Laryngeal Diseases, Voice Disorders PDF

LARYNGITIS Laryngitis refers to inflammation of the larynx. This is often due to an acute viral infection, which is typically a mild and self-limiting condition that lasts for a period of 3 to 7 days. There are non-infectious causes and more serious conditions that can present with acute laryngeal s...

LARYNGITIS Laryngitis refers to inflammation of the larynx. This is often due to an acute viral infection, which is typically a mild and self-limiting condition that lasts for a period of 3 to 7 days. There are non-infectious causes and more serious conditions that can present with acute laryngeal symptoms, and practitioners must be familiar with the differential diagnosis and workup. This activity reviews the evaluation and treatment of acute laryngitis and highlights the role of the interprofessional team in caring for patients with this condition. The most common cause of acute laryngitis is viral upper respiratory infection (URI), and this diagnosis can often be obtained from taking a thorough history of present illness from the patient. In the absence of infectious history or sick contacts, additional causes of non-infectious laryngitis must be explored. Presenting symptoms often include voice changes (patients may report hoarseness or a "raspy" voice), early vocal fatigue (particularly in singers or professional voice users), or a dry cough. Breathing difficulties are rare (though possible) in acute laryngitis, but the presence of significant dyspnea, shortness of breath (SOB), or audible stridor should alert the clinician that a more dangerous disease process may be present. Suspicion should be heightened in smokers and the immunocompromised, as these patients are at higher risk for malignancy and more dangerous infections that may otherwise mimic acute laryngitis. Similarly, the presence of significant dysphagia, odynophagia, drooling, or posturing are very rare in simple acute laryngitis and warrant additional workup. Etiology The etiology of acute laryngitis can be classified as either infectious or non-infectious. The infectious form is more common and usually follows an upper respiratory tract infection. Viral agents such as rhinovirus, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus, and influenza are all potential etiologic agents (listed in roughly descending order of frequency). It is possible for bacterial superinfection to occur in the setting of viral laryngitis, this classically occurs approximately seven days after symptoms begin. Acute infectious laryngitis in adults is most commonly caused by the viral organisms listed above. These same agents are common in pediatric acute laryngitis, though it is important to remember croup (laryngotracheobronchitis) in children, which is due to parainfluenza virus (most commonly parainfluenza-1). This may present with isolated vocal symptoms, but classically includes a characteristic "barking" cough and may progress to inspiratory or biphasic stridor. In about 3% of children, viral infections of the airways that develop in early childhood led to narrowing of the laryngeal lumen in the subglottic region resulting in symptoms such as hoarseness, a barking cough, stridor, and dyspnea. The predisposing factors for acute subglottic laryngitis in children are the shape and size of the larynx, a tendency for submucosal swelling (especially in the subglottic region), and airway hyperreactivity. These infections may eventually cause respiratory failure. The disease is often called acute subglottic laryngitis (ASL). Terms such as pseudocroup, croup syndrome, acute obstructive laryngitis and spasmodic croup are used interchangeably when referencing this disease. Although the differential diagnosis should include other rare diseases such as epiglottitis, diphtheria, fibrinous laryngitis and bacterial tracheobronchitis, the diagnosis of ASL should always be made on the basis of clinical criteria. Acute non-infectious laryngitis can be due to vocal trauma/abuse/misuse, allergy, gastroesophageal reflux disease, asthma, environmental pollution, smoking, inhalational injuries, or functional/conversion disorders. Vocal misuse or abuse can be acute in onset, as seen after a day or days of shouting/yelling. This is common in coaches, fans, and athletes after an event. This can also be seen in vocal performers, particularly those whose performance