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sleep_apnea_n_stidor in otorhinolaryngology.pptx
- 1. SLEEP APNOEA &STRIDOR DR. NEERAJ RAUNIYAR MS ENT RESIDENT, 3rd YEAR GMSMA For ENT – H & N STUDIES MMC, TUTH, IOM
- 2. SLEEP PHYSIOLOGY Sleep temporary state of unconsciousness that can be interrupted by external stimuli Stages of sleep Quiet/Non rapid eye movement sleep ( non-REM) Active/Rapid eye movement sleep (REM) Non-REM sleep 4 stages Stage 1,2 EEG wave is low voltage & mixed frequency Stage 3,4 high voltage & slow frequency so caleed Slow Wave Sleep (SWS) Stage 2 account for ½ of adult sleep.
- 3. REM speep Low voltage & high frequency 2 pattern Tonic REM depressed muscle tone Phasic REM rapid eye movement & twitching of face & limbs Dream, increased autonomic activity, fluctuation in BP, pulse, RR in sleep 1st REM occur after 90 min of onset of sleep REM account 25% of sleep As sleep progresses REM increase & non-REM shortened
- 4. Reticular activatingsystem promotes wakefulness when active & promotes sleep when inactive. Neurotransmitters in sleep Amines Amino acids Peptides Melatonin released in darkness & promotes sleep
- 5. SLEEP & RESPIRATION Respiratory centre in medulla Afferent central chemoreceptor sensitive to ph Peripharal chemoreceptor sensitive to P02 Mechanoreceptor in airway, lungs & chest wall Efferent phrenic nerve, peripheral nerve, respiratory muscle In non-Rem sleep no diaphragmatic activity & increased intercostal activity In REM sleep increased diaphragmatic activity & decreased intercostal activity
- 6. Reduction ofmetabolic rate by 10-25% during sleep due to inhibition of motoe activity & decreased body temp. Upper airway muscle activity decreases during sleep with associated increase in upper airway resistance predisposing to partial upper airway obstruction Snoring low frequency sound produced by vibration of upper airway walls (esp. soft palate) during partial upper airway obstruction
- 7. SLEEP DISORDERS Respiratorysleep disorder Obstructive sleep apnoae/hypopnoae (OSAH) Central sleep apnoae/hypopnoae Cheyne- Stokrs breathing Sleep hypoventilation Non- respiratory sleep disorder Narcolepsy Periodic limb movement disorder Idiopathic hypersomnia
- 8. OBSTRUCTIVE SLEEP APNOAE/HYPOPNOAE (OSAH) Recurrent episodes of partial or complete upper airway obstruction during sleep which are usually terminated by an arousal
- 9. CAUSES Congenital Nasal obstruction b/l choanal atresia Neonatal rhinitis Congenital cyst of nasal cavity Facial skeletal abnormalities Nasopharyngeal airway obstruction Apert’s ,Crouzon’s syndrome Oropharyngeal obstruction Treacher Collins syndrome Pierre Robin syndrome Macroglossia Down’s syndrome, Beckwith syndrome, cystic hygroma Pharyngeal swelling Lingual thyroid mass Lingual thyroglossal duct Cong tumors of pharynx (teratoma, thorwald's cyst)
- 10. Acquired Traumatic Inflammatory Adenotonsillar hypertrophy Nasal polyp, rhinitis Peri/para/retropharyngeal abscess Neoplastic Angiofibroma, neuroblastoma, lymphoma Iatrogenic Post tonsillectomy adenoidectomy, PNP Pharyngeal airway dysfunction Obesity Pickwickian syndrome Chubby puffer syndrome (Stool 1997)
- 11. PATHOGENESIS Sleep decreased upperairway muscle activity upper airway collapse Stimulate increased respiratory effort hypercapnia/ hypoxaemi hypoventilation Arousal resumption of normal upper airway muscle activity relief of upper airway obstruction cycle repeats sleep resumes Correction of hypercapnia/hypoxeamia
- 12.
