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Eustachian tube dysfunction

Eustachian tube dysfunction (ETD) is a medical condition in which the —a narrow passage connecting the to the back of the and upper —fails to open or close properly, disrupting the normal equalization of air , of fluid, and protection of the from pathogens. This malfunction can lead to a buildup of fluid or negative in the , resulting in symptoms such as ear fullness, pain, muffled hearing, and increased susceptibility to infections like . ETD is classified into types, including obstructive (where the tube does not open adequately) and patulous (where the tube remains abnormally open), with the obstructive form being the most prevalent. The plays a critical role in ventilation and , opening intermittently during actions like , yawning, or to balance with that in the . In children, the tube is shorter, more horizontal, and floppier than in adults, contributing to higher rates of dysfunction and related complications such as recurrent ear infections. Common causes include upper respiratory infections, allergies, , acid reflux, environmental irritants like smoke or pollution, and anatomical factors such as enlarged adenoids or nasal polyps. Less frequently, it may stem from rapid , hormonal changes, or even in patulous cases. Symptoms of ETD vary by type but often include a sensation of ear pressure or blockage, popping or clicking sounds, (ringing in the ears), , and temporary . In obstructive ETD, patients may experience pain exacerbated by altitude changes or during , while patulous ETD can cause autophony (echoing of one's own voice or ). typically involves a of the ear, to assess middle ear pressure, and sometimes endoscopic evaluation of the nasopharynx by an otolaryngologist. ETD affects approximately 1% of the general adult population but is far more common in children, with up to 40% experiencing transient episodes and a prevalence estimated at 4% to 20%. In the United States, obstructive ETD has a prevalence of about 4.6% among adults and 4.4% among adolescents, underscoring its significant public health impact. Treatment options range from conservative measures like nasal decongestants, antihistamines, and steroid sprays to surgical interventions such as tympanostomy tube placement or Eustachian tube balloon dilation for chronic cases. Early management is essential to prevent complications like chronic otitis media or hearing impairment.

Anatomy and physiology

Structure of the Eustachian tube

The , also known as the auditory tube, is a narrow passageway that connects the cavity to the nasopharynx. In adults, it measures approximately 3 to 4 cm in length, with a of about 3 that is widest at its ends and narrowest at the . The tube is divided into two main portions: a bony segment comprising the lateral third, which is embedded within the petrous portion of the and opens into the at the tympanic orifice; and a cartilaginous segment forming the medial two-thirds, which consists of fibroelastic and extends to the nasopharyngeal opening known as the . The bony portion is nearly horizontal and rigid, while the cartilaginous portion is more flexible and descends at an angle of 30° to 40° relative to the . Key structural components include the tubal , which provides support with its broad medial lamina, thin lateral lamina, and accessory cartilages; Ostmann's fat pad, located medially to maintain closure by filling the surrounding space; and associated muscles such as the tensor veli palatini, which inserts onto the cartilaginous portion via a bilaminar structure; the levator veli palatini, originating from the inferior and ; and the salpingopharyngeus, which aids in tubal dynamics. The inner lining of the Eustachian tube is composed of pseudostratified ciliated columnar epithelium containing goblet cells and submucosal glands, which contribute to by producing and transporting mucus toward the nasopharynx. Developmentally, the Eustachian tube in children is shorter, narrower, and more —sloping at about 10° to the compared to 35° in adults—which alters its anatomical configuration. In adults, the tube is angled at approximately 45° to the , with variations in length, diameter, and cartilage flaccidity observed across individuals.