intensity or frequency has increased recently, and who have not had formal voice or singing coaching. Gastroesophageal reflux (GERD), more specifically extra-esophageal GERD, termed laryngopharyngeal reflux (LPR), is an exceptionally common cause of voice symptoms and laryngitis. These symptoms can be acute or chronic and may be episodic. They may not follow or accompany the classic GERD symptoms, and 1/3 of patients with GERD will experience only laryngeal/voice symptoms. Hallmarks include a history of GERD, frequent throat-clearing or coughing, globus pharyngeus sensation, or coarseness to the voice. Singers may note a loss of their higher range. Asthma may predispose to laryngitis due to chemical irritation from inhaler use, and chronic steroid inhaler use can predispose to fungal laryngitis, particularly if patients are not drinking plain water after their steroid inhaler use as instructed. There is also cough-variant asthma that may cause a repetitive injury to the vocal cords, leading to voice changes that mimic acute laryngitis. Environmental causes such as seasonal and environmental allergies, or seasonal or constant air pollution, can cause irritation to the vocal cords that may trigger acute laryngeal symptoms. Inhalation of noxious substances, whether intentional from smoking or other drug use or from unintentional exposure, irritates the larynx and can cause edema of the vocal folds and voice symptoms. Certain patients may be sensitive to perfumes, colognes, detergents, or other commonly-used aromatics in daily life. Functional dysphonia is a term for a group of true conversion disorders and encompasses a wide range of voice symptoms and physical examination findings. This is a diagnosis of exclusion, but recent major life stressors such as loss of a job or loved one are well-known triggers. The evaluation of an acute laryngitis patient must always begin with a thorough history and physical examination. Special attention should be directed at recent URI or other illnesses, sick contacts, or any other signs of systemic illness. The physician should also explore past medical history including immune status, immunization status, allergy and travel history, and history of other confounding pathologies such as GERD. These can include: Change in quality of voice, in later stages there may be a complete loss of voice (aphonia) Discomfort and pain in the throat, particularly after talking Dysphagia, odynophagia (if present, exercise caution - may hint at additional pathology) Dry cough General symptoms of dryness of throat, malaise, and fever Frequent throat-clearing Early voice fatigue or loss of vocal range Diagnosis can usually be made based on history. The examination of the larynx can confirm the diagnosis. Indirect examination of the airway with a mirror or with a flexible laryngoscope is warranted. Laryngeal appearance can vary with the severity of the disease. In the early stages, there is erythema and edema of the epiglottis, aryepiglottic folds, arytenoids, and vocal cords. As the disease progresses the vocal cords can become erythematous as well as edematous. The subglottic region may be involved, depending upon the inciting agent, though this is rarer. Sticky, ropy, secretions may also be seen between vocal cords or in the inter-arytenoid region. In the case of vocal abuse or misuse, several changes can be seen in the vocal folds. Reinke's edema is a common finding in both acute and chronic laryngitis. Submucosal hemorrhage may be seen in acute vocal trauma, or previously undiagnosed nodules or pseudo-nodules may be present. If left untreated, all of these can progress to chronic voice pathology. Treatment Treatment is often supportive in nature and depends on the severity of laryngitis. Voice rest: This is the single most important factor. Use of voice during laryngitis results in incomplete or delayed recovery. Complete voice rest is recommended although it is almost impossible to achieve. If the patient needs to speak, the patient should be instructed to use a "confidential voice;" that is, a normal phonatory voice at low volume without whispering or projecting. Steam Inhalation: Inhaling humidified air enhances moisture of the upper airway and helps in the removal of secretions and exudates. Avoidance of irritants: Smoking and alcohol should be avoided. Smoking delays prompt resolution of the disease process. Dietary