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    B3b Section V: Voice 1 Traumatic laryngitis is usualy self-limited and is best managed conservatively with voice rest, hydration, and humidification, 1 Angioedema involving the larynx requires aggressive treatment aimed at suppressing the inflammatory response. 1 The incidence of laryngeal tuberculosis is increasing, and it should be strongly considered in patients with laryngitis and systemic symptoms, in patients who are immunosuppressed, orn patients who immigrated from endemic areas, 1 Patients with laryngitis who are immunocompromised must have close follow-up. Failure of empiric treatment requires biopsy and epproprate cultures. 1 Radiation laryngitis must be differentiated from recurrent cancer LPR radionecrosis, nd hypothyroidism, ‘The larynx possesses a complex and organized architecture of immunologically active cells with the laryngeal mucosa presenting a strong barrier of innate and acquired immunity. Is continued study should lead to further understanding of inflammatory diseases of the larynx. REFERENCES 1. Koufman JA. The otolaryngologic manifestations of gastroe- Sophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an ex perimental investigation of the role of acid and pepsin inthe de- ‘velopment of laryngeal injury. Larygoscope 1991;101(suppl 53): 1-78. 2 Berger G, Landau, Berger S, et al. The rising incidence of adult acute epiglotiis and epiglotic abscess. Am J Ot 2003;24: 374-383. ‘Nakamura H, Tanaka H, Matsuda A, etal. Acute epiglotts: a re- view of 80 patients. J Laryngol Otol 2001;115(1):31-34. 4, Mehanna H, Kuo, Chaplin J, etal. Fungal laryngitis in immuno- ‘competent patients J Laryngol Otol 2004;118:379-381. 5. Hanson JM, Spector G, ELMofty SK. Laryngeal blastomycosis: a commonly missed diagnosis. Report of two cases and review of the literature. Ann Otel Rhinol Laryngol 2000;109(3):281-286, 6. Lee KC, Schechter G. Tuberculous infections of the head and neck, Ear Nose Throat 1995;74:395-399. 7. Fajardo-Dole G, Chavolla R, Lamadrid-Bautista E, etal. Laryn- geal scleroma, J Otolaryngol 1999 Aug;28(4):229-231. 8, Postma GN. Laryngeal manifestations of AIDS. Curr Opin Oto lanygol Head Neck Surg 1997;5:112-116. 9. Langford CA, Snell MC, Hallahan CW, et al. Clinical features and therapeutic management of subglottic stenosis in patients with Wegne’s granulomatosis Arthritis Rheum 1996;39:1754-1760, to, Pribitkin E, Friedman O, O'Hara B, et al, Amyloidosis upper aerodigesive tract. Laryngoscope 2003;113:2095-2191" 11, Letko E,Zafiraks P, altatzs S, etal. Relapsing polychond clinical review. Semin Arthritis Rheum 2002 Jun:31(6) 384-390" 12, Dean CM, Sataoff RT, Hawkshaw MI, eal Laryngeal sarois J Voice 2002 Jun;16(2):283-288. . 13, Liu RM, Papsin BC, de Jong AL. Epidermolyss bullosa of head and neck: a case report of laryngotracheal involvement i, 10-year review of cases at the Hospital for Sick Children. J Qs Laryngol 1999 Apr;28(2):76-82. 14, Koufman JA, Amin MR, Panetti M. Prevalence of reflux 113 consecutive patients with laryngeal and voice disorder. 0. laryngol Head Neck Surg 2000;123:385-388. 15, Hanson DG, Kamel PL, Kahrilas PJ. Outcomes of antirefhut th, apy for the treatment of chronic laryngitis. Ant Otol Rina Lary 1995;104:550-555. 16. Koufman J, Aviv J, Casiano R, Shaw G. Laryngopharyngea refi. Position statement of the Committee on Speech, Voice and Sia) lowing Disorders of the American Academy of Otolaryngoop, Head and Neck Surgery. Otolanngol Head Neck Sug 2 July;127:32-35, 17, Postma GN, Tomek MS, Belafsky PC, et al. Esophageal mo: function in laryngopharyngeal reflux is superior to that of dase {gastroesophageal reflux disease, Ann Otol Rhinol Layngi 2001;110(12):1114-1116, 18, Johnson P, Koufman J, Nowak L, et al. Ambulatory 24-hour dow ble probe pH monitoring: the importance of manometry. Lana _goscope 2001;111:1970-1974, 19. DelGaudio JM, Waring P. Empiric esomeprazole in the weatmez cof laryngopharyngeal reflux. Laryngoscope 2003;113:598-601 20. Westcott Cj, Hopkins MB, Bach KK, et al. Fundoplication fr laryngopharyngeal reflux. J Am Coll Surg 2004;199(1):23-30. 