Normal function and regulation

The Eustachian tube serves three primary physiological roles in maintaining health: pressure equalization between the and the ambient atmosphere to facilitate optimal tympanic membrane mobility and sound transmission; protection of the from nasopharyngeal pathogens, secretions, and pressure fluctuations; and drainage of mucoid secretions from the to the nasopharynx. These functions ensure the remains aerated and free from fluid accumulation under normal conditions. At rest, the remains passively closed due to of its fibrocartilaginous structure and surrounding tissue pressure, preventing reflux of nasopharyngeal contents. Active opening occurs intermittently through contraction of the , primarily during , yawning, or the , with assistance from the levator veli palatini; this allows brief airflow for pressure equilibration, typically lasting about 0.4 to 0.5 seconds per event. In normal adults, the tube opens approximately 1 to 1.4 times per minute during typical activities, with intervals lengthening during rest or sleep. Mucociliary clearance is facilitated by ciliated epithelial cells lining the tube, particularly in its anteroinferior portion, which propel secretions unidirectionally from the toward the nasopharynx through coordinated ciliary beating at a rate of 8 to 16 Hz, augmented by airflow during tube opening and gravitational effects in the angled adult configuration. Regulation of Eustachian tube function involves the , which modulates and mucosal vascularity, alongside hormonal influences such as , which can affect tube patency. Age-related maturation enhances efficiency: in children, the more horizontal tube orientation (angle ~10°) and smaller volume (~62 mm³) impair drainage and increase infection susceptibility, whereas adults exhibit a steeper angle (~35°) and larger volume (~111 mm³), supporting more effective ventilation and clearance.

Pathophysiology

Mechanisms of dysfunction

Eustachian tube dysfunction (ETD) arises from disruptions in the tube's normal mechanisms of opening, closure, and clearance, which under physiological conditions maintain pressure equilibrium and protect against . These disruptions can manifest as obstructive, patulous, or clearance-related failures, each contributing to pathology through altered pressure dynamics and fluid accumulation. Obstruction primarily occurs due to failure of the tube to open adequately, often from or of the mucosal lining, which narrows the and prevents passive or active dilation during or yawning. This leads to negative middle ear pressure relative to the atmosphere, promoting transudation of fluid into the space and subsequent , as gas absorption by the mucosa outpaces replenishment. Mechanical blockage from mucosal folds or adhesions can exacerbate this, further impairing ventilation and increasing the risk of during rapid ambient pressure changes, such as in air travel. In contrast, a patulous state involves abnormal patency of the tube, where it fails to close at rest, allowing continuous airflow between the nasopharynx and . This excessive opening results in pressure instability, with the tympanic membrane oscillating with respiration, and can produce autophony through direct transmission of voice or breath sounds into the ear. The underlying physiology may involve reduced tissue mass or elasticity in the tube walls, preventing the necessary for closure. Impaired contributes to ETD by disrupting the transport of secretions from the to the nasopharynx, often due to reduced ciliary beat frequency or hypersecretion of viscous . damages ciliated , leading to of and inflammatory products within the tube, which traps fluid and perpetuates obstruction. Inflammatory cascades play a central role in many forms of ETD, where allergens or irritants trigger the release of inflammatory mediators, including cytokines such as interleukin-4 and , causing mucosal swelling and altered tube compliance. This swelling increases the opening required for , while vasodilatory effects from mediators like further impair mucociliary function and promote . Biomechanical factors, particularly inefficiency in the , reduce the contractile force needed to overcome mucosal adhesion or elasticity during tube opening. Dysfunction in this muscle, often linked to neuromuscular coordination issues, diminishes the tube's ability to ventilate the , compounding pressure imbalances.

Classification of ETD

Eustachian tube dysfunction (ETD) is classified into three primary types based on the functional abnormalities of the tube: dilatory (also known as obstructive), patulous, and baro-challenge-induced. This classification, established in a international statement, emphasizes the tube's role in ventilation and pressure regulation, distinguishing failures in opening from failures in closing or context-specific dysfunction. Dilatory ETD, the most common form accounting for the majority of cases, involves inadequate opening of the , leading to negative pressure and impaired ventilation. It is subdivided into acute (symptoms lasting less than 3 months, often following an upper respiratory infection) and (symptoms persisting beyond 3 months) subtypes, with further categorization into functional obstruction (due to or mucosal ), dynamic dysfunction (resulting from abnormal function), and anatomical obstruction (from structural narrowing). Patulous ETD, a rarer affecting approximately 0.3% to 6.6% of the population, occurs when the tube remains abnormally open, allowing continuous airflow and transmission of nasopharyngeal sounds to the . It is frequently idiopathic or associated with significant , , or disorders that lead to of the tubal lining. Baro-challenge-induced ETD represents a mixed or situational form where dysfunction manifests primarily under conditions of rapid pressure change, such as during , , or altitude shifts, without persistent abnormalities at rest; it does not fit neatly into pure dilatory or patulous categories. Classification also varies by age group, with obstructive (dilatory) ETD being more prevalent in children (estimated at 4% to 20% overall ETD ) due to their shorter, narrower, and more horizontal Eustachian tubes, which predispose to and poor . In adults, patulous ETD is relatively more common, linked to age-related , while overall ETD drops to about 0.77% to 4.6%. Diagnostic criteria for these types rely on a combination of symptoms and objective tests, particularly . Obstructive ETD typically shows a type B (flat) curve indicating reduced tympanic membrane mobility from or , while patulous ETD often presents a normal type A curve but with confirmatory signs like tympanic membrane excursions synchronized to respiration observed during nasal airflow testing.