modification: dietary restriction is recommended for patients with gastroesophageal reflux disease. This includes avoiding caffeinated drinks, spicy food items, fatty food, chocolate, peppermint. Another important lifestyle modification is the avoidance of late meals. The patient should have meals at least 3 hours before sleeping. These dietary measures have been shown to be effective in classic GERD, though their efficacy in LPR is disputed, they are often still employed. Medications: Antibiotics prescription for an otherwise healthy patient with acute laryngitis is currently unsupported; however, for high-risk patients and patients with severe symptoms antibiotics may be given. Some authors recommend narrow-spectrum antibiotics only in the presence of identifiable gram stain and culture. Fungal laryngitis can be treated with the use of oral antifungal agents such as fluconazole. Treatment is usually required for three weeks period and may be repeated if needed. This should be reserved for patients with confirmed fungal infection via laryngeal examination and/or culture. Mucolytics like guaifenesin may be used for clearing secretions. In addition to lifestyle and dietary modifications, LPR-related laryngitis is treated with anti-reflux medications. Medications that suppress acid production such as H2 receptor and proton pump blocking agents are effective against gastroesophageal reflux, though proton pump inhibitors are found to be most effective for LPR. These may require higher doses or twice-daily dosing schedule to be effective in this setting. Prevailing data do not support the prescription of antihistamines or oral corticosteroids for treating acute laryngitis. Differential Diagnosis includes: Spasmodic dysphonia Reflux laryngitis Chronic allergic laryngitis Epiglottitis Neoplasm Prognosis As this is often a self-limiting condition, it carries a good prognosis. If the patient completes the recommended therapy, the prognosis for recovery to a premorbid level of phonation is excellent. If vocal maladaptation has occurred, a course of speech therapy can resolve these problems. Acute laryngitis is often a self-limiting condition, but the clinician must be astute and attuned to potential underlying conditions or other problems that can mimic acute laryngitis. Any acute laryngitis that does not respond to appropriate treatment warrants further reconsideration, and potential referral to an otolaryngologist for a formal laryngeal examination. Voice rest is recommended. (Level 1) Antihistamines and oral steroids have no role in treatment. (Level 1) References: 1. Jaworek AJ, Earasi K, Lyons KM, Daggumati S, Hu A, Sataloff RT. Acute infectious laryngitis: A case series. Ear Nose Throat J. 2018 Sep;97(9):306- 313. [PubMed] 2. Mazurek H, Bręborowicz A, Doniec Z, Emeryk A, Krenke K, Kulus M, Zielnik- Jurkiewicz B. Acute subglottic laryngitis. Etiology, epidemiology, pathogenesis and clinical picture. Adv Respir Med. 2019;87(5):308-316. [PubMed] 3. Ghisa M, Della Coletta M, Barbuscio I, Marabotto E, Barberio B, Frazzoni M, De Bortoli N, Zentilin P, Tolone S, Ottonello A, Lorenzon G, Savarino V, Savarino E. Updates in the field of non-esophageal gastroesophageal reflux disorder. Expert Rev Gastroenterol Hepatol. 2019 Sep;13(9):827-838. [PubMed] 4. Naunheim MR, Dai JB, Rubinstein BJ, Goldberg L, Weinberg A, Courey MS. A visual analog scale for patient-reported voice outcomes: The VAS voice. Laryngoscope Investig Otolaryngol. 2020 Feb;5(1):90-95. [PMC free article] [PubMed] 5. Kavookjian H, Irwin T, Garnett JD, Kraft S. The Reflux Symptom Index and Symptom Overlap in Dysphonic Patients. Laryngoscope. 2020 Nov;130(11):2631- 2636. [PubMed] 6. Stachler RJ, Francis DO, Schwartz SR, Damask CC, Digoy GP, Krouse HJ, McCoy SJ, Ouellette DR, Patel RR, Reavis CCW, Smith LJ, Smith M, Strode SW, Woo P, Nnacheta LC. Clinical Practice Guideline: Hoarseness (Dysphonia) (Update). Otolaryngol Head Neck Surg. 2018 Mar;158(1_suppl):S1-S42. [PubMed] 7. Khodeir MS, Hassan SM, El Shoubary AM, Saad MNA. Surgical and Nonsurgical Lines of Treatment of Reinke's Edema: A Systematic Literature Review. J Voice. 2021 May;35(3):502.e1-502.e11. [PubMed] 8. Cohen SM, Thomas S, Roy N, Kim J, Courey M. Frequency and factors associated with use of videolaryngostroboscopy in voice disorder assessment. Laryngoscope. 