- 13. EPIDEMIOLOGY OF OSAH 4 % male and 2% female ( Young et al,. 1993) Approx. 5% in a given population ( Young et al,. 2002) More common & severe in male 3-7 yrs of age in children with equal in both sexes Greater in Chinese origin Risk factor for OSAH Obesity Gender ( male) Increased age Sex hormone ( progesterone increases upper airway dilating muscle activity) Individual variation in mandibular, tongue & soft palate size and position Adenotonsillar hypertrophy
- 14. Associated medicalconditions:- Cardiovascular disease HTN CAD Cerebrovascular disease Stroke Metabolic syndrome Obesity DM HTN Insulin resistance
- 15. SYMPTOMS Snoring Fatigue Witnessed breath-holds Gasping & choking Excessive daytime sleepiness (EDS) Fragmented sleep • Unrefreshing sleep • Reduced alertness • Mood changes • Nocturia • Impaired work performance • H/O DM, HTN, Hypertriglyceridaemai In children • Failure to thrive • Sweet during sleep • Unusual sleeping position • Tracheal tug • Hyperactivity Vs EDS in adult
- 16. EXAMINATION Central obesity BMI > 28 Neck circumference > 47 cm (have predictive value) Detailed nasal & oropharyngeal examination including Mallampati score Retrognathia Craniofacial abnormality Adenotonsillar hypertrophy History & examination has sensitivity & specificity of 50% only (Hoffstein et al,. 1993) EDS measured with Epworth Sleepiness Scale (ESS) ???????put scoring table
- 17. THE EPWORTH SLEEPINESSSCALE Score situation Sitting and reading Watching TV Sitting inactive in a public place (eg, theater, meeting) As a passenger in a car for an hour without break Lying down to rest in the afternoon when circumstances permit Sitting and talking to someone Sitting quietly after a lunch without alcohol In a car, while stopped for a few minutes in the traffic Normal score 2-10 Mod – severe OSA > 16 0 - Would never doze off 1 - Slight chance of dozing off 2 - Moderate chance of dozing off 3 - High chance of dozing off
- 18. INVESTIGATIONS Videondoscopy Polysomnography Sleep nasendoscopy +/- Video Oesopharyngeal manometry Cephalometry with Mueller manoeuver Fluroscopy 3D CT Dynamic ultrafast MRI Acoustic analysis Nasal spray test Can identify site of snoring
- 19. SLEEP NASENDOSCOPY- Cansite of snoring be identified? Widely used in UK Procedure-: Sleep Nasendoscopy Grading Grade Obstruction 1 Simple palatal level snoring/palatal flutter 2 Single level palatal obstruction 3 Palatal level obstruction with intermittent oropharyngeal involvement 4 Sustained multisegmental obstruction 5 Tongue base obstruction 6 Isolated epiglottic involvement
- 20. Other wayto classify level of obstruction is level 1 adenoid or valopharyngeal obstruction Level 2 tonsillar obstruction Level 3 tongue base obstruction Level 4 supraglottic obstruction Fig Findings at sleep nasendoscopy. The photographs show the endoscopic view of the obstruction at each level from 1 to 4.
- 21. Polysomnography EEG EOG EMG Overnight oximetry Domiciliary multichannel testing Apnoae complete cessation of airflow for al least 10 sec. regardless of where there is associated o2 desaturation or aurosal. In children its 6 sec duration Hypoapnoae reduction in airflow of 50 – 90%with or without =/>3% o2 desaturation &/or EEG changes OR reduction in airflow of <50% accompanied by =/>3% o2 desaturation &/or EEG changes
- 22. OVERNIGHT OXIMETRY Measureo2 saturation & pulse rate >97% SpO2 excludes hpoxia/ hpercarbia < 87% SpO2 coexistient cardiac or broncho-pulmonary disease Principle when apnoea/hypoanoae 02 saturation falls & when apnoae/hyponoae relieved o2 saturation recovered Rise & falls in 02 saturation o2 dip A dip of fall in o2 saturation of 4% significant O2 desaturation index (ODI) no. of times of o2 saturation falls by 4% averaged our per hr
- 23. A ODIof > 15/hr OSA Other features in diagnosis of OSA are ESS > 10 BMI > 28kg/m2 Co-morbidities HTN CAD DM Metabolic syndrome O2 saturation monitored with wristwatch device which pt. wear at night It’s a screening tool which has good specificity but lack sensitivity It may miss OSA who do not desaturate
- 24. HOME MULTICHANNEL TESTING Usually consist of oronasal cannulae, thoracic & abdominal band & finger oximeter probe Thoracic & abdominal band determine type of upper airway obstruction OSAH chest & abdominal band display movement Central Sleep apnoae/hypoapnoae no chest & abdominal movement Advantages- Pt. comfort Cost saving Prevention of hosp. admission Rapid analysis of data
- 25. Disadvantages- Sensorfailure Loss of signal A classic example of OSA with repetitive apnoeas. X-axis is five minutes. 1st - trace is the oronasal cannulae flow, 2nd - thoracic band, 3rd - abdominal band, 4th - trace is oxygenation and 5th - is pulse rate.