21, Steward D, Wilson K, Kelly D, etal. Proton pump inhibitor th. apy for chronic laryngo-pharyngitis: A randomized placebo cor tuol trial. Otolaryngol Head Neck Surg 2004;13:342-350. 22. Chiu AG, Newkirk KA, Davidson Bi, et al. Angiotensin-convening ‘enzyme inhibitor-induced angioedema: a multicenter review and an algorithm for airway management. Ann Otol Rhinol Lang 2001 Sep10(9}834-640. 23, Dixon HS. Allergy and laryngeal disease. Otolaryngol Allg 199; 25:229-250. 24, Peer), Fennelly KP, Balkissoon , etl tant associated vol cord dysfinaton.j Oceup Enron Med 1998 Feb 40(2) 136-16, 25. Reidy PM, Dworkin JP, Krouse JH. Laryngeal effects of antiga stimulation challenge with perennial allergen Dermatophagoides pteronyssinus, Otolaryigol Head Neck Surg 2003 Apr/128(¢} 455-462, 26. Roland N}, Bhalla RK, Earis J. The local side effects of inhaled co ticosteroids: current understanding and review of the litertwe ‘Chest 2004 Jul;126(1):213-219. 27. Mirza N, Schwartz §, Antin-Ozerkis D. Laryngeal findings in uses of combination conicosteroid and bronchodilator therapy aye g0sepe 2004;114:1566-1569. 28, Rees LE, Ayoub O, Haveron K, etal Differential majorhisoca- patibility complex class II locus expression on human larynged epithelium. Clin Exp Immunol 2003 Dec;134(3):497-502. 29, Johnston N, Bulmer D, Gill GA, et al. Cell biology of larynged epithelial defenses in health and disease: further studies. Ann Out Rhinol Largo! 2003 Jun:112(6)481~491 Dipindai dengan CamScanner tife threatening if the larynx is involved. Etiologic agents include certain medications (particularly angiotensin. converting enzyme, or ACE, inhibitors), foods, insect bites, transfusions, and infections (22). It is not thought to be an immunoglobulin E (IgE)-mediated allergic reaction; itis puild up of bradykinin. Treatment must be aggressive supplemental oxygen, epinephrine, corticosteroids, anti- tistamines, and aminophylline are the mainstays of ther- apy; however, ACE inhibitor-related angioedema is not believed to be IgE mediated, and such patients therefore may be refractory to this therapy. If airway obstruction de- ‘elops, intubation or tracheotomy may be required, Hereditary angioedema is an autosomally dominant de- fidency of C1 esterase inhibitor that leads to recurrent at- tad of mucocutaneous edema. Diagnosis is based prima- rly on the history, although the offending agent may not be readily apparent. Patients present with rapid-onset edema that may involve the face, oral cavity, oropharynx, of larynx. Chronic pretreatment of hereditary angioedema with danazol appears to elevate levels of functional Cl esterase inhibitor and may help to prevent recurrent episodes. ‘Acute events or prophylaxis before surgical procedures are treated with C1 esterase inhibitor replacement. Allergic Laryngitis Allergy-mediated inflammation involving the larynx is a common condition, but exact prevalence is controversial. Itmay be responsible for symptoms of chronic and recur- rent dysphonia in some patients (23,24). Evaluation for allergic laryngitis begins with a careful history, noting spe- fic or chronic environmental exposures or association of symptoms with certain foods (24). Examination may reveal laryngeal edema and polypoid mucosa. Associated findings of “allergic shiners,” a supratip nasal crease, boggy nasal mucosa, or nasal polyps also may suggest an atopic etiology. The most common triggering sub- stances are insecticides, phenol, petroleum-based com- pounds, formaldehyde, and a variety of common environ- mental allergens (24). Diagnostic testing may indude a standard allergy evaluation (skin test or RAST {radioaller- gosorbent test}); challenge testing with the suspected trigger- ing agents has yielded equivocal results (25). More common causes of laryngitis, such as LPR, should be ruled out prior to Proceeding to a diagnosis of primary alesgic laryngitis. Treatment primarily involves the avcidance of the incit- ing agent and the judicious use of antihistamines, steroids, and immunotherapy. Adjunctive treatrient measures may include optimizing vocal hygiene with hydration and voice therapy to avoid pathologic compensatory behaviors. Radi Radiation therapy for laryngeal malignancies can result in a patient with dysphonia, dysphagia, pain, or globus pharyn- Beus. Examination may reveal an erythematous, swollen, tion Laryngitis Chapter 59: Laryngitis. 