2014 Sep;124(9):2118-24. [PMC free article] [PubMed] 9. Mosli M, Alkhathlan B, Abumohssin A, Merdad M, Alherabi A, Marglani O, Jawa H, Alkhatib T, Marzouki HZ. Prevalence and clinical predictors of LPR among patients diagnosed with GERD according to the reflux symptom index questionnaire. Saudi J Gastroenterol. 2018 Jul-Aug;24(4):236-241. [PMC free article] [PubMed] 10. Reveiz L, Cardona AF. Antibiotics for acute laryngitis in adults. Cochrane Database Syst Rev. 2015 May 23;2015(5):CD004783. doi: 10.1002/14651858.CD004783.pub5. PMID: 26002823; PMCID: PMC6486127. 11. Chae M, Jang DH, Kim HC, Kwon M. A Prospective Randomized Clinical Trial of Combination Therapy with Proton Pump Inhibitors and Mucolytics in Patients with Laryngopharyngeal Reflux. Ann Otol Rhinol Laryngol. 2020 Aug;129(8):781- 787. [PubMed] 12. Ringel B, Horowitz G, Shilo S, Carmel Neiderman NN, Abergel A, Fliss DM, Oestreicher-Kedem Y. Acute supraglottic laryngitis complicated by vocal fold immobility: prognosis and management. Eur Arch Otorhinolaryngol. 2019 Sep;276(9):2507-2512. [PubMed] HOARSENESS Hoarseness can be caused by acute (42.1%) and chronic laryngitis (9.7%), functional vocal disturbances (30%), and benign (10.7–31%) and malignant tumors (2.2–3%), as well as by neurogenic disturbances such as vocal cord paresis (2.8–8%), physiologic aging of the voice (2%), and psychogenic factors (2–2.2 %). Hoarseness is very rarely a manifestation of internal medical illness. The treatment of hoarseness has been studied in only a few randomized controlled trials, all of which were on a small scale. Voice therapy is often successful in the treatment of functional and organic vocal disturbances (level 1a evidence). Surgery on the vocal cords is indicated to treat tumors and inadequate vocal cord closure. The only entity causing hoarseness that can be treated pharmacologically is chronic laryngitis associated with gastro-esophageal reflux, which responds to treatment of the reflux disorder. The empirical treatment of hoarseness with antibiotics or corticosteroids is not recommended. Voice therapy, vocal cord surgery, and drug therapy for appropriate groups of patients with hoarseness are well documented as effective by the available evidence. In patients with risk factors, especially smokers, hoarseness should be immediately evaluated by laryngoscopy. Dysphonia, with the cardinal symptom of hoarseness, has a prevalence of around 1% among patients in general (1) and a lifetime prevalence of approximately 30% (e1). The term dysphonia is used to describe any impairment of the voice—alteration in the sound of the voice with hoarseness, restriction of vocal performance, or strained vocalization. The pathophysiology of hoarseness is characterized by muscle tone– related irregularity in the oscillation of the vocal cords owing to hypertonic dysphonia, incomplete closure of the glottis on vocalization, or an increase in vocal cord bulk, perhaps due to a tumor (Figure 1a, ,bb). The causes of hoarseness are diverse: Acute and chronic laryngitis (accounting for 42.1% and 9.7% of cases respectively) Functional dysphonia (30%) Benign and malignant tumors (10.7 to 31.0% and 2.2 to 3.0% respectively) Neurogenic factors such as vocal cord paralysis (2.8 to 8%) Physiological aging (2%) Psychogenic factors (2.0 to 2.2%) (1, e5). Very occasionally hoarseness can be attributed to manifestations of laryngeal disease other than tumors (Table 1). Causes and characteristics of hoarseness Open in a separate window Pathology Proport Typical Treatment Evide ion of symptoms nce all cases Functiona Hyperfunctional 30% Hoarseness Voice therapy 1a/A l dysphonia with vocal dysphoni strain a Secondar Vocal cord nodules Include Hoarseness Voice therapy 1a/A y d in with vocal (phonosurgery manifesta benign strain ) tion of tumors functiona (10.7– l 31%) dysphoni a Organic Laryngiti Acute 42.1% Hoarseness No medicinal 1a/A dysphoni s. infection treatment. a self-limiting Chronic 9.7% Constant Avoidance of 4/X hoarseness noxae.. laryngostrobo dysphonia. scopic throat _monitoring _sensation s. compulsio n to clear throat Benign Polyps/cys 10.7– Hoarseness Phonosurgery. 