces rapid pressure changes within the middle ear. Some clinicians create a second tympanic membrane perforation to permit air egress during injection or place a tympanostomy tube in patients who require repeated intratympanic therapy. However, these techniques are not routinely necessary and are generally reserved for selected clinical circumstances or operator preference.[33]

Postprocedural Care

Following injection, the patient remains in the supine or semireclined position with the treated ear facing upward for approximately 20 to 30 minutes to maximize contact between the corticosteroid solution and the round window membrane. Patients are commonly instructed to avoid swallowing, speaking, yawning, or excessive jaw movement during this period to reduce eustachian tube opening and minimize medication loss into the nasopharynx, although evidence supporting these measures is limited.[33] The patient should be observed briefly for transient vertigo, nausea, vasovagal symptoms, or discomfort before discharge. Most patients tolerate the procedure well and may resume normal activities shortly thereafter. Patients should be instructed to seek medical attention if they experience persistent otorrhea, severe otalgia, fever, prolonged vertigo, or worsening hearing loss. The need for repeat intratympanic corticosteroid injections depends on the underlying disease, treatment protocol, and clinical response. Although no universally accepted regimen exists, treatment typically consists of 1 to 4 injections administered over several days or weeks, with follow-up audiometry performed to assess treatment response and guide further treatment.

Complications

Intratympanic corticosteroid injection is generally a safe, well-tolerated outpatient procedure with a low incidence of serious complications. Most adverse effects are mild, self-limited, and resolve without intervention. Patients should be counseled regarding expected transient symptoms and uncommon but clinically important risks before providing informed consent.

The most frequently reported adverse effects include transient injection site pain or discomfort, a burning sensation during corticosteroid instillation, temporary vertigo or dizziness, and a sensation of ear fullness immediately after the procedure.[34] These symptoms typically resolve within minutes to several hours without treatment. Less common complications include persistent tympanic membrane perforation, otitis media, transient tinnitus, headache, vasovagal or syncopal episodes, dysgeusia or tongue numbness resulting from irritation of the chorda tympani nerve, and temporary worsening of hearing.[34] Persistent tympanic membrane perforation is uncommon and may require surgical repair if the perforation does not close spontaneously.

Although rare, sensorineural hearing deterioration, prolonged vertigo, and middle ear infection have been reported after intratympanic injection. Careful patient selection, meticulous sterile technique, accurate needle placement, and appropriate postprocedural monitoring minimize the risk of these complications. Patients should be instructed to seek prompt medical evaluation if they develop persistent otorrhea, fever, severe otalgia, worsening hearing loss, prolonged vertigo, or symptoms suggestive of middle ear infection after the procedure.

Clinical Significance

Intratympanic corticosteroid injection is an established, minimally invasive procedure that enables targeted delivery of corticosteroids to the inner ear while minimizing systemic drug exposure. This procedure has become an important treatment option for patients with idiopathic sudden sensorineural hearing loss, particularly as salvage therapy after incomplete recovery with systemic corticosteroids and as primary therapy when systemic corticosteroids are contraindicated. Intratympanic corticosteroids also provide an effective, hearing-preserving treatment option for patients with active Ménière disease whose vertigo persists despite noninvasive treatment.

Compared with systemic corticosteroid therapy, intratympanic administration achieves substantially higher intracochlear drug concentrations while reducing the risk of systemic adverse effects.[35] The procedure is generally well tolerated, can be performed safely in an outpatient setting under topical or local anesthesia, and has a low complication rate when performed by appropriately trained clinicians. Because hearing recovery in idiopathic sudden sensorineural hearing loss is highly time-dependent, prompt diagnosis, timely referral, and early intervention are essential to optimize patient outcomes. Intratympanic corticosteroid injection therefore represents an important component of contemporary, evidence-based otologic practice and expands treatment options for patients with cochleovestibular disorders.

