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LARYNGITIS and chronic inflammation ppt
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- 3. ACUTE LARYNGITIS • Infections-Streptococcus pneumonia, H.influenza, Hemolytic streptococcus, S.aureus • Noninfectious- Vocal abuse, allergy, trauma, burns ( chemical /thermal) • Clinical features- abrupt onset, hoarseness of voice, Pain and vocal fatigue, fever • Laryngeal edema, erythema , interarytenoid secretion • Submucosal hemorrhage in vocal cord
- 6. MANAGEMENT • Video laryngoscopy •Flexible fiberoptic laryngoscopy • Voice rest • Smoking and alcohol cessation • Vocal hygiene • Steam inhalation • Anti tussives • Antibiotics and analgesics • Steroids
- 7. ACUTE EPIGLOTTITIS • Inflammationof the supraglottis • Life threatening • Children, H.influenza • Adults less common • Sudden in onset • Fever- High grade , toxic look • Dyspnea and stridor
- 8. • 4D’s ofepiglottitis • Dyspnea • Drooling • Dysphagia • Dyspnea • Tripod position
- 9. • Laryngeal examinationis better avoided – red swollen angry epiglottis • X-ray Soft tissue Neck lateral- Thumb sign
- 11. TREATMENT • Immediate hospitalization •Antibiotics – 3rd generation cephalosporin • Steroids • Humidification with oxygen • Intubation/ Tracheostomy
- 12. ACUTE LARYNGOTRACHEO BRONCHITIS •Etiology- Parainfluenza type I and III • Age- 6 months to 3 years • Male • Secondary bacterial infection with gram positive cocci • Edema of loose areolar tissue of subglottic area, tenacious secretion occlude the airway
- 14. • Onset isslow, non toxic • Hoarseness and croupy cough- Barking seal like • Fever low grade • Respiratory difficulties is slow in onset with intercostal and suprasternal recession • Xray neck- AP view – Steeple sign
- 17. TREATMENT • Immediate hospitalization •Antibiotics – 3rd generation cephalosporin • Steroids • Nebulisation with adrenaline • Humidification with oxygen • Intubation/ Tracheostomy
- 19. LARYNGEAL DIPHTHERIA • Secondaryto faucial diphtheria • Less than 10yrs • Infective material- nasopharyngeal secretion • IP-2 to 6 days • Portal of entry- respiratory or non respiratory • Droplet and direct • Period of infectivity-14 to 28 days from onset
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- 22. • Fever>101 • Toxemiaand tachycardia • Hoarse voice, croupy cough • Inspiratory stridor and dyspnoea leading to significant upper airway obstruction. • Membrane. Greyish white membrane is seen on the tonsil, pharynx and soft palate. It is adherent and its removal leaves a bleeding surface. Similar membrane is seen over the larynx and trachea. • Cervical lymphadenopathy.- BULL’S NECK APPEARANCE
- 27. MANAGEMENT • Isolation • Diphtheriaantitoxin -20,000 – 1,00,000 Units in I.v infusion • DOC- Benzylpenicillin and erythromycin • Intubation • Tracheostomy • Complete bed rest • Three negative cultires at 24 he intervals
- 28. COMPLICATIONS • Asphyxia ,,death • Laryngeal, palatal paralysis • Toxic myocarditis
- 29. PERTUSSIS • Bordetella pertussis •Exotoxin and endotoxin – stop cilia function and epithelial necrosis • Spread by sneezing and coughing (Droplets) • Notifiable disease • IP- 7 to 14 days • Period of communicable – 1 week after Exposure to 3 weeks after onset of cough • Cough – paroxysmal attacks with gasping and whoop • Throat swab and PCR
- 31. TREATMENT • Erythromycin 7to 14 days • Steroids • Beta 2 adrenergic • Pertussis specific immunoglobulin
- 32. INFECTIOUS MONONUCLEOSIS • EBV •Affinity to B lymphocytes , Infect epithelium of oropharynx • Transmitted through bodily secretions • Common in adolescent • IP 4 to 7 weeks • Sore throat, tonsillar enlargement, periorbital edema and edema of the lower lips- HOGALAND SIGN • Palatal petechiae, hepatomegaly, splenomegaly