2a/B tumors ts 31%. reduced if applicable volume of voice therapy voice. _vocal fatigue Reinke Hoarseness Avoidance of 2a/B edema. vocal noxae. fatigue. phonosurgery. deep voice _if applicable voice therapy Recurring Hoarseness Phonosurgery 2a/B _papilloma. dyspnea tosis Pathology Proport Typical Treatment Evide ion of symptoms nce all cases Vocal cord 2.2–3% Hoarseness (Laser) 2a/B malignancies as early surgery. symptom radiotherapy Vocal cord scarring n.d. Constant Voice therapy 4/X hoarseness (phonosurgery. quiet ) voice Presbyphonia 2% Hoarseness Voice 2a/B. high- therapy. pitched phonosurgery voice Manifesta Laryngopharyngeal Include Only slight With signs of 2b/C tion of reflux d in hoarseness reflux: PPIs internal_ chronic. throat Without signs 2a/B disease laryngiti sensations of reflux: no s (9.7%) _predomin PPIs antly at night Tubercul n.d. Dyspnea. Tuberculostati 3/D osis cough c treatment Rheumat Rheumatoi n.d. Hoarseness Antirheumatic 3/D oid d arthritis. dyspnea. treatment diseases Collagenos n.d. or es dysphagia. (systemic _dependin lupus g on site erythemato sus) Vasculitid n.d. es (Wegener disease) Sarcoidosi n.d. s Amyloidosis n.d. Hoarseness Phonosurgery. 3/D. dyspnea. internal / or hematological dysphagia. _treatment _dependin g on site Pathology Proport Typical Treatment Evide ion of symptoms nce all cases Lymphoma n.d. Dysphonia Internal / 4/X. dyspnea hematological treatment Neurolog Vocal cord paresis 2.8– Hoarseness Voice 1a/A. ical 8.0%. impaired therapy. 2a/B diseases speech phonosurgery breathing Spasmodic dysphonia n.d. Variable Administratio 2a/B hoarseness n of botolinumtoxi nA Vocal n.d. Hoarseness Discuss with 4/X cord during an patient. dysfuncti episode of breathing on respiratory therapy. distress _psychotherap (few y seconds) Psychoge 2–2.2% Sudden Psychological 4/X nic hoarseness and dysphoni (hours or psychosomati a days) c treatment. psychotherapy Dysphonia Etiological classification of dysphonias according to causes. typical symptoms and characteristics of hoarseness. showing each cause’s percentage contribution to the total. Phonosurgery is an operative intervention to improve the voice. usually using microinstruments inserted transorally via a laryngoscope. sometimes by means of laser. n.d.. no data or prevalence 90% of boys, ca. 50% of girls) (2, e4, e23, e24). Organic dysphonia Acute laryngitis Acute laryngitis is the most common cause of hoarseness, accounting for 40% of cases (1), and is almost always viral in origin. It occurs in infections of the upper respiratory tract and is self-limiting, subsiding after 1 to 2 weeks (2, e25, e26). Patients are counseled to limit how much they talk, but absolute voice rest is not advised in order to avoid the risk of overcompensation to the point of aphonia (4). Routine antibiotic treatment is discouraged (evidence level 1a, recommendation grade A) (2, 5, e4); antibiotics are prescribed only in exceptional circumstances, e.g., in the presence of bacterial superinfection or laryngeal tuberculosis (Table 1). Indirect or direct laryngoscopy is indicated in such severe cases (evidence level 4, recommendation grade C) (Figure 2). Corticosteroids should not be administered in acute laryngitis (evidence level 3, recommendation grade B) (2). Chronic laryngitis Chronic laryngitis has an incidence of 3.5 /1000 in the general population (e27) and is a precursor of vocal cord cancer (6, 7). The following have been proposed as important etiological factors: Nicotine abuse Inhaled corticoid treatment Inhaled environmental noxae Gastroesophageal reflux with laryngopharyngeal involvement. Not infrequently leukoplakia arises (Figure 3). Possible clinical signs of chronic laryngitis are dysphonia, sensations in the throat, and a constant urge to clear the throat (e27). The principal therapeutic measures are avoidance of noxae and regular laryngeal stroboscopy for early detection of malignancy (4, 6). Meta-analyses have shown that laryngeal dysplasia or leukoplakia progresses to cancer in 14 to 16% of patients after a mean interval of 43 months (range 4 to 192 months) (e28, e29). Figure 2 Algorithm for diagnosis of hoarseness. ENT, ear, nose, and throat; VCD, vocal cord dysfunction; PPI, proton pump inhibitor; EGD, esophagogastroduodenoscopy; VC, vocal cord Benign and malignant tumors Vocal cord polyps/vocal cord cysts – Vocal cord polyps are unilateral tissue proliferations on the free margin of the vocal cord and thus hamper phonation (8). Men are more frequently affected (55%) (e30). The factors promoting the formation of vocal cord polyps include smoking (51 to 90%) (8), chronic laryngitis, and phonation trauma, i.e., microvascular trauma with local edematous remodeling