835 larynx with exudate and crusting Treatment involves hydration, humidification, and acid suppression, with steroids and antibiotics occasionally. The symptoms gradu- ally resolve following treatment. The differential diagnosis ‘must indude recurent cancer, LPR, radionecrosis, and hypothyroidism, Inhaled Steroids One half ofthe patients taking inhaled corticosteroids no- tice some untoward laryngeal symptoms. It is unclear why an antiinflammatory steroid preparation would cause in- flammation in the upper airway; however, the cartier sub- stance and turbulent flow may play a role. Symptoms vary between odynophagia, dysphonia, dysphagia, and globus. Laryngoscopy often reveals diffuse inflammation, leuko- plakia, candida infection, or blood vessel dilation. Symp- tomatology appears to be dose related but unaffected by the use of a spacer (26,27), IMMUNOLOGIC DEFENSES OF THE LARYNGEAL MUCOSA The larynx has historically been regarded as without im- ‘mune function. However, recent research has shown a com- plex architecture of immunologically active cells with the la- ryngeal mucosa presenting a strong bartier of innate and acquired immunity. Below a layer of mucins lie epithelial cells that express major histocompatibility complex (MHC) 1 and IL as well as nonclassical MHC. The epithelium con- tains many immune cells including cytotoxic (CD8) T cells, which are important for control of vial infections and im- munosurveillance. The lamina propria contains helper (CD4)T cells. Located on either side of the basement mem- brane are dendritic cells or antigen-presenting cells. Studies ‘of how immunologic defenses respond to insults such as re- flux, tobacco, and pathogens should lead to further under standing of inflammatory diseases of the larynx (28,25). HIGHLIGHTS 1 Laryngitis is nota synonym for hoarseness; it refers to.an inflammatory condition of the larynx, most commonly vocal fold edema, 18 An understanding that carcinoma of the larynx often presents with similar symptoms is central to the evaluation of lanngits 1 In adults, the most common causes of lay upper respiratory infection and LPR. LPR may cause dysphonia, cough, frequent throat clearing, of a globus sensation in children and adults; however, patients with reflux laryngitis often do not report having heartburn or regurgitation. is are viral Dipindai dengan CamScanner and erythema, also are seen. Although granulomas of the vocal process may be caused by vocal abuse and endotra- cheal intubation, available data indicate that LPR plays @ role in many cases ‘Ambulatory 24-hour double-probe pH monitoring is the current gold standard for the diagnosis of LPR. The distal probe i placed 5 cm above the lower esophageal sphincter (LES) junction and the proximal probe just above the upper esophageal sphincter (UES). This technique is highly sensi- tive and specific for LPR and also delineates each patient's reflux patter, allowing individualized treatment (18). ‘Treatment of LPR includes making dietary and lifestyle modifications and taking antireflux medication, such as proton pump inhibitors (PPI), histamine (H) blockers, or both. PPis are the most effective antireflux medicine avai- able. With H, blockers, treatment fails in at least one-third of patients with LPR (1). Failures on PPIs occur less com- monly and are often the result of inadequate dosing, poor compliance, or poor timing of drug administration. In some patients, itis necessary to treat with both a PP! and an Hy antagonist (16). Ofien, dosing is adjusted by per- forming ambulatory pH monitoring while the patient is taking medication (so-called drug efficacy tests). Within 2 to 3 months of treatment, most patients report significant symptomatic improvement; however, it may take 6 months cor longer for the laryngeal findings of LPR to resolve. Usu- ally symptoms improve before objective laryngeal findings ‘occur (19). Some patients may require prolonged tapering, chronic treatment, or both (16,19). Patients who do not benefit from medical