- 26. POLYSOMNOGRAPHY Gold standard Sleep state EEG EOG EMG Respiratory variables O2 saturation Oronasal airflow Chest & abd movement Tracheal microphone Oesophageal balloon manometer Non respiratory variable ECG Anterior tibialis EMG Sleeping position detector Video monitoring
- 27. Values calculated Apnea/hypoanoae index(AHI) Mild OSA = 5-20 / hour. Moderate OSA = 20-40 / hour. Severe OSA = >40 / per hour Apnea type Apnea duration Degree of O2 saturation Time spent at each level of desaturation
- 28. OVERNIGHT POLYSOMNOGRAPHY Indication- Complex OSA such as OHS Neuromuscular disorder which need ventilatory support Narcolepsy Periodic leg movement syndrome
- 29. OESOPHAGEAL MANOMETRY Usedwith sleep screening studies To diagnose apnoae/hypoapnoae Also used to evaluate relationship between reflux & OSA C) Ultrafast MRI Used in awake and asleep pt. Also used to quantify surgical tissue volume resection to achieve resolution of snoring
- 30. 3D COMPUTERIZED TOMOGRAPHTY Esp. imp to evaluate retropalatal space
- 31. CEPHALOMETRY Esp forpt. undergoing UPPP & MAS
- 32. NASAL SPAY TEST Decongestant on alternate night compare severity of snoring & apnoae treat nasal pathology Improvement in symptoms
- 33. Which testshould be used? Oximetry as 1st line screening in borderline/ uncertain cases PSG
- 34. Apnoae/hypoapnoae index(AHI) no. of apnoae/hypoapnoae averaged per hr. American Apnoae Association grading of sleep apnoae AHI Level of OSA < 5 No OSA 5-20 Mild 20-40 Moderate > 40 Severe
- 35. TREATMENT When totreat? OSA without EDS &/or co-morbidity as HTN, DM, CAD no treatment Lifestyle modification like reducing wt. particularly if BMI > 25 kg/m2 & treating any co-morbidity Mils OSA with EDS &/or co-morbidity as HTN, DM, CAD Moderate/ Severe OSA with/ without EDS & co-morbidity Treatment A) medical B) Surgical Need treatment
- 36. Medical management Exclude hypothyroidism/ acromegaly Alcohol advice Drug review Weight loss Nasal medication Nosovent Drugs Protryptyline Acetazolamide, theophylline, doxapram, buspirone, nocotine
- 37. MEDICAL TREATMENT 1.) Continuouspositive airway pressure (CPAP) Acts as pneumatic splint MOA blowing air through a tube & mask through nasal &/or oral passageway will support pharyngeal & palatal walls thus preventing collapse of airway The equipment Fixed pressure CPAP constant blowing pressure Auto CPAP vary pressure depending on presence of apnoae/hypoapnoae Predicted pressure for CPAP ( cm H2O) = (0.16 x BMI) + ( 0.13 x NC) + (0.04 x AHI) -5.12 Where NC = neck circumference Used in children who are syndromic, obese, CP
- 38. S/E ofCPAP Claustrophobia Nasal stuffiness Leaks Coryzal illness Skin abrasions Ulceration of bride of nose Air swallowing Pulmonary barotrauma
- 39. Treatment Failure Mainly due to poor tolerance to CPAP Lead to continued symptoms + risk of co-morbidity esp. cardiovascular, cerebrovascular & DM Compliance & Troubleshooting By 3 yr, 12-25% discontinued CPAP Compliance increased =/>4 hrs of using CPAP for at least 5 nights/weeks Close f/u Adequate education abt. CPAP Consequences of not treating OSA Influence long-term use of CPAP
- 40. 2.) Nasopharyngeal airway:- In new born & few days old baby Length adjusted acc. to site of obstruction e.g. in Pierre Robin sequence lies just above epiglottis In Apart Syndrome free edge of soft palate 3.) Mandibular Advancement Splint (MAS):- Not tolerate CPAP Not fit for surgery
- 41. NEW TREATMENT inspire®Upper Airway Stimulation (UAS) therapy is a new treatment option for obstructive sleep apnea patients who are unable to use Continuous Positive Airway Pressure (CPAP) Inspire is a fully implanted system that is designed to sense breathing patterns and deliver mild stimulation to a patient’s airway muscles to keep the airway open during sleep.
