ENT Paediatric

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Kianoosh
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146347
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ENT Paediatric
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2012-07-13 01:52:14
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ENT ORL otorhinolaryngology paediatric Kian Kianoosh Nahid
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ENT flashcards for paediatric ENT Disclaimer: These flashcards are designed to help ENT residents/master's student in their preparations for final exams. The sources are different textbooks, lecture notes, and pictures uploaded in internet. Please send suggestions/feedbacks to dr.kian@ymail.com
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  1. The causes of acute epiglottitis?




    Causes of parapharyngeal abscess?
    infection from tonsil or peritonsillar abscess, or suppuration of local lymph nodes.








    Causes of paediatric airway obstruction?
    Congenital:
    -laryngomalacia
    -glottic web
    -hemangioma
    -vascular ring
    -hypoplastic mandible
    Infectious:
    -Tracheitis (Staph, H.influ, Strep.P, MC)
    -Croup: Para Influ 1,3, RSV
    -Acute epiglotitis: H.Influ Type B
    -Diphteria
    -ATH 
    Syndromes:
    -Robin
    -Treacher Collin
    -Goldenhar
    -Nager 
    Trauma
    FB




    Indication for pediatric tracheostomy?
    airway abnormality
    airway neoplasm
    airway infection/inflammation (rare)
    Prolonged ventilation >50days
    VC paralysis
    subglottic stenosis




    Size of ETT?
    Preterm 2.5-3
    Term to 6 m: 3-3.5
    6m to1y: 3.5-4
    1-2y: 4-4.5
    >2: (age+16)/4





    PHACE's syn?
     
    • Posterior cranium deformity
    • Hemangioma >5cm
    • Arterial lesions
    • Cardiac abnormality
    • Eye abnormality
  2. Padiatric laryngospasm
    Definition?
    types?
    risk factors?
    Incidence?
    • reflex closure of upper airway as a result of glottic spasm
    • partial/complete
    • infant (flexible chest, high vagal tone)/URTI/Passive smoking/ asthma/viral(RSV) 
    • 21% intraoperative/13% postoperative
  3. Rathke's pouch?
    a dimple above adenoid, remniscent of buccal mucosa invagination to form the anterior lobe of pituitary gland
  4. Snius of morgagni?
    • between skull base and s.constrictor m.
    • ET, LVT, TVP, and ascending palatine a. pass through it
  5. Passavant's ridge?
    soft palate touches it during swallowing or speech
  6. The most common benign neoplasm seen by ENT?
    rate in children/ adults?
    cause?
    types?
    Tx?
    • RRP
    • 4.3 and 1.8 in 100000
    • HPV 6,11, (16,18 risk of malignancy, 3-5% totally)
    • Cesarian does not reduce the risk
    • types: Juvenile(always 6,11, in 2-4y, may regress on puberty)/adult (solitary, more of carpet variant)
    • TX: 
    • surgery: CO2 laser, micrdebrider, cold instrument
    • other: Cidofovir, vaccin, interferon
    • H-influ type B
    • Group A strep
    • strep pneumoniae
    • Staph aureus
    • Klebsiella Pneumoniae
  7. Treatment for acute epiglottitis?
    • Treatment should be with intravenous antibiotics and 100 percent humidified oxygen. The antibiotics of choiceare second- and third-generation cephalosporins. Ampicillinwas often prescribed but resistant H. influenzae arenow emerging.
    • Airway support: intubation, KIV tracheostomy
  8. what is LARYNGOTRACHEOBRONCHITIS or CROUP?
    • an acute illness with hoarseness, a barking cough, stridor and varying degrees of airway distress. Croup affects mainly young children, aged 6 monthsto 3 years, in which subglottic oedema leads to early respiratory distress and biphasic stridor.
    • Cause: Viral: paramyxoviruses, para-influenza virus type I and type II
  9. What is the cause of whooping cough or Pertussis?
    Symptoms?
    Bordetelia pertussis

    symptoms of a runny nose, dry cough and mild pyrexia, similar to a common cold. The cough occurs in prolonged paroxysms after one to two weeks and is followed by gasping and the characteristic whoop in children.
