Acute laryngeal infection

1. Scott brown learning 2020
Volume : 2 "Paediatrics
The ear skull base"
Chapter : 29.Acute laryngeal infections( p.no :325 to 332 )
30. Congenital disorders of larynx , trachea and bronchi
( p.no : 333 to 346 )

2. Acute laryngeal infections &
Congenital disorders of larynx ,
trachea and bronchi
Dr. Vinoth .S , postgraduate in department of ENT ,
Madurai medical college

3. Acute laryngeal infections – croup ( ALTB)
• Croup typically presents as hoarseness with distinctive barking cough
progressing to inspiratory or biphasic stridor.
• usually a preceding history of upper respiratory tract symptoms,
malaise and pyrexia.
• Children with croup do not typically drool or appear toxic, in contrast
to children presenting with epiglottitis.
• The symptoms are thought to be due to mucosal oedema of the
larynx and trachea following a viral illness.

4. caused by parainfluenza virus type I , parainfluenza virus type II,
respiratory syncytial virus (RSV) virus types A and B and rhinovirus.
• The diagnosis of croup is a clinical one and laboratorytests and
radiological tests are generally not needed
• Croup is usually self-limiting , is rare
• critical symptom of stridor is due to oedema in the subglottis, the
narrowest part of the paediatric

5. Chest x-ray :
• radiograph of the thoracic inlet will show characteristic narrowing of
the subglottis on an anteroposterior view(‘steeple’ or ‘pencil-tip’ sign)

6. Westley Croup Score :
A maximum score is 17, a score of
2–3 equates to mild croup
4–7 to moderate croup and
8 or more to severe croup

7. Treatment
• For mild croup, can be supportive humidified environment or mist
tent
Medical - Corticosteroids
• The mainstay of treatment for croup is corticosteroids.
• Corticosteroids have a systemic anti-inflammatory effect.
• There is a reduction in capillary endothelial permeability and
therefore in mucosal oedema, and stabilization of lysosomal
membranes, decreasing the inflammatory reaction.
• Topical corticosteroids have alpha-mediated vasoconstriction.

8. Nebulized epinephrine
• Nebulized epinephrine (1 mL of 1 in 1000 epinephrine diluted in 3 mL
of 0.9% saline) has an established role in the acute paediatric airway
in reducing mucosal oedema by an alpha-agonist effect causing
vasoconstriction and bronchodilation;
• a maximum effect is achieved within 30–60 minutes but there is no
lasting benefit beyond 2 hours.

9. Heliox
• HelioxR is a mixture of helium and oxygen generally supplied with a helium
: oxygen ratio of 70 : 30
• produce laminar flow in the presence of a partially obstructed airway than
air or oxygen.
• Inhaled helioxR delivered through a high-flow system should reduce the
work of breathing and result in larger tidal volumes and improved gas
exchange.
• Helium has a high thermal conductivity and so care is needed with
humidification in order to avoid hypothermia

10. BACTERIAL LARYNGOTRACHEOBRONCHITIS
also known as
• PSEUDOMEMBRANOUS CROUP,
• BACTERIAL TRACHEITIS,
• MEMBRANOUS LARYNGOTRACHEOBRONCHITIS,
• NEONATAL NECROTIZING TRACHEOBRONCHITIS

11. • a severe form of laryngotracheobronchitis characterized by the
presence of profuse mucopurulent secretions with sloughing of the
respiratory epithelium.
• Secretions are often adherent, are not effectively cleared by
coughing and may occlude the airway causing respiratory
compromise.
• Bacterial tracheitis must be differentiated from croup and other
causes of infectious upper airway obstruction in order to initiate
proper management.

12. • Classically the child with bacterial tracheitis appears toxic with high
fevers and worsening stridor that fails to respond to treatment with
steroids and nebulized epinephrine.
• It typically affects children older (mean age 4–8 years) than the usual
age group for croup.
• Bacterial tracheitis is a much less common condition than croup.
• However, there is increased susceptibility in children with Down
syndrome or immunodeficiency

13. • Diagnosis can only be confirmed on airway endoscopy; there is a
pseudomembrane in the subglottis and trachea and thick mucopus
and debris extending into the bronchi
• Direct laryngotracheobronchoscopy under general anaesthesia and
removal of all tracheal secretions, with pulmonary toilet, is
mandatory.
• to secure the airway by endotracheal intubation for a period of days.