- 42. MULLER MANOEVER Scoring system( Sher et al 1985) Degree of pharyngeal obstruction at each level 1+ minimal collapse 2+ collapse decreasing cross section area by 50% 3+ collapse decreasing cross section area by 75% 4 + obliteration of the airway Soft palate level lower pharyng level UPPP 3+ 4+ - ideal 3+ 4+ 1+2+ suboptimal <3+ > 2+ not suitable
- 43. Indication forsurgery:- Patient with severe antisocial snoring Without OSA Localized obstruction at one level in upper airway usually at palatal level Multisegmental obstruction with predominant obs. at palatal level Patient with mild-to-moderate sleep apnoae With severe antisocial snoring Failed or inadequate response to CPAP Localized obstruction at one level in upper airway usually at palatal level Patients with moderate-to-severe sleep apnoae With severe antisocial snoring Failed or inadequate response to CPAP Multisegmental obstruction RFTVR LAUP UPPP Combination of procedure on Palate Tongue base Lateral pharyngeal walls
- 44. SURGICAL TREATMENT A)Adenotonsillectomy : Treatment of choice in children Treatment acc. To level of obstruction :- Level 1 adenoidectomy Level 2 tonsillectomy Level 3 nasopharyngeal airways, glossopexy, MAS, CPAP Level 4 LASER supraglottoplasty, anterior epiglottopexy
- 45. SURGICAL TECHNIQUE B)Uvulopalatopharyngoplasty Resection of a strip of soft palate & uvula in combination with tonsillectomy tonsillar pillar sutured together Principle to stiffen the soft palate by scarring and to increase space behind the soft palate to minimize obstruction Complication:- Severe post-op pain Haemorrage (2-14%) Airway obstruction Post-op pulmonary oedema & hypoxia(2-11%) Nasal regurgitation (13%)
- 46. valopharyngeal stenosis Dry throat Excessive pharyngeal hypersecretion (10%) Swallowing problems (9%) Voice changes (7%) Taste disturbance Short tern success rate 76-95% Long term success rate 45% (Hicklin et al,. 2000)
- 47. C) Laser-assisteduvulopalatoplasty (LAUP) OPD procedure & done under local anaesthesia Principle stiffen the soft palate and thereby minimize snoring due to palatal flutter Procedure Bilateral vertical incisions are made in the soft palate followed by partial vaporization of the uvula with a CO2 laser after giving local inj. Adv. no post-op nasal regurgitation Disadv. 1-5 procedure 1 month apart to complete treatment
- 48. Complication:- Comparativelyless than UPPP bt depend on degree of vaporization Globus type sensation Post-op pain Fungal infection Short tern success rate 79% Long term success rate 55% (Berger et al,. 2001)
- 49. D) RadiofrequencyTissue Volume Reduction (RFTVR)/ Thermal ablation Principle thermal injury to specific submucosal sites in the soft palate resulting in fibrosis of the muscular layer and volumetric tissue reduction Advantages:- Day care surgery under local Less post-op pain Less other complication
- 50. Complications:- Ulcerof tongue base & soft palate Dysphagia Temporary CN XII palsy Abscess at tongue base Short tern success rate 50-85% (Johnson et al,. 2002) Long term success rate 52% (Said et al,. 2003) Recent advances in treatment in RFTVR Somnus device Celon device bipolar electrode tip so reduced procedure time Coblater unit larger electrode tip so more complication
- 51. NASAL OBSTRUCTION ANDNASAL SURGERY IN THE PATHOGENESIS AND TREATMENT OF SNORING AND OBSTRUCTIVE SLEEP APNOEA Exact role unclear reduced nasal cross-sectional area promotes increased nasal resistance to airflow and promotes inspiratory collapse of both the oroand hypopharynx If nasal obstruction contributes to OSA development, correction of the obstructed airway should improve OSA but its not the case in most of OSA
- 52. OCCASIONAL PROCEDURES FORSNORING AND OBSTRUCTIVE SLEEP APNOEA Injection snoroplasty technique Outpatient uvulopalatal flap Palatal inplants Repose tongue base suspension suture Mandibular Advancement Surgery (MVS) Brings tongue base forwards thus increasing dimension of upper airway Adv. simplicity Reversibility Cost effectiveness
- 53. FOLLOW UP Aimto Determine compliance Minimize intolerance Improve symptoms Continue to modify cardiovascular risk factor Some centre uses repeat overnight oximetry with CPAP