  10. Clinical features of Infectious mononucleosis?
    • The characteristic features include an acute sore throat with large red infected tonsils, cervical lymphadenopathy with grossly enlarged bilateral lymph nodes, pyrexia and general malaise. There may also be palatal petechiae, oral ulceration, splenomegaly and hepatomegaly.
  11. What should be avoided in treatment of infectious mononucleosis? why?
    • Ampicillin, amoxicillin
    • maculopapular rash
  12. General ENT problems in Down syndrome?
    • Frequent upper respiratory tract infections (URTI)
    • Thyroid disease
    • Sialorrhoea
    • Atlantoaxial instability (manipulate the head with extreme care under anaesthesia)
  13. Airway problems in Down syn?
    • Airway obstruction
    • Narrow subglottis and trachea - may need smaller endotracheal tube during anaesthesia
    • Midfacial hypoplasia - increased incidence of obstructive sleep apnoea syndrome (OSAS)
    • Hypotonic pharyngeal airway
    • Macroglossia
  14. Ear disorders in Down syn?
    • Deafness
    • Frequent acute otitis media and otitis media with effusion
    • Small pinna and external meatus
    • Premature ossification of the cochlea
    • Facial nerve dehiscence common
    • Ossicular fixation
    • Mondini malformation more common
  15. Kernahan-Stark classification of cleft lip-cleft palate?
    (a) GroupA, incompleteunilateral cleft of primary palate; (b) group B.complete unilateral cleft of primarypalate;(c) group C, complete bilateral cleft of primarypalate; (d) group D. incomplete midline cleft of secondary palate; (e)group E,complete midline cleft of primaryand secondary palates; (f) groupF.complete unilateral cleft of primary and secondary palates; (g) group G, complete bilateral clefts of primary and secondary palates;(h) group H, cleft of primary palate and incomplete cleft of secondary palate.
  16. Types of oesophagyeal atresia?
    (a) Oesophageal atresia with distal trachaeooesophageal fistula, 87 percent; (b)oesophageal atresia without distal trachaeo-oesophageal fistula, 6-7 percent; (c) oesophageal atresia with proximal trachaeo-oesophageal fistula, 2 percent; (d) oesophageal atresia with proximal and distal trachaeooesophageal fistula, < 1 percent, (e) trachaeooesophageal fistula without oesophageal atresia,3-4 percent.
  17. Name the parts:
    BM. basilar membrane; IS, inner sulcus; DC, organ of Corti; OS, outer sulcus; RM, Reissner'smembrane; ScM, scala media; SeT,scala tympani; ScV, scala vestibuli; SP, spiral prominence; SV, stria vascularis; TM, tectorial membrane; TZ, transitional zone. Yellow areas show bone.
  18. Hearing tests in children based on their age?
    • 0-6m:
    • -Electrophysiologic tests (OAE, ABR)
    • -Behavioral observation audiometry (BOA)
    • 6-12m:
    • -Distraction test
    • 6m-3y:
    • -Visual reinforcement audiometry (VRA)
    • 2-5y:
    • -Performance testing
    • 3y onwards:
    • -PTAauditory speech discrimination tests
    • 18-30m:
    • -The co-operative test (normal child can discriminate instruction at 35-40dB)
    • 30m onwards:
    • -Toy discrimination tests
    • 6 years onwards:
    • -Consonant discrimination tests
  19. What is permanent childhood hearing impairment (PCHI), and how common is it?
    • confirmed permanent bilateral hearing impairment exceeding 40dBHL (hearing level) (average of pure tone thresholds at 0.5, I, 2 and 4 kHz in the better hearing ear).
    • 1/1000 born
  20. Congenital Causes of permanent childhood hearing impairment (PCHI):
    • Genetic:
    • -Syndromic
    • -nonsyndromic (LVA the commonets)
    • Nongenetic:
    • -Congenital rubella
    • -CMV
    • -Congenital syphilis
  21. Environmental causes of permanent childhood hearing impairment (PCHI):
    • Perinatal:
    • -Hypoxia
    • -Hyperbilirubinemia
    • -LBW
    • Aquired:
    • -Infections: CSOM, Meningitis, Mumps, Measles, AIDS
    • -ototoxicity
    • -Trauma
    • - Neoplasm
  22. What are the main statistics regarding congenital hearing loss?
    • Genetic factors: 50% of cases
    • AR: 77% (mostly prelingual)
    • AD: 22% (mostly postlingual)
    • x-linked: 1%
    • 30% syndromic: Pendred, Branchio-oto-renal, Usher, Wardenburg
  23. what is the relationship between increased risk for hearing loss and being admitted in NICU?