14. • Staphylococcus aureus( is the pathogen most commonly isolated from
tracheal cultures) Haemophilus influenzae, Moraxella catarrhalis,
Streptococcus pneumoniae and Pseudomonas aeruginosa
• Viral cultures are also frequently positive, indicative that many cases
of bacterial tracheitis represent a secondary bacterial infection that
follows a viral respiratory tract infection.
• Most commonly influenza A is identified, although other viruses
including the H1N1 strain of influenza A and metapneumovirus have
also been isolated.2,

15. Complications
include
• airway stenosis,
• acute respiratory distress syndrome,
• respiratory failure,
• toxic shock syndrome,
• anoxic encephalopathy and
• death.

16. Diphtheria
• Diphtheria remains an important differential in the diagnosis of acute
laryngeal infection in children, particularly in those who have
travelled to endemic areas or have not been vaccinated
• The causative organisms in pathogenic diphtheria are the toxogenic
strains of Corynebacterium diphtheria and Corynebacterium ulcerans.
• The early clinical picture of upper respiratory tract symptoms is due
to the effects of the organism itself.
• Delayed effects are due to the release of exotoxin.

17. • Symptoms of diphtheria come on gradually and typically begin 2–5
days after exposure.
• Initial symptoms are of pharyngitis with sore throat and malaise.
• The child is feverish and on examination there is a typical appearance
of the pharyngeal tonsils with necrosis and the development of a
characteristic grey pseudomembrane over the surface.
• This consists of necrotic tissue, bacteria and a rich fibrinous exudate.
• Early removal causes bleeding but the pseudomembrane may
separate more easily in the later course of the disease.
• There may be a bull-neck appearance due to cellulitis and regional
lymphadenopathy

18. • Diphtheria infection may also involve the larynx.
• After initial symptoms of dysphagia and toxaemia, symptoms may progress to
inspiratory stridor and a barking cough;
• the cough is frequently paroxysmal and exhausting.
• Death may follow owing to acute airway obstruction or as a result of the later
effects of the exotoxin.
• The exotoxin can cause a toxic myocarditis in the second week of the disease and
this may be fatal.
• Peripheral neuritis may also occur, palatal paralysis being the most common
effect of peripheral neuropathy and presenting with nasal regurgitation of food
and hypernasal speech.

19. • Successful treatment depends on early diagnosis, and the timely administration
of high-dose benzylpenicillin and antitoxin (10 000–100 000 units, depending on
the severity of infection).
• Delaying the administration of the antitoxin is associated with increased mortality
as the antitoxin does not neutralize toxin that is already bound to tissues.
• The decision, therefore, to administer antitoxin should be made based on clinical
suspicion and should not await microbiological confirmation.
• Airway management consists of removal of the laryngeal membrane,
administration of oxygen and humidification, and endotracheal intubation or
tracheostomy if necessary.
• Systemic steroids may reduce the need for airway intervention.
• Bed rest is recommended until the danger of myocarditis is past.

20. It is of a toxic child with a short history of sore throat, inspiratory stridor,
muffled voice and drooling due to odynophagia and dysphagia.
Untreated results in progressive respiratory distress.
The child is febrile, tachypnoeic and classically will be sitting upright, with
the neck extended to optimize the airway, and using then arms to provide support
to the shoulder girdle to maximize the efficiency of the accessory muscles of
respiration.
It is commonest between the ages of 2 and 8 and there is an increased
prevalence in winter

21. Acute epiglottitis
• When acute epiglottitis is suspected, pharyngeal examination should
not be attempted, as simple manipulation with a tongue depressor
may precipitate acute airway obstruction,
• although the use of a fibreoptic or small rigid endoscope can assist
the diagnosis in patients with an atypical presentation.
• Direct examination of the airway should not be delayed, but should
be undertaken in a controlled setting such as an operating room or
paediatric intensive care unit by personnel skilled in airway
intervention;