- 54. CENTRAL SLEEP APNOEA Causes Ondine’s curse Altitude Cheyne-Stokes respiration Congestive heart failure Myxoedema Neurological lesions Brainstem infarct, encephalitis Bulbar poliomyelitis Supratentorial space-occupying lesions Treatment Medical therapy Theophylline Ventilation via tracheostomy Diaphragm pacing with implanted b/l phrenic nerve electrodes
- 55. STRIDOR Stridor noisy sound of high pitch generated from turbulence of airflow in larynx & trachea. Stertor low pitch snoring type of noise produced by obstruction of naso & oropharynx Characteristics of stridor Inspiratory extrathoracic obstruction from supraglottis Expiratory obstruction in thoracic trachea or primary or secondary bronchi Biphasic obstruction in glottis or subglottis or cervical trachea Bernoulli law – velocity increases, pressure decreases – collapse of airway Pascal’s principle – pressure same at every point on containing walls Type of stridor n site of origin
- 56. CAUSES OF STRIDOR Larynx Congenital 1.Laryngomalacia 2.Subglotticstenosis 3.Webs, cyst, laryngocele Inflammatory 4.Croup 5.Epiglottitis 6.Angioneurotic oedema 7.Diphtheria 8.Fungal infections 9.Tuberculosis Vocal cord paralysis 1. Nerve damage, post thyroidectomy Trauma 2. Intubation 3. Neck trauma 4. FB Neoplasam 5. Benign –subglottic hemangioma, laryngeal papilloma, lymphangioma 6. Malignant – Ca larynx Laryngospasm
- 57. Trachea & bronchi Congenital 1.Vascular anomalies 2. Webs, cysts 3. Tracheal stenosis 4. Tracheoesophageal fistula Inflammatory 5. Tracheitis 6. Bronchitis 7. Cruop FB 1.Esophageal 2.Tracheal/bronchial Neoplasm 3.Tracheal 4.Extraluminal 1.Thyroid 2.Esophageal 3.Thymus Trauma
- 58. Lesion outsiderespiratory tract Congenital: Vascular rings, oesophageal atresia, tracheo- oesophageal fistula, cystic hygroma. Inflammatory: Retropharyngeal and retro-oesophageal abscess . Traumatic: FB oesophagus (secondary tracheal compresssion) . Tumours: Masses in neck
- 59. Age of onsetPossible Aetiology Birth Vocal cord paralysis choanal atresia, laryngeal web, vascular ring 4-6 weeks Laryngomalacia 1-4 years Croup, epiglottitis, foreign body aspiration Chronicity Acute Foreign body aspiration, croup, epiglottitis, retropharyngeal abscess chronic Structural lesion laryngomalacia, laryngeal web or larynogotracheal stenosis ASSESSMENT
- 60. Precipitating Factors PossibleAetiology Worsening with straining or crying Laryngomalacia, tracheomalacia, macroglossia, micrognathi Worsening in a supine position Viral or spasmodic croup Worsening at night Viral or spasmodic croup Worsening with feeding Croup, bacterial tracheitis Antecedent upper respiratory tract infection Tracheoesophageal fistula, tracheomalacia, neurologic disorder, vascular compression Choking Foreign body aspiration, tracheoesophageal fistula
- 61. Associated symptoms PossibleAetiology Barking cough Croup Brassy cough Tracheal lesion Drooling Epiglottitis, foreign body in esophagus, retropharyngeal or peritonsillar abscess Weak cry Laryngeal anomaly or neuromuscular disorder Muffled voice Supraglottic lesion Hoarseness Croup, vocal cord paralysis Snoring Adenoidal or tonsillar hypertrophy
- 62. Past history PossibleAetiology Intubation trauma Vocal cord paralysis, larynogotracheal stenosis Birth trauma Vocal cord paralysis Birth marks Hemangioma Atopy Angioneurotic edema, spasmodic croup Family history Down syndrome Hypothyroidism
- 63. PHYSICAL EXAMINATION General PossibleAetiology Cyanosis Cardiac disorder, hypoventilation with hypoxia Fever Underlying infection Toxicity Epiglottitis Tachycardia Cardiac failure Bradycardia Hypothyroidism Quality of stridor Inspiratory Extrathoracic obstruction from supraglottis Expiratory Obstruction in thoracic trachea or primary or secondary bronchi Biphasic obstruction in glottis or subglottis or cervical trachea