    more than 48 h: 10 times more chance of hearing loss
  24. Investigations of a deaf child?
    • History
    • Family history
    • Clinical examination
    • Audiology in patient and first degree relatives
    • Imaging (MRI, CT temporal bone)
    • ECG
    • blood, RF, UFEME, seorlogic tests for rubella, CMV
    • Thyroid tests
    • connexin 26 and 30 and other genetical councelling and chromosomal analysis
    • Ophtalmic assessment
    • Vestibular investigations
  25. What could be found in CT scan of a deaf child?
    • On CT scans, a large vestibular aqueduct is the most common isolated finding, while cochlear dysplasia is the most common abnormality in scans showing multiple abnormalities.
    • Other abnormal findings include lateral semicircular canal dysplasia, otic capsular lucency, small internal auditory canals and hypoplastic cochlea.
  26. Why universal neonatal screening can only detect 50% of CMV related SNHL?
    As it is largely a progressive HL, and if the sampling is done after 3 weeks of being born, it could be due to acquired infection.
  27. What syndrome is related to Large vestibular aqueduct (LVA)?
    Pendred syn
  28. The main nonsyndromic congenital causes of hearing loss?
    • Large vestibular Aqueduct
    • DFNB1 (50% of AR types of it)
  29. The main causes of CHL in children?
    Conductive hearing loss in children is usually acquired. The most common aetiology is otitis media with effusion (OME) but it may be the result of chronic otitis media (mucosal or squamous). In the presence of severe congenital deformity of the external ear, associated abnormalities of the ossicular chain are common but in isolation they are rare and often have a delayed diagnosis, particularly if unilateral.
  30. How is Congenital ossicular fixation and defect defined?
    a malformation affecting the ossicular chain, present at birth, which leads to a dysfunction of the ossicular mechanism due to immobility or discontinuity of the ossicular chain.
  31. What are the congenital middle ear ossicular malformations?
    • isolated stapes ankylosis,
    • ankylosis with other ossicular anomaly,
    • isolated ossicular anomaly,
    • aplasia or severe dysplasia of the oval or round windows.
  32. The main symptoms of cholestrol granuloma of petrous apex?
    tinnitus, vertigo, and facial twitching
  33. Differential diagnosis of petrous apex lesion?
    congenital entities (asymmetric fatty marrow, cholesteatoma), infection (apical petrositis),benign obstructive processes (effusion, mucocele,cholesterol granuloma), benign tumor (meningioma,schwannoma), malignant tumor (chordoma, chondrosarcoma, osteosarcoma, plasmacytoma, metastasis),and miscellaneous lesions (histiocytosis X, Paget disease, fibrous dysplasia, petrous carotid artery aneurysm, meningocele/encephalocele)
  34. Describe the MRI:
    MRI demonstrating abnormal lesion of the right petrous apex. a- The lesion had a homogenous hyperintensity on T1- weighted image b- and heterogenous hypointensity on T2- weighted image. Compressions of cranial nerves V, VII, and VIII were also evident.
  35. Cremers' classification of minor congenital anomalies of the ossicular chain?
    • Isolated congenital stapes ankylosis (or fixation)
    • Stapes ankylosis associated with another congenital ossicular chain anomaly
    • Congenital anomaly of the ossicular chain but mobile stapes footplate (commonest)
    • Congenital aplasia or severe dysplasia of the oval or round window.
  36. Clinical presentation of children with congenital ossicular abnormalities?
    Children with bilateral ossicular abnormalities will often present at a similar age to children with OME because of poor hearing performance and speech delay. It is not unusual that the children are managed with one or more sets of ventilation tubes before the diagnosis is made. The observation of a conductive hearing loss, normal tympanic membrane and normal middle ear pressures should lead to the general diagnosis.