Clinical presentation

Symptoms

Patients with Eustachian tube dysfunction (ETD) commonly report a sensation of fullness or pressure in the affected , often described as aural fullness, which arises due to inadequate equalization of middle pressure. This is frequently accompanied by popping or clicking sensations during or yawning, resulting from intermittent attempts by the tube to open. Muffled hearing is another prevalent symptom, where sounds appear dulled as if underwater, stemming from the pressure imbalance affecting sound transmission to the . , manifesting as ringing in the or autophony (echoing of one's own voice or breathing), may also occur, particularly in cases of patulous ETD where the tube remains abnormally open. Ear pain, or otalgia, is a frequent complaint, often exacerbated by changes in such as during air travel or diving, leading to that intensifies the discomfort. In acute ETD, symptoms typically emerge suddenly and resolve within days to weeks as the underlying trigger subsides, whereas chronic forms persist for months or years, potentially resulting in ongoing hearing impairment if untreated. ETD symptoms can significantly impair , with disrupting sleep and concentration, while persistent ear pressure may contribute to disturbances or vertigo-like sensations due to altered vestibular function. The severity of these symptoms is often assessed using validated tools such as the 7-item Eustachian Tube Dysfunction Questionnaire (ETDQ-7), which quantifies patient-reported experiences like pressure, fullness, and muffled hearing on a scale from 1 to 7, aiding in clinical evaluation of ETD impact. In children, ETD manifestations may present differently, with , frequent ear tugging, and potential speech delays arising from chronic muffled hearing, as young patients are less able to articulate discomfort verbally.

Signs and associated findings

In obstructive Eustachian tube dysfunction (ETD), otoscopic examination often reveals a retracted due to negative , along with possible air-fluid levels or indicative of with . In patulous ETD, the may appear normal but can exhibit hypermobility or synchronous inward and outward movement with nasal respiration, reflecting the abnormally open tube. Audiometric evaluation typically shows ranging from 20 to 40 dB in cases with persistent , accompanied by reduced compliance as evidenced by a type B tympanogram on . Nasal and pharyngeal signs contributing to tube blockage include mucosal edema or inflammation visible on flexible nasoendoscopy, from associated , and obstructing the tubal orifice, particularly in children. Associated conditions may involve vertigo or imbalance due to altered pressure transmission affecting the , though this is uncommon; rare cases include involvement, such as alternobaric facial paresis from pressure differentials. Untreated chronic ETD can progress to serous , manifesting as persistent effusion and tympanic membrane retraction pockets. Pneumatic otoscopy is a key examination technique to assess tympanic membrane , revealing immobility or poor response in obstructive ETD and exaggerated in patulous cases.

Causes and risk factors

Acute causes

Acute causes of Eustachian tube dysfunction (ETD) primarily involve transient inflammatory or mechanical obstructions that impair the tube's ability to ventilate the , often resolving with the underlying trigger. These factors lead to rapid onset of symptoms through mechanisms such as mucosal or direct pressure imbalance, distinguishing them from chronic predispositions. Upper respiratory infections, including rhinitis and acute , are the most common acute triggers, causing inflammation and swelling of the mucosa that blocks its orifice. Bacterial can also contribute, particularly when it extends to the nasopharynx, exacerbating local . These infections often peak during winter months due to increased viral transmission, aligning with higher ETD incidence in colder seasons. Allergic reactions, such as those from seasonal allergens, induce and mucosal inflammation, leading to temporary blockage. This is particularly evident in individuals with , where histamine-mediated edema reduces tube patency. results from rapid changes, as seen in , , or even , preventing equalization and causing transudation of fluid into the . Otic barotrauma affects approximately 9% of air passengers, highlighting its prevalence among flyers. Trauma, including nasal fractures or iatrogenic injury from endotracheal , can acutely compromise tube patency by distorting surrounding structures or inducing formation. Environmental exposures, such as cigarette smoke or air pollutants, irritate the nasopharyngeal mucosa, provoking acute and that hinders function. Epidemiologically, acute ETD affects about 1% of the adult population annually, often linked to these reversible triggers.