22. • endoscopic evaluation will confirm gross erythema and oedema of
the supraglottic structures
• When the diagnosis is confirmed, the airway should be secured by
endotracheal intubation
• a soft-tissue lateral radiograph of the neck will typically show a
thickened oedematous epiglottis – the ‘thumb sign’

23. Etiology :
• acute epiglottitis has been a manifestation of invasive Hib infection
• meningococci,
• group A streptococci, pneumococci, Haemophilus parainfluenzae and
Staphylococcus aureus.
• Immunocompromised individuals are at increased risk of epiglottitis.
due to atypical organisms such as Herpes simplex type 1, Varicella
zoster, Parainfluenza or Candida albicans.

24. Treatment :
• Treatment is with intravenous antibiotics; ampicillin resistance due to beta-
lactamase production is now over 50% in Haemophilus influenzae, so empirical
treatment with third-generation cephalosporins for 5–7 days is advised.
• Rifampicin prophylaxis has been recommended to eradicate the carrier state for
the index case as well as household and school contacts.
• Haemophilus influenzae type b immunization

25. AIRWAY MANAGEMENT
• Endotracheal intubation is now considered preferable to tracheostomy
• If endotracheal intubation is to be undertaken, it should be performed in an
operating room or paediatric intensive care unit with personnel and equipment
available and ready to undertake tracheostomy if the airway cannot be secured.
• humidified air should be administered to discourage the development of
tenacious secretions

26. Nasotracheal intubation
• When a prolonged period of intubation is anticipated, the
nasotracheal rather than the orotracheal route is preferred
• In acute epiglottitis, visualization of the epiglottis with a flexible
nasendoscope can be useful in monitoring resolution of
inflammation.
• in laryngotracheobronchitis, whether viral or bacterial, the airway
can be monitored using endoscopy until a reduction in tracheal
inflammation shows that it is safe to extubate.

27. • Systemic steroids administered 6 hours prior to removal of the tube
will minimize post-intubation oedema, and nebulized epinephrine can
assist with airway patency after extubation.
• For acute epiglottitis the period of intubation is usually less than 48
hours but for croup and bacterial laryngotracheobronchitis it may be
up to a week.
• Tracheostomy is no longer considered the first choice to secure the
airway in acute laryngeal infection.

28. Congenital conditions of
larynx

29. Congenital conditions of larynx -Laryngomalacia
• Laryngomalacia is characterized by partial or complete collapse of the
supraglottic structures on inspiration
• is the most common congenital cause of stridor
• Signs- the epiglottis is long and curled (omega-shaped)
the aryepiglottic folds are short and tightly tethered to the epiglottis;
there may also be redundant mucosa and submucosa of
the aryepiglottic folds medially resulted in a tall,
narrow supraglottis with a deep interarytenoid cleft

30. - epiglottis is soft and may curl and collapse and the
mucosa may prolapse into the airway .
- due to neuromuscular immaturity and consequent
incoordination of arytenoid movements

31. • high-pitched, fluttering inspiratory stridor is usually present at, or
shortly after, birth , increases during activity and decreases at sleep
The severity of the stridor increases during the first 9 months
of life, and disappears at two years of age ,
rarely may persist into late childhood.

32. • The diagnosis can be confirmed by flexible fibre-optic laryngoscopy
• Treatment :
• for mild, no intervention is needed and the parents can be reassured
• In severe laryngomalacia, there is serious respiratory obstruction with
substantial sternal and intercostal recession together with feeding
difficulties results in failure to thrive
• May associated with congenital cyanotic heart disease

33. • Children who show signs of failure to thrive should undergo an endoscopic
aryepiglottoplasty (sometimes termed a supraglottoplasty)
• In this procedure, each aryepiglottic fold is first divided to release it from the
edge of the epiglottis, and any redundant mucosa and submucosal tissue are
then excised from over the arytenoids, together, if necessary, with part or all of
the cuneiform cartilages.
• The ‘bridge’ of mucosa between the arytenoids is carefully preserved to prevent
interarytenoid scarring.