  37. Investigation results in congenital ossicular anomalies?
    • average threshold of approximately 50 dB,producing a flat air conduction line, with no low frequency bias as with otitis media. There is an average air-bone gap of 35 dB between 0.5 and 2 kHz (Carhart notch). Tympanometry usually demonstrates a normal middle ear pressure with reduced compliance due to fixation of the ossicular chain. (As)
    • CT may be useful.
    • endoscopy through ET
    • direct vision through endaural approach
  38. Treatment options for congenital ossicular malformation?
    • Air conducted hearing aid (ACHA)
    • middle ear surgery by deidacted otologist
  39. Why the stapedectomy/stapedotomy is abandoned if the persistant stapedial artery is found intraop?
    Traditional teaching has been that the presence of the artery is an absolute contraindication to stapedectomy, due ot its bleeding if injured, and partly as it was thought that damage to the artery would lead to ischaemic damage to the facial nerve.
  40. paediatric congenital middle ear deformities?
    • congenital ossicular malformations
    • persistant stapedial artery
    • aomalous facial nerve course or dehiscence
    • Congenital perilymph fistula
    • High jugular bulb (reaching bony annulus)
    • Aberrant ICA (DD of glomus tympanicum)
  41. Types of malformous course of facial nerve in middle ear?
    • facial nerve partially obliterates the stapesfootplate
    • bifurcation of the facial nerve
    • facial nerve rests on the footplate with deformed stapes or oval window
    • facial nerve rests on the promontory
  42. Where is the fluid in OME come from?
    OME is primarily caused by an inflammation of the goblet cells of respiratory epithelium in the Eustachian tube and hypotympanum, preceded by an episode of acute otitis media with otalgia and fever.
  43. Does middle ear effusion contain bacteriae?
    • mostly there in no growth after culturing the middle ear fluid which has been present for more than 6 months. Otherwise, these bacteriae may be found:
    • Streptococcus pneumoniae, Haemaphilus influenzae, Branhamella cotarrhalis, Streptacaccus pyogenes
  44. Percipitating factors for OME?
    • Cleft palate: 40% incidence
    • GERD?
    • AOM, or previous AOM
    • more siblings
    • history of OME in family
    • Down's syn
    • Allergy, sex, parental smoking is not a factor
  45. Peak age of OME?
    • First year of age
    • 20%: 2 years
    • 16%: 5 years
  46. Peak incidence of OME in a year?
    Winters twice summers (but not in Malaysia!)
  47. Methods of detecting OME?
    • otoscopy
    • pneumatic otoscopy
    • Tympanometry (the most common reference test)
    • Aspiration of fluid during M&G or otologic surgery
    • PTA?
  48. What is the outcome of OME?
    Majority of identified cases resolve in 9 months, although it may recur.
  49. Treatment options for OME?
    • Autoinflation in bigger childern
    • medical therapy (antihistamine)
    • M&G (>3years, bilateral 25dB HL over a 12-week-period)
    • Adenoidectomy
    • Hearing aid (Bone conducted)
    • No role for steroid nasal spray
    • Antibiotics maybe useful, only for a short term
  50. What are the complications of OME?
    • attic retractions
    • Pars tensa retraction
    • tympanosclerosis (risk icreased by M&G)
    • atrophy of pars tensa (risk icreased by M&G)
    • Persistant CHL even after resolution of OME
    • Language development problems
    • cognitive/intellectual flaws
    • Behavioral changes more common than normal children
    • imbalance (30%)
  51. Should M&G patients avoid swimming?
    There is no reason to advise against getting water in the ear in children who are fitted with ventilation tubes.
  52. Definition of AOM?
    acute infection of middle ear cleft with effusion, TM intact.
  53. Subytpes of AOM?
    • Sporadic
    • Persistant: >3-5 days taking A/B
    • Resistant: Within 6 days after finishing A/B
    • Recurrent : >3 times in 6 months
  54. Infective agents of AOM?
    • Viral 60-90%
    • respiratory syncytial virus (RSV);
    • influenza A virus;
    • parainfluenza viruses;
    • human rhinovirus;
    • adenoviruses.