processes and accompanying inflammation as a result of misuse of the voice (9). Retention cysts arise when the excretory ducts of the mucous glands are obstructed. The symptoms are hoarseness together with reduced volume and fatigue of the voice. The treatment of choice for polyps is phonosurgical excision at the base. Cysts must be removed in toto with the capsule (evidence level 2a, recommendation grade B) (2) (9, e24, e31). Reinke edema – Reinke edema is caused predominantly by tobacco smoke and mainly affects women (80%) between the ages of 40 and 60 years (ca. 47%) (e30). Phonosurgical removal of the edema results in improvement of the pitch, resonance, and also resilience of the voice. Dysplasia is rare (50,000 before proceeding with any airway surgery. Anatomically the anterior jugular veins can usually be retracted laterally; however, aberrant or bridging anterior jugular veins may be present, which should be ligated. A small percentage of patients, approximately 5%, will have a thyroidia ima artery, which courses along the anterior surface of the trachea. Once divided, it can retract inferiorly and contribute to ongoing bleeding, so meticulous technique is required when ligating it. As previously mentioned, careful ligation of the thyroid isthmus with transfixing ligatures can minimize bleeding risk from this site. A rare but disastrous intraoperative complication is that of airway fire. This occurs due to the presence of high concentrations of oxygen in the anesthetic tubing and an ignition source provided by the electrocautery unit. This can be prevented by precise communication between the surgical and the anesthetic team. If a fire occurs, the entire circuit should be removed from the patient, and the patient bagged with a mask until the tracheostomy is placed. The aerodigestive tract should then be evaluated for any potential thermal injury via laryngoscopy, bronchoscopy, and esophagoscopy. A final operative complication is that of pneumothorax or pneumomediastinum. This can occur with the inadvertent creation of a false passage if the tracheostomy tube is placed anterior to the trachea. A ruptured bleb or injury to the apex of the lung may result in a pneumothorax as well. Pneumomediastinum is generally self-limited, if the pneumothorax is a concern, a chest radiograph should be obtained postoperatively, and chest tube placed if indicated. This is also extremely rare after a routine tracheostomy, though some surgeons obtain postoperative chest X-rays on all tracheostomy patients. Early Complications Infections after tracheostomy are very rare, and those requiring antibiotics even more so. The majority of "infections" can be treated by local wound care, as they are typically just leakage of secretions from the new stoma into the field. Some deep infections or frank abscesses may require antibiotics specific for the infecting organism and are more significant in the immunocompromised patient. Acute obstruction of the tracheostomy tube may be caused by blood or mucus and is more likely in the immediate and early postoperative periods. Postoperative protocols involving scheduled flexible tracheal suctioning, use of humidified oxygen, and scheduled replacement or cleaning of the inner cannula (daily) can minimize the risk of complete obstruction. Tube dislodgement can also result in acute obstruction, where the distal tip of the tracheostomy tube exits the tracheal lumen and rests in the soft tissue or a false-passage. Placement of stay sutures in the lateral trachea during the operative procedure can facilitate tube replacement, as can skin sutures to secure the tracheostomy tube to the neck skin while the fistula matures. Reintubation can be required to re- establish a definitive airway and is best performed via flexible laryngoscopy through the tracheostomy tube to visually confirm an intra- lumenal placement. Late Complications The most dreaded late complications are associated with pressure necrosis due to over-inflation of the cuff of the tracheostomy tube. These are rarer than in the past due to advancements in low-pressure cuffs and the awareness of cuff pressure as a risk factor. Tracheostomy cuff pressure should be measured regularly to prevent this occurrence, ideally at a maximum of 20cm H2O. High pressure in the trachea can lead to necrosis of the wall due to ischemia. Subsequent healing results in scanning