34. Vocal cord paralysis
• Vocal cord paralysis is the second most common congenital anomaly
of the larynx after laryngomalacia.
• patients may have other, coexisting airway pathology
• Diagnosed by flexible fibre-optic laryngoscopy
Laryngeal ultrasound

35. • Unilateral vocal cord paralysis is usually not congenital, most cases being acquired
as a result of surgical injury to the left recurrent laryngeal nerve, often following
correction of a congenital cardiac anomaly.
• Patients present with mild stridor, dysphonia and sometimes aspiration.
• If the vocal cord lies in an intermediate position, surgical intervention is not
usually necessary, and the voice can be expected to improveby compensation.
• If the vocal cord lies in a more abducted position, the dysphonia may be more
pronounced and aspiration more likely.
• Vocal cord medialization procedures such as thyroplasty and augmentation
injection can improve the dysphonia and aspiration, but these may result in
worsening of the stridor.

36. • Bilateral vocal cord palsy is usually a congenital abductor paralysis.
• The vocal cords lie in the paramedian position with consequent
inspiratory stridor,
• and a tracheostomy is necessary for airway management
• Presented with the Arnold-Chiari malformation
• If it have no movement ,then an endoscopic laser cordotomy or
arytenoidectomy should be considered at the age of 11

37. Laryngocoeles :
• Laryngeal cysts divided into laryngocoeles and saccular cysts.
• laryngocoele is an air-filled dilatation of the laryngeal ventricle which
communicates with the laryngeal lumen.
• uncommon lesion which usually occurs in middle age but may rarely be seen in
infancy,
• can produce respiratory distress which typically becomes worse on crying due to
increased distension of the laryngocoele with air.
• a laryngocoele may obstruct and fill with mucus or become infected
(laryngopyocoele), thus becoming indistinguishable from a saccular cyst

38. • A also represents an abnormal dilatation or herniation of the saccule
of the ventricle of the larynx;
• it differs from a laryngocoele in that there is no opening into the
larynx and it is filled with mucus instead of air.
• result from a developmental failure to maintain patency of the
orifice between the saccule and the ventricle, and may be of anterior
or lateral type.
Saccular cyst

39. The anterior saccular cyst extends medially
and posteriorly from the saccule and so
protrudes into the laryngeal airway
between the true and false vocal cords.
The lateral saccular cyst is most common in
infants and
expands posterosuperiorly into the false
cord and
aryepiglottic fold

40. • Laryngeal cysts are classified as internal or type 1 if contained entirely within the
laryngeal framework, and external or type 2 if it pierces the thyrohyoid
membrane.
• Diagnosis is confirmed by endoscopy, except in an external laryngocoele where
no abnormality may be seen except on imaging.
• Saccular cysts are best treated at the initial endoscopy by wide endoscopic
marsupialization
• If the cyst recurs, then the procedure of choice is a lateral cervical approach
extending through the thyrohyoid membrane at the superior margin of the ala of
the thyroid cartilage, with subperichondrial resection of a portion of the upper
part of the ala. Through this ‘window’ the cyst can be completely excised, using
short-term intubation to secure the airway post-operatively.

41. Vascular malformations
• include lymphatic malformations, venous malformations, av malformations
• Lymphatic malformations (also termed lymphagiomas or cystic hygromas) are
cystic malformations that result from abnormal development of the lymphatic
vessels.
• In the head neck they may be macrocystic (usually infrahyoid), microcystic
(usually suprahyoid) or a combination of the two.
• Occasionally, a microcystic lymphatic malformation may extend into the tongue
base, valleculae and supraglottis, and airway obstruction may result.
• If the lymphatic malformation is very extensive, a tracheostomy may be required,
• Surgical modality is to debulk the lesion by endoscopic vaporization using a CO2
laser or radiofrequency ablation.