Chronic and predisposing factors

Anatomical predispositions significantly contribute to chronic Eustachian tube dysfunction (ETD), particularly in individuals with craniofacial anomalies that alter tube structure and function. Conditions such as cleft palate impair the tensor veli palatini muscle's ability to open the tube, leading to persistent obstruction and higher rates of effusion. Similarly, is associated with abnormal Eustachian tube anatomy, including a shorter and more horizontal orientation, increasing susceptibility to chronic dilation failure and . In children, the is naturally shorter, narrower, and more horizontal compared to adults, contributing to with effusion in up to 90% of preschool-aged children, often due to associated ETD. Lifestyle factors can exacerbate or perpetuate ETD through ongoing mucosal irritation or pressure imbalances. Smoking is a well-established risk, roughly doubling the odds of obstructive ETD (odds ratio approximately 2.0), as tobacco smoke induces ciliary dysfunction and inflammation in the tubal mucosa. Obesity contributes by altering the peritubal fat pad and promoting negative middle ear pressure, often compounded by associated obstructive sleep apnea. Frequent air travel or high-altitude exposure further amplifies risk in susceptible individuals by repeatedly challenging tubal dilation mechanisms, leading to chronic barotrauma in those with underlying vulnerabilities. Comorbidities involving chronic inflammation or secretory deficits often underlie persistent ETD. irritates the nasopharyngeal mucosa via acid exposure, causing edema and impairing tube opening. Autoimmune conditions like Sjögren's syndrome reduce glandular secretions, resulting in mucosal dryness and obstruction that manifests as recurrent issues. Iatrogenic factors from medical interventions can lead to long-term tubal impairment. for frequently causes and mucosal in the , resulting in chronic dysfunction in 30% to 50% of survivors. Prolonged overuse of nasal corticosteroids, while typically beneficial, may contribute to iatrogenic atrophy or rebound inflammation in rare cases, though evidence remains limited. Genetic influences play a role in familial or syndromic forms of chronic ETD, particularly patulous variants. Collagen disorders such as Ehlers-Danlos syndrome weaken connective tissues around the tube, promoting abnormal patency and autophony through laxity in supporting structures. Similarly, , caused by mutations in genes like COL2A1, is linked to Eustachian tube anomalies and progressive in affected families. Recent data highlight as an emerging chronic trigger for ETD, with post-viral inflammation leading to persistent patulous or obstructive patterns in a subset of cases, including associations with with effusion. This recognition has grown since 2023, underscoring neurotrophic or inflammatory sequelae in respiratory recovery.

Diagnosis

Clinical evaluation

The clinical evaluation of Eustachian tube dysfunction (ETD) begins with a detailed history to identify the onset, duration, and triggers of symptoms, which helps differentiate acute from chronic cases and guides suspicion toward ETD. Acute ETD is typically defined as lasting less than and often linked to triggers such as upper respiratory infections, allergies, from flying or , or gastroesophageal , while chronic ETD exceeds and may involve persistent or anatomical factors. Associated symptoms commonly include aural fullness, muffled hearing, , autophony, otalgia, and imbalance, frequently accompanied by or , which can exacerbate Eustachian tube obstruction. To quantify symptom severity and support diagnosis, the Eustachian Tube Dysfunction Questionnaire-7 (ETDQ-7) is administered; this validated seven-item tool assesses symptoms over the past month on a scale from 1 (no problem) to 7 (severe problem), with a total score of ≥14.5 indicating clinically significant ETD with high sensitivity and specificity. Physical examination follows the history and focuses on basic otoscopic and nasopharyngeal assessment to detect supportive findings without relying on advanced instrumentation. Otoscopy reveals tympanic membrane retractions, negative middle ear pressure, or effusion in obstructive ETD, while patulous ETD may show a mobile membrane without retraction. Flexible nasopharyngoscopy allows visualization of the nasopharynx, torus tubarius, and adenoidal tissue for signs of hypertrophy, inflammation, or masses that could impede tube function; dynamic observation during swallowing can demonstrate tube dilation in patulous cases. Differential diagnosis is pursued through targeted historical questions to exclude mimics such as (TMJ) disorder (probe for jaw pain or clicking exacerbated by chewing), (inquire about vertigo episodes and low-frequency hearing loss), or (assess for chronic discharge or foul odor). Red flags warranting urgent referral include unilateral symptoms suggestive of nasopharyngeal tumor or malignancy, or associated neurological signs like facial weakness or cranial nerve involvement, which may indicate more serious pathology beyond isolated ETD. In pediatric patients, evaluation relies heavily on parental reports due to limited verbal expression, emphasizing history of feeding difficulties (e.g., poor or regurgitation during bottle feeds), recurrent acute , or persistent with effusion, which affects up to 90% of children before school age but often resolves by age seven as the tube matures. The overall workflow prioritizes taking to establish diagnostic suspicion, followed by physical examination, with objective testing reserved for confirmation if initial findings are equivocal.