- 33. MANAGEMENT • CBC, LFT,RFT • Leucocytosis (50%), atypical leukocytes (10%, >20%) • Monospot test, Paul bennell test • Positivity to monospot test first 6weeks , and repeated after 7 days • Repeated negative test-CMV, HIV, Rubella and toxoplasmosis • Fluid, analgesics and steroids • Penicillin group of antibiotics avoided as it may cause maculopapular rash
- 34. COMPLICATIONS • Airway obstructiondue to cervical lymphadenopathy • Anaemia, thrombocytopenia , encehapilitis, GBS • Pericarditis and myocarditis
- 35. OEDEMA OF LARYNX •Airway obstruction • Inspiratory stridor • IDL • Treatment • Intubation of larynx • Tracheostomy • Inj.adrenaline • Steroids
- 36. CHRONIC LARYNGITIS HYPEREMEIC HYPERTROPHIC Symmetricalinflammatory condition of whole larynx localised Acute laryngitis Chronic infection of sinus Occupational hazard Smoking Vocal abuse Same Ciliated columnar – squamous Keratinization Mucus glands dryness of larynx Hoarseness Constant hawking discomfort Males 8:1 Mucosa is thickened Vocal cords red & swollen Mobility restricted Hyperemeia of larynx Vocal cords congested Stripping of vocal cords Voice rest Remove the irritant
- 37. REINKE’S EDEMA • Bilateralsymmetrical swelling of vocal cord- membranous part • Middle aged man /woman • Edema of subepithelial space of vocal cords • Etiology • Vocal abuse, chronic smoking, chronic sinusitis& LPR • Hoarseness • Pt uses false cords for voice production, low pitched & rough voice
- 38. • IDL- fusiformswelling with pale translucent look • Ventricular bands- hyperemic, hypertrophy & obscuring the view of vocal cords • Treatment • Stripping of vocal cords in stages • Voice rest • Speech therapy
- 40. PACHYDERMIA LARYNGITIS • Posteriorpart of larynx- interarytenoid, posterior part of vocal cords • Hoarseness of voice, throat pain • IDL- red / grey granulation tissue in interarytenoid & post. 1/3 of vocal cords • Ulceration – contact ulcer • Treatment- removal of granulation tissue , LPR treatment, speech therapy
- 41. LARYNGITIS SICCA • Atrophyof laryngeal mucosa • Seen in woman esp- atrophic rhinitis • Dry irritation & cough • Crust formation • Treatment- humidification • Laryngeal sprays with glycerine – crust removal
- 42. TB LARYNX • Secondaryto pulmonary TB • Haematogenous/ bronchogenic spread • Posterior part of larynx – esp interarytenoid region • Pseudoedema • Voice fatigue, voice change & dysphagia • Mouse bitten vocal cord • Turban epiglottis • Mammilated appearance of interarytenoid region
- 44. • Vocal cordpalsy • Investigation- sputum, videolaryngoscopy, chest xray • Treatment
- 45. JRP • Common benignlesion in children • HPV 6,11 • Infected from mother with vaginal HPV • Usually supraglottis & glottis • 3- 5yrs • Hoarseness, respiratory distress/ stridor • Flexible fibreoptic laryngoscopy • Care need to be taken if child has tracheostomy
- 47. • Co2 LASER •Interferon alpha • 13 cis retinoic acid
- 48. FB IN AIRWAY •Non irritating type • Irritating type- vegetable/ nuts- edema • Choking • Symptomless period • Laryngeal- obstruction - death
- 49. LOCATION •In decreasingorder Offrequency, 1.Bronchus (right> left) 2.Trachea 3.Larynx 4.lungs
- 50. • Tracheal- cough,hemoptysis, wheeze, audible slap • Bronchial
- 51. DELAYED PRESENTATION •Common inchildren •Maybe treated as asthma due to low grade cough and noisy breathing •Delay in diagnosis- granulation tissue formation, pneumonitis, bronchiectasis, lung abscess
- 52. • Chest xray •Xray neck ap/ lateral view • Fluroscopy • CT chest • Hemlich • Cricothyrotomy • Tracheostomy • Direct laryngoscopy • Bronchoscopy
- 53. RIGID BRONCHOSCOPY •Mainstay oftreatment •done under general anaesthesia •Position: barking dog position •Technique: direct method, through laryngoscope •Limitations: supraglottic area is difficult to evaluate can reach only up to segmental bronchi •Technically difficult •On prolonged procedure it causes Subglottic edema