    • Bacteriae:
    • H influ,
    • Moraxella C
    • Strep
    • Staph
  55. Routes of spread of infection in AOM?
    • ET
    • TM perforation
    • Hematogenous
  56. Risk factors of AOM?
    • Genetic
    • poor economic condition
    • Day-care attendance
    • Down's & Turner's syn
  57. Management of AOM?
    • Conservative:
    • analgesic
    • A/B (Amoxicilline 80mg/kg/day for 10days)
    • Surgery:
    • M&G for complicated cases or to relieve the pain
  58. Management of recurrent AOM?
    • Alteration risk factors: reduce exposure to other kids
    • Medical: prophylactic A/B
    • Xylitol consumptoin
    • Vaccination (Viral, bacterial)
    • Surgical: M&G, adenotonsillectomy
  59. Complications of AOM?
    • Extracranial: TM perforation (10%), acute mastoiditis ( in younger children), Petrositis (needs mastoidectomy), FN palsy ( in 80% needs only A/B, M&G, KIV mastoidectomy in 20%), labyrinthitis (serous, suppurative)
    • Intracranial: Meningitis (commonest), Extradural abscess, Subdural abscess, Subdural empyema, sigmoid sinus thrombosis (MRI, A/B, M&G, KIV mastoidectomy, needle the sinus and removal of thrombosis), focal encephalitis, brain abscess, otitic hydrocephalus.
  60. What is Griesinger sign?
    mastoid tenderness and oedema secondary to thrombophlebitis of the mastoid emissary vein.
  61. What is COM?
    • Chronic infection with submucosal and mucosal changes, tissue destruction, incomplete healing.
    • The reason for chronicity: repeated infection from nasopharynx, or EAC in case of TM perforation.
  62. Bacterial causes of COM?
    Pseudomonas Aeroginosa
  63. Treatment of COM?
    • keep ear dry
    • topical antbiotic
    • tympanoplasty in cases of unhealed TM perforation
  64. What is the diagnosis?
    Retraction of pars tensa and atrophy of TM.
  65. Sade's grading of retraction of pars tensa?
    • 1: TM slightly etracted
    • 2: TM touching incus or stapes
    • 3: TM touching promontorium
    • 4: TM adherent to promontorium
  66. causes of cholesteatoma by aetiology?
    • Congenital: Vestigial, Hamartoma, Metaplasia, Invagination, Amniotic migration
    • Acquired: Invagination, Invasion, Basal cell hyperplasia, Metaplasia, Trauma, Iatrogenic (residual)
  67. canal atresia epidemiology?
    • 63% in boys
    • 58% in Right ear
    • 20% bilateral
    • No canal cholesteatoma before age of 3 years, If untreated after 12 years, 91% can get cholesteatoma ( even in only stenotic canals)
  68. In assessing the patient with canal atresia, what is the most important fact in planning the management?
    The presence of normal canal and hearing level in the other ear.
  69. Causes of facial nerve palsy in children?
    • Bell's palsy (commonest), trauma, infections, congenital and neoplasm.
    • Bell's palsy in children is considered to have a betterprognosis than in adults, regardless of treatment.
  70. Causes of congenital facial paralysis?
    • Mobius syn: underdeveloped CN VII, VIII, +- autism or MR
    • Goldenhar syn: (oculoauriculovertebral dysplasia) deformity of 1st and 2nd branchiar arch organss (e.g. IAC) + HL
    • Asymmetric crying facies: congenital hypoplasia or agenesis ofthe depressor anguli oris muscle on one side of themouth.
    • CHARGE syn: colobomata, heart defect, atresia of the choanae, retarded development, genital hypoplasia and ear anomalies and hearing loss.
    • Familial facial paralysis: male members of family
  71. acquired causes of paediatric facial nerve palsy?
    • Infections: AOM, CSOM, Lyme, viral, TB
    • Trauma: perinatal trauma, temporal bone #, penetrating trauma, iatrogenic
    • Neoplasm: leukemia in temporal bone, h&n rhabdomyosarcoma
    • Idioplathic: Bell's, Melkersson-Rosenthal, Wegener's, hypertension
  72. Causes of Nasal obstruction in children?
    • Congenital
    • skeletal anomaly: choannal atresia, pyriform aperture stenosis, nasal agenesis.
    • nasal cyst: dermoid cyst, NLD cyst, thornwaldt cyst, nasoalveolar cyst, dentigerous cyst, mucous cyst
    • nasal masses: encephalocoele, meningocoele, glioma, hemangioma.