42. Bifid epiglottis
• is a rare laryngeal anomaly in which the epiglottis fails to fuse in the
midline and thus has a cleft extending down to its tubercle.
• It may be seen as a feature of Pallister–Hall syndrome
• presents with feeding difficulties due to aspiration and with stridor
because of collapse and enfolding of the two halves of the epiglottis.
• Endoscopy establishes the diagnosis,
• treatment options include amputation of the epiglottis and
tracheostomy.

43. Glottis - Laryngeal webs
• Failure of complete canalization of the larynx during embryogenesis
may result in a glottic or, very rarely, a supraglottic web.
• Mostly involves anterior glottis , associated with congenital vocal cord
paralysis .
• Due to delayed maturation in the vagal nuclei
• glottic enlargement surgery in order to avoid a tracheostomy
• an endoscopic laser cordotomy or arytenoidectomy if presented with
stridor

44. Laryngeal atresia
• Laryngeal atresia is incompatible with life unless there is an
associated tracheo-oesophageal fistula (TOF)
• emergency tracheostomy is performed in the delivery room.
• now recognized antenatally on ultrasound imaging and managed with
ex utero intrapartum treatment (EXIT) procedure,
• whereby a tracheostomy is undertaken following elective Caesarean
section with the neonate still on placental circulation.

45. Congenital subglottic stenosis
• due to defective canalization of the cricoid cartilage and/or conus elasticus,
resulting in either gross thickening of the anterior lamina of the abnormal cricoid
• a small, elliptical, thickened cricoid with excessive submucosal soft tissue
• there may be anterior fusion of the vocal cords, forming a web with subglottic
extension, as seen in 22q11 deletion syndromes.
• Subglottic stenosis is said to be the third most common congenital anomaly of
the larynx
• may be a combined congenital plus acquired stenosis for intubation

46. The Myer-Cotton grading system
• Grade I : 0–50% obstruction
• • Grade II: 51–70% obstruction
• • Grade III: 71–99% obstruction
• • Grade IV: 100% obstruction.
• If the airway is not severely compromised, surgery may not be
required
• a strict contraindication to dilatation or laser resection:
• any type of endoscopic treatment is liable to worsen the initial
condition, and attempted dilatation is inevitably ineffective as the
thickened ring of cricoid cartilage cannot be expanded

47. Milder degrees of stenosis present as
inspiratory or biphasic stridor as the
child becomes older and more active, or
as recurrent ‘croup’ owing to
superimposed oedema from upper
respiratory tract infections

48. • If the airway is severely compromised, a tracheostomy is needed.
• The surgical options have evolved from the classical castellated
laryngotracheoplasty designed by Evans and Todd
• The LTR involves augmentation of the laryngotracheal complex by
anterior and/or posterior midline incision of the cricoid with insertion
of costal cartilage grafts to expand the airway

49. Treatment :
• Grade I subglottic stenosis usually requires no surgical intervention.
• Grade II stenosis can be reconstructed by means of an LTR with
anterior cartilage grafting +/− posterior cricoid split.
• Mild grade III stenosis needs an anterior graft with posterior cricoid
split +/− posterior cartilage grafting.
• Severe grade III stenosis (a pinhole airway) requires both anterior and
posterior grafts.
• Grade IV stenosis demands anterior and posterior grafts with
prolonged stenting

50. Subglottic haemangioma
• Infantile subglottic haemangioma causes gradually worsening
inspiratory or biphasic stridor presenting in the first few weeks of life
• Associated with cutaneous haemangioma
• The natural history is typically a proliferative phase lasting 6–12
months followed by complete involution over 1–5 years
• At endoscopy the typical appearance is of a compressible, pear-
shaped red swelling in the subglottis on one side, left more
commonly than right

51. • Subglottic haemangioma is life-threatening
because of its situation in the narrowest part
of the airway and therefore requires rapid
intervention.
• Tracheostomy will maintain the airway
until involution
• radiotherapy, CO2 laser ablation, systemic steroids,
intralesional steroid injection followed by intubation, and interferon
alpha-2a