and stenosis. Persistent Tracheocutaneous Fistula On removal of the tracheostomy tube, the stoma will usually close within 24-48 hours spontaneously. On occasion, granulation tissue will persist at the site and can be a nuisance. This can typically be treated with topical silver nitrate. If surgical closure is required, debridement and closure in layers utilizing the strap muscles to bolster the repair will usually be successful. Tracheoesophageal Fistula Tracheoesophageal fistula is a very rare complication occurring in less than 5% of tracheostomies. They generally arise due to excessive pressure on the posterior membranous trachea (the party wall shared by the trachea and esophagus). This can be caused by over-inflation of the cuff of the tracheostomy tube. The tracheostomy tube may also be oriented posteriorly placing excessive pressure on the posterior tracheal wall, and if ventilatory pressures are higher than expected, a flexible scope should be passed via the tracheostomy tube to ensure the proper intra-lumenal orientation of the tracheostomy tube. Re-sizing or replacement with a proximal or distal XLT tube may alleviate such an issue. The presence of an indwelling nasogastric tube, in addition to the rigid tracheostomy tube, increases the risk of this complication, and alternate enteral feeding is advised (gastrostomy tube) for patients requiring tracheostomy. Patients with a tracheoesophageal fistula may present with bronchopulmonary suppuration or tracheobronchial contamination with food/gastric contents, or simply with recurrent or severe pneumonia. The length of the fistula is generally 1-4 cm and requires attention to the trachea as well as the esophagus.[7-8] Post-Tracheostomy Care Tube cuffs should be monitored to maintain pressure in the 20 to 25 mm Hg range. Humidification of gases is important as this will aid in preventing thick or dried out secretions, which are more prone to cause obstruction. The head of the bed should be elevated to minimize the risk of aspiration, and oral feeding should be initially evaluated by a speech pathologist. For the first 24 hours, the lumen should be suctioned hourly. This can be extended to every four hours until the first tracheostomy tube change at 5 to 7 days postoperatively. The skin sutures and any stay sutures are removed at this time as well. If patients are alert, awake, and cooperative, the caliber of the tracheostomy tube may be able to be downsized at this time. It is inadvisable to change the tracheostomy tube within the first five days of placement as the cutaneous-tracheal tract is immature and easily lost, which can result in loss of the airway. If tube changes are necessary during this time period, emergency equipment and adequate lighting similar- to the operating suite or, in the operating room, should be considered. Additional measures include the availability of smaller sized trach tubes, endotracheal tubes, exchange catheters, as well as possible bronchoscopic guidance. Clinical Significance A tracheostomy provides a secure, durable airway for prolonged mechanical ventilatory support in patients. It can also provide a means of the pulmonary toilet in individuals unable to clear secretions. Quality of life issues, as well as end-of-life issues, should be addressed preoperatively with the patient or surrogates before proceeding, especially in the terminally ill and elderly. Tracheostomy aerosolizes respiratory particles from the patient to a higher degree than many other surgeries, and in cases of virulent airborne pathogens (tuberculosis, COVID-19, etc.), special precautions should be taken to protect operating room staff. Tracheostomy is a safe, effective procedure that can be performed via an open or percutaneous technique. Indications include relief of airway obstruction, secretion management, and secure access for prolonged mechanical ventilation. The precise timing of tracheostomy remains controversial, but most centers proceed within 5-14 days, depending on the prognosis of the patient and the cause of initial intubation. Complications can be categorized as intraoperative, early, and late. The most devastating complication is that of a tracheoinnominate fistula. Post- operative management is best carried out by a multidisciplinary team. References 1. Alidad A, Aghaz A, Hemmati E, Jadidi H, Aghazadeh K. 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