antireflux therapy may require surgi- cal treatment of reflux (20) Lifestyle modifications to minimize LPR include avoid- ance of fatty meals, caffeine, alcohol, smoking, and oral take within 2 hours of lying down or bedtime; head of bed Figure 59.2 Pseudosuleus vocals variable fz ing n ptt wth ryngopharngel rf Unie ‘rue sulcus, which is located within the true vocal fis 2 “pscudosuleus" is located between the tre yo folds and the reflux induced swelling of the subglcts elevation also is indicated. Some studies have shown lifestyle modifications to improve reflux symptoms as vel as PPI therapy does (21). Traumatic Laryngitis ‘Traumatic laryngitis is commonly caused by vocal abuse but it also can result from persistent coughing, muscle tr sion dysphonia, or direct endolaryngeal injury. Such pe tients present with various degrees of dysphonia and ‘odynophonia. The mucosa of the true vocal folds is hype: ‘emic from dilated vessels on the vocal fold surface. Edema within Reinke’s space develops, and submucosal hemor rhage may occur. This form of laryngitis is self-limited and subsides within a few days when treated with voice conser vation and humidification. Thermal Injury Laryngitis as a result of thermal damage to the larynx well-recognized. Patients report dysphonia, odynophagi and odynophonia. Exposure of the larynx to steam, smoke or very hot liquids or food (particularly if microwave) leads to supraglottic edema and erythema, It is more com ‘mon in children. Laryngeal edema as a result of exposureto freebase cocaine also may present in a similar fashion ‘Treatment of such injuries is with humidification, conico steroids, and airway observation or intubation if the larynx is severely edematous. Angioedema ‘Acquired angioedema is an inflammatory reaction character ized by vascular dilation and increased vascular permeability It can be caused by a variety of substances and is potentially Dipindai dengan CamScanner gelapsing Polychondritis gelapsing polychondritis is characterized by episodes of inflammation and fibrosis with destruction of the cartilage ofthe ears, nose, larynx, and tracheobronchial tree. Laryn- al disease occurs in more than half the cases and is man- ifested by dysphonia, dysphagia, and throat pain. Airway jqvolvement leads to the high mortality seen with this dis- ‘ase. The etiology of relapsing polychondritis is unknown, put the pathogenesis seems to be an immunologic reac- sion to type Il collagen. The diagnosis is usually made on dinical findings alone, with several criteria required for di agnosis (11). Treatment for milder cases includes non- sceroidal antiinflammatory agents, dapsone, and colchicine. Corticosteroids and other immunosuppressive drugs such as methotrexate or azathioprine are required in more se- rere cases (11). Tracheotomy may be necessary. systemic Lupus Erythematosus systemic lupus erythematosus may produce laryngeal in- flammation in as many as one-third of patients. Symp- toms range from intermittent dysphonia to airway obstruc- tion, but dysphonia and dyspnea are the most common laryngeal symptoms. Examination may reveal edema (par- ticularly of the supraglottis), ulceration, or even vocal fold paralysis. Most patients readily respond to systemic corti- costeroid therapy. Sarcoidosis Sarcoidosis is a multisystem granulomatous disease of unknown etiology. The diagnosis is based on finding noncaseating granulomas and pale diffuse edema of the supraglottis and on excluding tuberculosis, Wegener gran ulomatosis, and fungal disease. Patients present with dys- phonia and varying degrees of airway obstruction. Lesions usually resolve with the use of systemic and intralesional conicosteroids. Endoscopic surgery, low-dose radiation therapy, and inhaled steroids have been used as alternative therapies (12). Tracheotomy is rarely necessary Epidermolysis Bullosa and Cicatricial Pemphigoid Epidermolysis bullosa and cicatricial pemphigoid represent autoimmune disorders manifested by mucosal blister for mation (13). Bullae or ulcerations heal by car tissue forma- tion. Involvement of the larynx is relatively uncommon but may result in dysphonia and airway obstruction. Laryngeal