Objective tests

Objective tests for Eustachian tube dysfunction (ETD) provide quantitative measures to confirm and characterize the condition, often following initial clinical evaluation to guide test selection. These assessments focus on , tubal patency, and auditory function, helping differentiate obstructive from patulous subtypes. is a primary objective tool, measuring and via acoustic immittance in response to changes. In obstructive ETD, a Type B tympanogram (flat curve) indicates reduced due to negative or , while a Type A curve (normal peak) may occur in patulous ETD despite symptoms, with peak typically around 0 to -50 daPa. demonstrates approximately 91-100% sensitivity and 67-100% specificity for detecting obstructive ETD when using thresholds like -50 daPa. Specialized Eustachian tube function tests extend tympanometry to evaluate active tubal opening. Inflation-deflation tympanometry, such as the nine-step test, applies positive and negative pressures to assess the opening threshold, with normal active opening at pressures below +30 daPa during or Valsalva maneuvers. For patulous ETD, the reflux test monitors pressure equalization during , revealing abnormal inward movement or persistent openness. Audiometry complements these by quantifying hearing impacts. often reveals mild to moderate (10-30 dB) in obstructive ETD due to middle ear pressure imbalance, with air-bone gaps most evident at low frequencies; remains normal unless other pathologies exist. thresholds may be elevated, reflecting impaired sound transmission. Imaging modalities are reserved for complex cases, not routine first-line use. Computed tomography (CT) delineates bony Eustachian tube anatomy, identifying anomalies like narrowing or masses contributing to obstruction. Nasal enables dynamic visualization of the nasopharyngeal ostium, assessing mucosal inflammation or abnormal movement during . Emerging tests as of 2024 include sonotubometry, which uses acoustic signals to detect real-time airflow through the tube during maneuvers, offering higher specificity for patency than traditional methods. Tubomanometry measures pressure changes during to quantify opening efficiency, aiding in precise dysfunction grading.

