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Laryngeal infections
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- 2. INTRODUCTION • Laryngitis isone of the most common conditions identified in the larynx. Laryngitis, an inflammation of the larynx, manifests in both acute and chronic forms. • Acute laryngitis has an abrupt onset and is usually self-limited. If a patient has symptoms of laryngitis for more than 3 weeks, the condition is classified as chronic laryngitis.
- 3. The etiology ofacute laryngitis includes vocal misuse, exposure to noxious agents, or infectious agents leading to upper respiratory tract infections. The infectious agents are most often viral but sometimes bacterial.
- 6. INFECTIOUS: Viral Bacterial NON INFECTIOUS Inhaled fumes Allergy Pollutedatmospheric conditions Vocal abuse Iatrogenic trauma Gastroesophageal reflux disease (GERD) AETIOLOGY
- 7. Pathophysiology 1.The mucosa ofthe larynx becomes congested and may become oedematous. 2.A fibrinous exudate may occur on the surface. 3.Sometimes infection involves the perichondrium of laryngeal cartilages producing perichondritiis.
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- 9. CLINICAL PRESENTATION •Change orloss of voice; • Difficulty in breathing/stridor; • Sore throat and otalgia; • Difficult or painful swallow; • Tender larynx with/without cervical lymphadenopathy.
- 10. Acute Laryngeal infectionsin childhood • Acute Epiglottitis • Laryngotrachealbronchitis • Bacterial Laryngotrachealbronchitis • Diphtheria • Conditions which mimic laryngeal infections
- 11. Acute Epiglottitis • Mostfrightening pediatric emergency. • If unrecognized it can lead to death of the child. • 6-23 per 100,000 in chlidren. • Haemophilus influenzae type B , is the causative organism in most cases. • The disease is concentrated maximally on the epiglottis but the inflammation may involve whole supraglottic compartment. • Most cases seen between 1 and 6 years of
- 12. Clinical features • Classicalfeatures: – A child c/o sore throat which intensifies, with in half and hour dysphagia reported. – Inspiratory stridor develops and within 2 hours child becomes critical. – Child sits up and leans forward – Saliva is dribbling due to absolute dysphagia – Voice is muffled – As time goes child becomes quiet and respiratory distress appears to lessen. – An an ominous sign: respiratory & cardiac arrest imminent
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- 15. Investigations • Blood culture •Throat awab culture • WBC counts • X ray plain lateral soft tissue neck. • Computed tomography (CT) scans are useful if there is a complication such as an epiglottic abscess
- 16. Lateral X-ray ofneck may show classical ‘thumb’ sign of swollen epiglottis www.learningradiology.com/archives04/COW%2010 ...
- 17. Management • It isa surgical emergency • Admit and observe give i.v. antibiotics and 100% humidified oxygen. • Examination of throat by tongue depressor is particularly dangerous- sudden respiratory obstruction may occur. • If the clinical situation suggests that the diagnosis is epiglottitis , there is no point in confirming it what might turn out to be fatal X-ray.
- 18. • The childis shifted to OT and anesthetized in upright position • Laryngoscope inserted & diagnosis confirmed • An appropriate size orotracheal tube inserted • Otherwise rigid bronchoscope used to secure airway • Tracheostomy / nasotracheal tube • Culture swabs taken from epiglottis • Nasogastric tube inserted for feeding
- 19. Best Clinical Practice •Adults with suspected acute epiglottitis should be admitted and airway closely monitored • Patients should be treated with I/V second- or third-generation cephalosporins and 100% humidified oxygen • Airway obstruction should be treated early, ideally by intubation
- 20. Complications 1.Epiglottic abscess 2.Pulmonary oedemasecondary to relieving airway obstruction 3.Thrombosis of internal jugular vein
- 21. Laryngotracheobronchitis (Croup) • As namesuggests it involves larger proportion of respiratory tract • Area of maximum impact is sub-glottis • An acute illness with hoarseness, a barking cough, stridor and varying degree of respiratory distress • Affects young children (6 months to 3 years)
- 22. • In mostcases causative organism is paramyxovirus, para-infleunza virus type I and type II • In adults it may also occur from herpes simplex, cytomegalovirus & influenza virus • Adult croup is rare, more severe & impaired immunity should always be considered • The key feature is sub-glottic oedema
- 23. Investigations • Direct viralantigen detection by sampling mucus from nasopharynx • A plain neck radiograph may show narrowing of the subglottis (steeple sign) and ballooning of hypopharynx • Chest X-ray to exclude collapsed lobes or meditational shift
- 24. • Narrowing ofthe subglottis (steeple sign)