findings include edema, raw mucosa, bullae, ulcers, webs, and areas of stenosis in the larynx and tachea. Intubation should be avoided if possible because the larynx appears to be particularly sensitive to trauma, Patients may require a tacheotomy despite corticosteroid and immunosuppressive therapy. Stenosis may be treated by endoscopic techniques ‘once the primary disease is under control. Chapter 59: Laryngitis 833 INFLAMMATORY LARYNGITIS Laryngopharyngeal Reflux Of all the causes of noninfectious laryngitis in adults, LPR is probably the most common. It has been estimated that reflux affecs 50 million Americans and that as many as 50% of patients with laryngeal complaints have reflux as a causative or exacerbating factor (1,14). LPR may be associated with an acute, chronic, or inter- ‘mittent patter of laryngitis, LPR has been implicated in the development of vocal fold granulomas, laryngeal stenosis, recurtent laryngospasm, globus pharyngeus, cervical dys- Phagia, asthma, laryngeal carcinoma, and chronic cough (15,16). The highest reported association (92%) is with subglotic stenosis (1). Gastroenterologists consider patients with reflux who do not repor gastrointestinal symptoms to be atypical re- fluxers, but in fact they are quite typical of the patients en- countered in an otolaryngology practice. LPR is underdiag- nosed and undertreated because its signs, symptoms, and mechanisms are different from those seen in gastroenterol- ‘ogy patients, who characterstcally have heartburn, regur- gitation, and esophagitis. When compared with patients with esophagitis, patients with LPR. on aggregate, have up- right reflux, normal esophageal acid clearance, and normal esophagoscopy (17). Consequently, patients with LPR usu- ally present with symptoms of dysphonia, cough, and fre- ‘quent throat clearing but often do not report having heart- burn (Table 59.3) Examination of the laryrx may reveal a variety of find- ings. Posterior laryngitis demonstrating red arytenoids with interarytenoid mucosal hypertrophy is commonly seen with LPR. Infaglottc edema is seen frequently (Fig. 59.2). The larynx may show diffuse edema, Reinke’ edema, or mucosal thickening without significant ery- thema, which may cause ventricular effacement. Diffuse cenythema with granular, friable mucosa, and vocal process granulomas, with or without associated laryngeal edema COMPARISON OF OTOLARYNGOLOGY PATIENTS WITH LARYNGOPHARYNGEAL REFLUX (LPR) AND GASTROENTEROLOGY PATIENTS WITH GASTROESOPHAGEAL REFLUX (GER) LPR GER Respiratory symptoms Yes No Heartburn Uncommon Yes Dyzphonia Yes No Esophageal acd clearance Normal Delayed Good mucosal protection No Yes Upright efx Frequent Sometimes Supine/efx Sometimes Frequent © Dipindai dengan CamScanner al B52 Section VE volke Scleroma Scleroma is a chronic progressive infection caused by Kleb- siellarhinoscleromatis. It is endemic to North and Central Africa, Egypt, Central and South America, and Eastern Europe. It primarily involves the nasal cavity, but it may involve the laryngopharynx. The disease has three overlap- ping clinical stages. The catarrhal stage is characterized by purulent thinorthea, with nasal crusting and obstruction, followed by the granulomatous stage, in which nodular granulomas form within the upper respiratory tract. The subglotts is most commonly involved. The final, sclerotic stage is manifested as fibrosis and scar formation. Dyspho- nia and respiratory obstruction may develop during the sclerotic stage, bu this usually takes many years (7). The diagnosis is made by isolating the organism from the tissues of via immunohistochemical studies. Histologi- cally, foamy vacuolated histiocytes (Mikulicz cells) and degenerated plasma cells (Russell bodies) are seen. Treat- ‘ment is with tetracycline, fluoroquinolones, or clofaz- imine. Endoscopic laser resection and tracheotomy may be required. Immunocompromised Host Patients with immune systems compromised by acquired immunodeficiency syndrome, by immunosuppression for transplantation, or by chemotherapy or chronic cortico- steroid therapy are a risk for developing a variety of laryn- geal opportunistic infections and malignancies, including