Management

Initial and conservative treatments

Initial and conservative treatments for Eustachian tube dysfunction (ETD) primarily focus on non-invasive strategies to alleviate symptoms, promote patency, and address underlying contributors such as or allergies, particularly in acute obstructive cases. These approaches are recommended as first-line management for most patients, aiming to equalize pressure and reduce discomfort without procedural intervention. Evidence supports their use in resolving symptoms in the majority of acute presentations, with a trial period typically lasting 1 to 2 weeks to assess response. Lifestyle modifications form the cornerstone of initial management, emphasizing simple actions to facilitate Eustachian tube opening and ventilation. Patients are advised to perform frequent swallowing, yawning, or chewing gum to activate muscles like the tensor veli palatini, which help equalize pressure across the tube. Adequate hydration is also encouraged to thin mucus secretions and prevent dehydration-related thickening that could exacerbate obstruction. Avoidance of environmental triggers, such as allergens if implicated in the patient's history, may further support symptom relief, though this briefly ties to known predisposing factors like allergies. These measures are low-risk and can be implemented immediately upon symptom onset. Pharmacotherapy targets nasal and mucosal inflammation or congestion to indirectly improve Eustachian tube function. Oral decongestants, such as at a dose of 60 mg every 6 hours, are commonly prescribed to reduce swelling in the nasopharynx, though use should be limited to short-term to avoid effects. For inflammatory components, intranasal corticosteroids like fluticasone propionate (2 sprays per once daily for 2 to 4 weeks) are recommended to decrease mucosal , with from clinical trials showing potential benefits in symptom reduction despite mixed overall data. Antihistamines, such as loratadine 10 mg daily, are indicated specifically for allergy-associated ETD to mitigate histamine-mediated swelling. These agents are selected based on the suspected , with monitoring for side effects like from decongestants. Autoinflation techniques provide active methods to force air into the , bypassing passive equalization. Common maneuvers include the Valsalva (pinching nostrils closed, closing the mouth, and gently blowing to create positive pressure) and the Toynbee (pinching nostrils closed and swallowing simultaneously). Devices like the Otovent nasal balloon facilitate controlled autoinflation by having the patient inflate a balloon through the nose, typically 3 to 5 times daily. These techniques demonstrate benefits in resolving associated with obstructive ETD, based on tympanometric improvements in clinical studies. Success depends on patient cooperation and correct technique, with instruction from a recommended. For associated otalgia, involves over-the-counter analgesics such as acetaminophen (500 to 1000 mg every 6 hours as needed) or ibuprofen (400 to 600 mg every 6 to 8 hours), which effectively reduce discomfort from pressure imbalances without addressing the underlying dysfunction. These should be used judiciously, following dosing guidelines to minimize gastrointestinal or hepatic risks. A 1- to 2-week trial of these conservative measures is , during which many acute obstructive ETD cases resolve spontaneously or with , avoiding the need for escalation. Persistent symptoms beyond this period warrant reassessment. Guidelines from the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), such as the 2016 Clinical Practice Guideline on Otitis Media with Effusion (OME), explicitly recommend against routine use unless acute bacterial is confirmed, as prophylactic administration does not improve outcomes in uncomplicated ETD and contributes to resistance.

Advanced and surgical options

For patients with persistent Eustachian tube dysfunction (ETD) that does not respond to after at least 3 months, advanced interventions are indicated to address underlying structural or functional issues, with overall complication rates reported below 5% across procedures. represents a minimally invasive option for obstructive ETD, involving endoscopic placement of a into the , which is inflated to dilate the cartilaginous portion and improve patency. This procedure, FDA-approved in for adults and later expanded, achieves technical success in nearly 100% of cases and yields symptom improvement in 70-80% of patients at 2-year follow-up, as evidenced by reductions in ETD scores and enhanced ability to perform Valsalva maneuvers. Long-term studies confirm sustained benefits in chronic cases, with low complication rates of 3-4%, primarily minor epistaxis or transient pain. Myringotomy with tube insertion is employed for chronic effusion secondary to ETD, where a small incision is made in the tympanic membrane under local or general , often followed by placement of a or tube to facilitate and ventilation. Laser-assisted or cold knife techniques are used, with tubes typically remaining in place for 6-12 months to prevent recurrence, particularly effective in cases unresponsive to initial therapies. In pediatric patients with ETD due to , is a common surgical intervention that removes enlarged adenoidal tissue to relieve extrinsic compression on the , improving ventilation in approximately 70% of cases. This procedure is frequently combined with and tube insertion in about 50% of instances to address concurrent with effusion, demonstrating significant postoperative enhancements in and hearing thresholds. For dysfunction, where the tube remains abnormally open, targeted injections of bulking agents such as or autologous fat into the can restore closure function, achieving symptom relief in 60-80% of patients at mid-term follow-up (6-24 months). These minimally invasive procedures carry low risks, though repeat injections may be required in 20-30% of cases due to material resorption. Emerging therapies include laser tuboplasty, which uses targeted energy to ablate hypertrophic mucosa and remodel the tube; however, it remains investigational with limited evidence from early studies showing 50-70% improvement in small cohorts at 1 year. Larger randomized studies are needed. Recent developments as of 2025 also include eustachian tuboplasty for chronic cases, demonstrating efficacy in treating with effusion, and the AAO-HNS position statement affirming dilation as appropriate for pediatric obstructive ETD. Investigations into biologic agents, such as injectables, and devices for neural regulation of tube function remain in early phases, with limited clinical data available.

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