    • Acquired:
    • septal deformity, septal haematoma or abscess, FB.
    • Physiological rhinitis:
    • neonatal, pubertal rhinitis
  73. What is choanal atresia?
    • Complete obstruction of posterior nasal opening, due to persistance of the nasobuccal membrane.
    • 1 in 7000 live birth
    • bony or membraneous
    • Bilateral: emergency as neonates are obligate nasal breathers.
    • cyclical cyanosis: blue spells relieved by crying
    • resolving symptom by oral airway
    • Isolated anomaly or part of CHARGE
    • Unilateral: persistant profuse unilateral rhinorrhea in older child
    • Tx: surgery and dilatation ( transpalatal, transnasal)
  74. Surgeries for paediatric rhinosinusitis?
    • Adenoidectomy
    • Maxillary antral washout
    • Inferior meatal antrostomy
    • Turbinate reduction surgery
    • ESS
  75. Clinical grading of adenoid size?
    • Grade I: Adenoid tissue filling one-third of the vertical portion of the choanae
    • Grade II: Adenoidtissue filling from one-third to two-thirds of the choanae
    • Grade III: From two-thirds to nearly complete obstruction of the choanae
    • Grade IV: Complete choanal obstruction
  76. carniofacial syndromes with increased risk of OSA?
    Pierre Robin sequence, Crouzon syndrome, Goldenhar syndrome, Treacher Collins syndrome, Apert syndrome, Down syndrome, Hunter syndrome, Velocardiofacial syndrome, Beckwith-Wiedemann syndrome
  77. Systmic illnesses with increased risk of OSA in children?
    Cerebral palsy, Myotonic dystrophies, Obesity, Sickle cell disease, Glycogen storage disorder, Achondroplasia.
  78. what is the OSA level due to AHA?
    • mild: 5-20
    • Moderate: 20-40
    • Severe: >40
  79. Levels of obstruction is paeds OSA?
    • level I or adenoid pad and velopharyngeal obstruction;
    • level 2 or tonsillar obstruction;
    • level 3 or tongue base obstruction;
    • level 4 or supraglottic obstruction.
  80. Treatment of OSA in children?
    • Medical:
    • treat Rhinosinusitis
    • A/B in case of pulmonary atelectasia
    • CPAP
    • nasopharyngeal airway (especially for Pierre Robin sequence)
    • Mandibular advancement splints
    • surgical treatment:
    • Adenotonsillectomy
    • UPPP for CP patients
    • Laser supraglottoplasty or epiglottopexy
    • Tracheostomy
  81. Definition of stridor?
    Turbulent flow due to partial obstruction of the airway gives rise to abnormal or unwanted noise.
  82. Common causes of stretor?
    • Neonates:
    • Neonatal rhinitis, Choanal atresia/stenosis, Craniofacial abnormalities, Micrognathia
    • Children:
    • Allergic rhinitis, Adenoiditis, Adenotonsillar hypertrophy, Foreign bodies
  83. Common causes of Stridor?
    • Neonates:
    • Laryngomalacia, Intubation trauma, Reflux laryngitis, Laryngotracheal stenosis, Vocal cord palsy
    • Children:
    • Croup, Haemangiomas, Papillomatosis, Intubation trauma, Vocal cord palsy, Papillomatosis
  84. Congenital causes of stridor?
    Laryngomalacia, Posterior laryngeal cleft, Vallecula cyst, Laryngeal cysts, Webs, Laryngeal atresia, Laryngotracheal stenosis, Arytenoid fixation,Vocal cord palsy
  85. What is the pattern of stridor in Laryngomalacia?
    Typically, laryngomalacia is better with the child at rest and asleep but made worse by crying, feeding and when the child is distressed.
  86. Potential cause of progressive airway obstruction?
    Acute infection or FB inhalation
  87. Which one is a better indicator of severity of airway compromise? degree of stridor or subcostal/intercostal/supracostal recession?
    The recession, as the severity of stridor can paradoxically become less as obstruction worsens due to the diminishing airflow.
  88. Dose of propranolol for treating hemangioma in children?
    0.6mg/kg/dose/ TDS
  89. Bryce's sign?
    manual compression of laryngocele causes escaping gas/fluid escape to airway

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