Kaposi sarcoma, non-Hodgkin lymphoma, and squamous cell carcinoma, Patients who are immunosuppressed may present with symptoms and physical findings consistent with acute or chronic laryngitis. Opportunistic infections often mimic nonspecific laryngitis and carcinoma (8). Failure to im- prove rapidly with empiric therapy should lead to early di- rect laryngoscopy and biopsy in this patient population. A high index of suspicion for laryngeal opportunistic infec- tions and malignancies must be maintained when caring for the patient who is immunocompromised. SYSTEMIC INFLAMMATORY DISEASES CAUSING LARYNGITIS Wegener Granulomatosis ‘Wegener granulomatosis is a systemic disease characterized by necrotizing granulomas with vasculitis involving the res- Piratory tract and kidneys. Laryngeal involvement (25%) is much less common than nasal involvement (90%). We- gener’s may initially resemble acute laryngitis, but it can Drogress to the eventual development of granulomatous ul- cers within the larynx. Subglottic involvement isa difficult problem to manage. Surgical treatments including mechan- ical subglottic dilation, with or without intaachel in tion af lucocortioids topical aplication of mitomyen and laser therapy have demonstrated variable succes (¢ Progression can lead to airway obstruction, requiring, cheotomy and eventual laryngotracheoplasty follows, medical treatment. Diagnosis is based on the histology, findings of necrotizing granulomas and vasculitis. The » tinuclear at toplasmic autoantibody test (ANCA) jy highly specific (90%) for Wegener granulomatosis. Meg ical treatments include cyclophosphamide, conicostei methotrexate, and azathioprine. Rheumatoid Arthritis Rheumatoid arthritis is a relatively common autoimmune disease that involves inflammation of the synovial tissu. Laryngeal involvement is reported in 25% of cases. Symp. toms are variable but include globus, hoarseness, tide, and dysphagia. Two stages of laryngeal involvement hie been described, The first is an active phase in which the Jarynxis tender and erythematous. The second is a chronic phase in which the mucosa appears relatively normal bu the cricoarytenoid joint is ankylosed, submucosal noduls may be found on the true vocal folds, or both. Sjtenic ‘treatment includes corticosteroids or other immunosp. pressive agents. Surgical excision is performed for sympio. matic theumatoid nodules. Amyloidosis Amyloidoss is an idiopathic disorder characterized by the extracellular deposition of protein leading to tissue damag, with a peak incidence in the fifth decade. It often preens with laryngeal findings but may present as a componente systemic amyloidosis (10). Clinically, the systemic type a amyloidosis can be divided into two types: primary amy dosis, when associated with an immunocyte dyscrasia uh as multiple myeloma, or secondary amyloidosis, when toc curs as a result of an underlying chronic inflammatory con dition such as rheumatoid arthritis, inflammatory bord disease, or tuberculosis or with nonimmunocyte-deiel ‘tumors such as renal cell carcinoma or Hodgkin disease lr ryngeal amyloidosis ocours as diffuse mucosal thickening, submucosal nodules, or less commonly as polypoid leon. Clinical findings at laryngoscopy are dificult to distinguish from other laryngeal lesions. The diagnosis is made by pathologic examination of tissue samples (10) Patients 2 usually asymptomatic until the deposits involve the wal folds causing dysphonia or they critically narrow the away Biopsy reveals an amorphous Congo red-staining material with characteristic apple-green birefringence by polarized light microscopy. Symptomatic cases are treated by end scopic removal of lesions. Systemic disease is evaluated wid appropriate immunoelectrophoretic studies. Lifelong low-up is important with this condition because of is chronic and recurrent nature. G& Dipindai dengan CamScanner 59.1. Histoplasmosis ofthe larynx may present UFR Teorsuperical exophyti stone wich can {rue and become painful. Diagnosis is made by the Seeplement fixation test and culture. Tuberculosis ‘berculous laryngitis is the most common granuloma- ‘bus disease of the larynx and is often