- 64. Position of childPossible Aetiology Hyperextension of neck Extrinsic obstruction at or above larynx Leaning over and drooling Epiglottitis Lessening of stridor on prone Laryngomalacia, micrognathia, macroglossia Chest finding Prolonged inspiratory phase Laryngeal obstruction Prolonged expiratory phase Tracheal obstruction U/L decreases air entry Foreign body in ipsilateral bronchus Associated signs Arrhythmias, murmur, abnormal heart sound Structural heart disease Cutaneous heamangiomas Subglottic haemangioma Peripheral neuropathy Vocal cord paralysis Utricaria/ angioedema Angioneurotic oedema
- 65. INVESTIGATIONS I.) Pre-endoscopic ABGrespiratory acidosis Imaging A) plain chest x-ray Ground glass appearance bronchopulmonary dysplasia Mediastinal shift/ obstructive emphysema FB bronchus B) Videofluroscopy Young children with suspected FB Tracheomalacia C) Bronchography Tracheobronchial stenosis Tracheobronchial malacia
- 66. D) USGof vocal cord TVC palsy E) 24 hr oesophageal pH probe monitoring GERD F) PFT using flow-volume-loops To localize site of obstruction
- 67. II.) Endoscopy Confirmthe diagnosis 1) Flexible endoscopy in ward/OPD Without anaethesia Per-oral Vs transnasal Screening Miss second pathology Dynamic abnormalities like laryngomalacia, TVC palsy
- 68. 2) Laryngotracheobronchoscopy(LTB) Gold standard Team work Anesthesia iv induction intubation jet ventilation–short pulses of injected anesthetic gas laryngeal mask Maintenance of anaesthesia O2 + halothane
- 69. 3) Microlaryngotracheobronchoscopy(MLTB) With microscope/ rigid telescope Microscope (400 mm lens) +/- Hopkins rod telescopes Age appropriate bronchoscopes Laryngeal examination ET tube removed Superior view Mobility of cricoarytenoid joint assessed Post, laryngeal cleft
- 70. 4.) Bronchoscopy Ventilating bronchoscope Age-appropriate bronchoscope Main bronchi, carina, trachea & subglottis examined systemically Tracheomalacia use small bronchoscope Avoid +ve pressure to avoid splinting
- 71. 5.) Dynamicassessment of larynx on recovery from anesthesia Assess while withdrawing bronchoscope to just posterior to tip of the epiglottis Advantage:- Look cord mobility Posterior type of laryngomalacia Disadvantage Miss ant. collapse of epiglottis
Editor's Notes
- #6 Other sites of vibration tonsil, epiglottis, base of tongue
- #21 Since history n examination has poor sensitivity n specificity other tools used to diagnose OSAH
- #24 Oronasal canulae nasal or nasal air flow Thoracic/ abd. Band measure chest or abd. movenent
- #25 A classic example of OSA with repetitive apnoeas. X-axis is five minutes. The top trace is the oronasal cannulae flow, the second the thoracic band, the third the abdomi nal band, the fourth trace is oxygenation and the fifth is pulse rate. Note the marked desaturations of oxygen with each apnoea, which recovers once the apnoea has ended, and because of lag time effect, the nadir of oxygen saturation always follows the apnoea
- #27 Minisleep study
- #34 No. apnoae/hypoapnoae divided by total sleep time AHI
- #37 No significant difference betn fixed or (Sullivan et al 1981 auto CPAP
- #45 Described by Ikemastu in 1950s n popularized by Fugita in 1985
- #47 By kamami in france in 1993 Lignocaine with adrenaline is injected above the base of the uvula and 1 cm lateral to the midline in the inferior portion of the soft palate. Bilateral vertical incisions are made in the soft palate followed by partial vaporization of the uvula with a CO2 laser.
- #49 RFTVR treatment of choice now
- #59 History Perinatal history Birth laryngeal web, subglottic stenosis After 1st few weeks congenital vocal cord palsy Pattern od stridor Laryngomalacia better with siting, prone and asleep but worse with cry, feed and when distress Associated feature
- #68 Iv induction for older child, preop steroid, atopine for dry surgical field, gus for infant Intubation quickly ventilated to level so that endoscope passed without gag n maintain spontaneous resp. Jet ventilation child paralyzed, gas exchange maintained with short pulse of iv anaesthetic , s/e pneumothorax in neonates Laryngeal mask in difficult intubation n mandibular hypoplasia, also 4 fibre optic bronchoscopy
- #71 Excellent technique use fibre optic bronchoscope with laryngeal mask ventilation just above laryngeal inlet