Enhancing Healthcare Team Outcomes

Optimal outcomes after intratympanic corticosteroid injection require timely diagnosis, appropriate patient selection, and close collaboration among members of an interprofessional healthcare team. Primary care clinicians, emergency clinicians, urgent care clinicians, advanced practice clinicians, audiologists, and otolaryngologists should recognize the time-sensitive nature of ISSNHL and facilitate prompt audiometric evaluation and referral for definitive treatment. Because hearing recovery is strongly influenced by the interval between symptom onset and treatment, delays in diagnosis or referral may reduce the likelihood of meaningful hearing improvement.[36] Although spontaneous recovery occurs in a proportion of patients with ISSNHL, recovery cannot be predicted reliably at presentation. Therefore, current evidence supports prompt initiation of evidence-based therapy rather than observation alone.[37] Otolaryngologists are responsible for confirming the diagnosis, determining patient eligibility, obtaining informed consent, performing the procedure using meticulous sterile technique, and managing procedural complications when they occur.

Audiologists play a central role by performing baseline and follow-up audiometric testing to document hearing status, assess treatment response, and identify patients who may benefit from additional intervention. Repeat audiometry should be obtained after treatment to guide ongoing care, including consideration of salvage intratympanic corticosteroid therapy for patients with persistent hearing loss.[38] Clinicians contribute by educating patients, preparing equipment and medications, assisting during the procedure, monitoring for adverse events, reinforcing postprocedural instructions, and coordinating follow-up care. Pharmacists help ensure appropriate corticosteroid selection, preparation, storage, and safe medication handling while identifying potential contraindications or drug-related concerns. Clear communication, shared decision-making, and coordinated follow-up among all members of the healthcare team improve procedural safety, reduce treatment delays, enhance adherence to evidence-based practice, and optimize hearing and vestibular outcomes. A patient-centered, interprofessional approach remains essential for delivering high-quality care to patients undergoing intratympanic corticosteroid injection.

Nursing, Allied Health, and Interprofessional Team Interventions

Optimal outcomes after intratympanic corticosteroid injection depend on coordinated, patient-centered care delivered by an interprofessional healthcare team. Primary care clinicians, emergency clinicians, urgent care clinicians, and advanced practice clinicians should recognize the time-sensitive presentation of idiopathic sudden ISSNHL, obtain prompt audiometric evaluation, and expedite referral to an otolaryngologist. Early diagnosis and treatment are critical because delays may reduce the likelihood of hearing recovery.

Otolaryngologists are responsible for confirming the diagnosis, determining the appropriateness of intratympanic corticosteroid therapy, obtaining informed consent, performing the procedure using meticulous sterile technique, and treating procedural complications. Nurses and medical assistants prepare the equipment and medications, assist with patient positioning, maintain aseptic technique, monitor patients during and after the procedure, reinforce postprocedural instructions, and identify adverse events requiring clinician evaluation. Additionally, audiologists perform baseline and follow-up audiometric assessments to document hearing status, evaluate treatment response, and facilitate ongoing care. Pharmacists contribute by verifying the selection, concentration, preparation, storage, and compatibility of corticosteroids while ensuring safe medication handling practices. Effective communication among all members of the healthcare team, combined with shared decision-making and coordinated follow-up, improves procedural safety, enhances adherence to evidence-based practice, minimizes treatment delays, and optimizes hearing and vestibular outcomes for patients undergoing intratympanic corticosteroid therapy.

Nursing, Allied Health, and Interprofessional Team Monitoring

Patients undergoing intratympanic corticosteroid injection should be monitored for both treatment response and procedure-related complications through coordinated interprofessional follow-up. Immediately after the procedure, nursing staff or other trained healthcare professionals should observe patients for transient vertigo, nausea, vasovagal symptoms, pain, or other adverse effects before discharge. Patients should receive clear instructions regarding expected postprocedural symptoms and be advised to seek prompt medical evaluation if they develop persistent otorrhea, fever, severe otalgia, prolonged vertigo, or worsening hearing loss.

Audiologists play a critical role in monitoring treatment effectiveness by performing baseline and follow-up audiometric evaluations to assess hearing recovery, speech discrimination, and disease progression. Otolaryngologists interpret these findings, evaluate symptom resolution, determine the need for additional intratympanic injections or alternative therapies, and monitor for complications such as persistent tympanic membrane perforation or middle ear infection. Primary care clinicians and advanced practice clinicians reinforce follow-up recommendations, monitor overall patient progress, and coordinate care with otolaryngology and audiology services. Effective communication among all members of the healthcare team promotes timely recognition of an inadequate treatment response or complications, facilitates evidence-based treatment, and optimizes patient safety and hearing outcomes.