associated with ac- tive pulmonary tuberculosis, although there have been an increasing number of reports of isolated laryngeal lesions presenting as nonspecific laryngitis without perichondri- ts or cavitary lung disease. Today, in developed countries tuberculosis is seen more frequently as a sequelae of HIV infection; in a nursing home environment; and in imi gation populations from endemic areas such as India, China, southeastem Europe, and sub-Saharan Africa. Pa- tients present with symptoms of dysphonia, odynophagia, dyspnea, and odynophonia. Respiratory obstruction may develop in the advanced stages of the disease. Systemic complaints of fever, night sweats, and weight loss are common. Laryngeal examination may reveal diffusely edematous and hyperemic mucosa involving the posterior third of the larynx or granular exophytic lesions, which may re- semble carcinoma. The diagnosis is made by demonstrat- ing the organisms by smear and culture. Cultures ate crit cal in guiding therapy because of increasing rates of mycobacterial drug resistance (6). If tuberculous laryngi- tis is left untreated, stenosis may develop, necessitating tracheotomy. 831 Chapter 59: Laryngitis Syphilis ‘The larynx may become involved during the later stages of syphilis, Diffuse erythematous papules, edema, and ulcers that mimic carcinoma along with cervical lymphadenopa- thy are seen during the secondary stage. These may clear spontaneously within several weeks. Gumma formation during the tertiary stage leads to fibrosis, chondritis, and stenosis. Serologic tests for syphilis are diagnostic. Peni- aillin is the treatment of choice. Leprosy Laryngitis caused by Mycobacterium leprae is rare in the United States, but it is more common in Africa and the southem portion of the Indian subcontinent. It most commonly involves the supraglottic larynx, and the pa- tient presents with a muffled voice, odynophagia, and ‘cough. Laryngoscopy reveals a nodular, edematous supra- glottis with ulceration. Diagnosis is made by biopsy, which reveals a chronic inflammatory cell infiltrate with foamy cells that contain the M. leprae bacillus. Nasal ‘smears for the intracellular organisms may be diagnostic. Long-term combination treatment with rifampin and dapsone is indicated. Tracheotomy may be required if stenosis develons & Dipindai dengan CamScanner 830 Section V: Voice Gradual or sudden onset Stidor ‘Associated upper respiratory infection or “heartburn” Duration, chronicity of symptoms Intermittent or progressive symptoms Examination Listen to voice, breathing Indirect, miro lanngoscopy Fiberopti assessment Radiographic studies Skin ests Laboratory tests Biopsy less than 24 hours or present with drooling are at higher Tisk for airway compromise requiring intervention. Med- ical treatment includes humidification, hydration, corti- costeroids, and intravenous antibiotics (2,3). Epiglottic abscess is an uncommon complication of supraglotttis, and it occurs more commonly in adults than in children. Epiglottic abscesses usually occur on the lin- gual side of the epiglottis and may be diagnosed by direct visualization or computerized tomographic evaluation. Infectious laryngitis Viral—commonly rhinovirus, paainluenca; rere cytomegelovius, human papllomavius, herpes simplex virus Bacteral—Haemophitus influenzae, streptococcus, Mycobacterium Protozoan—rare leishmaniasis crptosporiisis Systemic diseases causing laryngitis Wegener granulomatosis Rheumated arthritis ‘Anyloidesis Relapsing polyehondiitis Systemic lupus enthematosus Sarcoidosis Epidermolysis bullosa Cicatrcal pemphigoid Reactive laryngitis in adults Laryngopharyngeal refx Smoking Voice abuse Inhaled steroids Inhaled exposure—Freon, formaldehyde, solvents Angioedema Allergy Management involves immediate operative airway m agement followed by drainage. Fungal Laryngitis Fungal laryngitis, especialy in the patient who is immung, competent, is often overlooked and misdiagnosed becase it usually mimics leukoplakia both clinically and histolog, cally. The causative organism is usually candida or ley commonly blastomyces, histoplasma, aspergillus, or cx,

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