- 27. Management • Oxygen, steroidsand nebulized epinephrine should be administered • Monitor airway and oxygen saturation, consider endotracheal intubation if necessary • Broad spectrum antibiotics to cover secondary infection • No evidence to support antiviral agents
- 28. Best Clinical Practice •Adult croup is rare but rapidly progressive • Once suspected patient should be admitted • Larynx inspected by flexible laryngoscope • Broad-spectrum ABx to prevent bacterial infection • If the airway deteriorates patient should be intubated and ventilated
- 29. Bacterial Laryngotrachealbronchitis • May bea separate disease or be caused by secondary bacterial infection of viral laryngotrachealbronchitis • Also called bacterial tracheitis since it involves trachea predominantly • Much more severe illness and much less common • More severe respiratory obstruction and artificial airway is often needed • Tracheostomy preferred over intubation
- 30. Whooping cough orPertussis 1.an acute illness that is usually caused by Bordetella pertussis. It is a notifiable communicable disease that affects all age groups and is transmitted by coughing and sneezing. 3.Most severe in children, particularly infants. Adults generally have a milder disease. Clinical features •Runny nose, •dry cough and mild pyrexia, • similar to a common cold
- 31. •The cough occursin prolonged paroxysms after one to two weeks and is followed by gasping and the characteristic whoop in children. •The disease is generally milder in adults and presents as protracted cough rather than the characteristic 'whooping cough' of children. Investigations confirmed by serum serology and nasopharyngeal aspirate culture and assay by (PCR).
- 32. M anagement•Pertussis isusually not diagnosed until the cough has developed. •A 7-14-day course of erythromycin is recommended. •Fluoroquinolones are also likely to be effective in adults. The cough should be treated symptomatically with cough suppressants.
- 33. Diphtheria • Caused byCorynebacterium diphtheriae • Spreads by droplet infection • Affects non-immunised children and susceptible adults particularly elderly • Usual site of infection is the tonsils and fauces but it can also occur in nasal cavities or spread to larynx
- 35. Clinical Features • Severesore throat, malaise, pyrexia • Examination of throat shows characteristic grey membrane in oropharynx which may spread to larynx. • Enlarged tender cervical lymph nodes
- 36. Investigations • A swabfrom throat for C/S • A sample of grey membrane for screening
- 37. Management • Treat withbenzyl penicillin and antitoxin • Acute obstruction should be managed with intubation • Complications: – The diffusible exotoxin has predilection for cardiac and renal tissues – Neurological complications soft palate paralysis, diaphragm & EOM
- 38. Conditions which mimiclaryngeal infections in childhood • Foreign bodies • Peritonsillar abscess • Retropharyngeal Abscess • Infectious mononucleosis
- 39. Infectious mononucleosis • Acommon disease often sub-clinical or mild • Caused by Epstein-Barr virus • Spread is usually transfer of infected saliva during kissing
- 40. Clinical Features • Acutesore throat with large infected tonsils • Cervical lymphadenopathy with grossly enlarged bilateral lymph nodes • Fever, Malaise • There may also be palatal petechiae, oral ulceration, splenomegaly and hepatomegaly
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- 43. Investigations • Full Bloodcount • Heterophil antibody test: Heterophil antibodies are antibodies that are stimulated by one antigen and react with an entirely unrelated surface antigen present on cells from different mammalian species • Specific EBV serology • HIV testing
- 44. Management • I/V fluids •Analgesia • In serious infections antibiotics, steroids and acyclovir should be considered • Ampicillin / amoxycillin are best avoided for fear of inducing a maculopapular rash
- 45. Complications • Gross swellingof tonsils and adenoids causes airway obstruction, but inflammation and ulceration can also extend to larynx • The severity of laryngeal involvement may be masked by upper airway obstruction • Splenic rupture • CNS complications like encephalitis, meningitis, CN palsies • Immune deficiency and HIV status be
- 46. MYCOTIC LARYNGITIS • Diseaseof both immunocompromised and immunocompetent hosts • May mimick leukoplakia or malignancy – White or gray pseudomembrane on mucosa – Mucosal erythema and edema (focal or diffuse) surrounding white plaques – Mucosal ulcerations – Contact bleeding
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- 48. Risk factors •Risk factors:LPR, smoking, inhaled steroids, prolonged antibiotic use, XRT •DM, immunosuppressants, CA, nutritional deficits •Compromise mucosal barrier
- 49. Investigation 1.A chest radiograph. 2.Directlaryngoscopy and biopsy may be necessary to confirm a diagnosis of fungal laryngitis. 3.Tissue samples should be sent for special fungal stains, such as methenamine silver and periodic acid-schiff, to identify the fungal hyphae.
- 50. Treatment of fungal laryngitis 1.Fluconazole x 3wks 2. Nystatin swish and swallow (100,000 units/ml, 10ml tid). 3. Prevention spacers for inhaled steroids oral rinse, gargle with water after use.
- 51. Chronic Laryngitis Is achronic inflammation of the mucosa of the larynx Definition Grade I Mild erythema, stasis of secretions, string sign, piling u p of i nter-arytenoid mucosa Grade II Diffuse oedema a nd mucosal thickening, but with little erythema Grade III Diffuse erythema, with granular friable mucosa or Ulceration Grade IV Discrete granuloma(s) with or without oedema and erythema
- 52. Etiology • Follows repeatedacute attacks but usually it arise insidiously due to : • Faulty use of voice. • Infection of teeth, tonsil, sinus, and lower respiratory tract infection. • Excessive alcohol consumption or smoking. • Dust or irritant fumes.
- 53. Clinical classification: Chronic nonspecificlaryngitis 1. Chronic simple laryngitis. 2. Hyper keratosis of larynx (chronic keratosis or leukoplakia). 3. Pachydermia laryngis. 4. Contact granuloma. 5. Atrophic laryngitis. Chronic specific laryngitis • Tuberculous laryngitis • Syphilitic laryngitis. • Leprosy of the larynx. • Scleroma of the larynx. • Wegener’s (malignant) granuloma of the larynx. • Mycosis of the larynx.
- 54. Simple chronic laryngitis Pathology: •Hyperaemiaof vocal cord. •Edema. •Myositis occurs in the intrinsic muscles. •Excessive secretion due to hyper activity of the mucous gland. •Hyperaemic and edematous stage often passes to a hypertrophic one and rarely to an atrophic one. Clinical Features: -Hoarseness (intermittent then persistent). -Cough (slightly dry). -Sore throat (very common).
- 55. Chronic laryngitis: thereis hyperemia of mucus membrane. Odema of the margins of the vocal cord(Rienkes edema
- 56. Laryngeal appearance Three types: 1.Hyperaemic. 2. Hypertrophic. 3. Edematous. In all types the larynx is always affected bilaterally & symmetrically.
- 57. Treatment: •Vocal rest •Elimination ofirritating factors such as dust and smoking. •Systemic antibiotics. •Carbocisteine ( a mucolytic ) when secretion are thick. •Stripping of the vocal cords is performed endoscopically in persistent cases.
- 58. REINKE'S OEDEMA 1. Polypoidcorditis 2. Proliferation of superficial lamina propria chronic irritant exposure Smoke, LPR, occupational exposures 3.Water-balloon outpouching from membranous VF 4. characterized by oedema of the vocal cords.
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- 60. •Surgery 1. Airway compromise 2.Preserve some superficial lamina propria and overlying epithelium to preserve mucosal wave •Stage for bilateral disease to prevent anterior web •Remove irritants and treat LPR Treatment
- 61. Vocal cord polyp •Polypoidallesion of cords •More in male •localised vascular engorgement and microhaemorrhage followed by oedema. •Gelatinous,fibrous,talengiectatic
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- 63. Effect of polypson mucosal waveAsymmetric mass produces more chaotic vibrations and aperiodic mucosal waves Larger polyps cause decreased wave amplitude Excessive air egress during phonation Fatigue Frequent voice breaks decreased vocal power
- 64. Treatment •Conservative for smallpolyps •Microsurgery mainstay of therapy •Hemorrhagic polyps Pulsed-dye lasers absorbed by hemoglobin (585 nm) Lasers more effective for smaller polyps.
- 65. Tuberculous laryngitis •Almost alwaysto secondary to pulmonary TB •Infected sputum •Younger age group •Tubercle formation is characteristic •Infilteration stage followed by proliferative stage •Posterior part of larynx involved
- 66. The typical siteand appearance of tuberculous lesion involving the posterior commissure in secondary-acquired tuberculous laryngitis.
- 67. To improve vocalhygiene • Drinking lot of fluids - Drink 7-9 glasses of water per day; also good are herbal tea and chicken soup. • maintaining good general health - Exercise regularly. • Avoiding smoking - They are bad for the heart, lungs and vocal tract. • Eating a balanced diet - Include vegetables, fruits and whole grain foods. • Avoid dry, artificial interior climates. • Do not eat late at night - may have problems when stomach acid backs up on the vocal cords. • Use a humidifier to assist with hydration.
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Editor's Notes
- #23 The inflammatory response and migration of dendritic cells, neutrophils and lymphocytes is much greater in the subglottis compared to the glottis