52. • propranolol is an effective treatment for cutaneous haemangioma
and subglottic haemangioma
• Submucous resection remains a valid alternative for non-
circumferential haemangiomas and those not involving the vocal
cords

53. Laryngeal and laryngotracheooesophageal
cleft
• Posterior laryngeal clefts result from failure of the posterior cricoid
lamina to fuse with incomplete development of the tracheo-
oesophageal septum.
• Benjamin and Inglis classification
- type I cleft extends down to the level ofthe vocal cords;
-type II cleft extends below the vocal cords into the cricoid
- type III cleft extends down into the cervical trachea
-type IV cleft extends into the thoracic trachea and may even reach
the carina
• With Opitz-Frias syndrome, TOF, Pallister–Hall syndrome

54. Symptoms :
• Type I clefts present with cyanotic attacks on feeding and recurrent chest
infections
• Type II and III clefts produce dramatic aspiration with recurrent
pneumonia, sometimes with stridor and an abnormal cry.
• Type IV clefts cause severe aspiration, cyanosis and incipient
cardiorespiratory failure.
• Suspension microlaryngoscopy to probe the arytenoids
• A plain chest X-ray may show changes secondary to recurrent aspiration
pneumonitis
• Videofluoroscopic contrast swallow studies may not differentiate laryngeal
incompetence from neuromuscular incoordination

55. Treatment :
• A short type I cleft with no aspiration requires no treatment. Minimal aspiration
may be managed by thickening the feeds
• A very short type II cleft may also be repaired endoscopically,
• a long type II or a type III cleft needs to be approached anteriorly through an
extended laryngofissure with a low tracheostomy
• type IV clefts may be managed by an anterior approach through a cervical
incision, if necessary pulling the trachea up into the neck to reach the lower end
of the cleft.
• Longer clefts will require a lateral cervical approach in combination with a
thoracotomy, or preferably an anterior cervicothoracic approach via a median
sternotomy with repair on extracorporeal membrane oxygenation (ECMO) or
cardiopulmonary bypass.

56. • Mortality remains significant, being approximately 14% overall
37 rising to 66% for type IV laryngotracheooesophageal clefts and
up to 100% for full-length clefts ending at the carina

57. Agenesis
• Tracheal agenesis may be complete (full-length) or partial, but in
either case there is no continuity between the larynx and the bronchi
• Occasionally, short-term survival may be possible if there is a
broncho-oesophageal fistula, which can permit some airflow into the
lungs, but surgical efforts to use the oesophagus as a tracheal
replacement have not been successful and long-term survival has not
proved possible

58. Stenosis
• Occasionally, a membranous web may be encountered in
the trachea with a normal underlying cartilaginous
ring structure. Such cases usually fare well with endoscopic
rupture and dilatation.
• Thicker congenital fibrous stenoses may be amenable to radial KTP laser incision
and balloon dilatation, followed by application of mitomycin C to reduce the risk
of restenosis42 or tracheal resection with end-to-end anastomosis.
• A short stenosis may also be associated with one or two absent tracheal rings,
although the most common finding in congenital tracheal stenosisis (CTS) is a
segment of complete tracheal cartilaginous rings with an airway lumen as narrow
as 2 mm

59. • Children with congenital tracheal stenosis usually present with
respiratory distress
• Symptoms may become apparent in the neonatal period with
biphasic stridor, respiratory distress, tracheal tug and episodes of
cyanosis in the first year of life
• Endoscopy remains the ‘gold standard’ investigation for a child with
stridor

60. • Bronchoscopy and bronchography (B&B) demonstrate the the size of the tracheal
lumen and outline the trachea and bronchi distal to the stenosis, which may be
too narrow to permit passage of a bronchoscope and also provides a dynamic
assessment of any malacic segments.
• Optical coherence tomography (OCT) can be combined with B&B to confirm the
presence of complete rings if there is any doubt.
• Contrast CT and an echocardiogram are essential in view of the high incidence of
associated anomalies of the heart and great vessels.
• CT is particularly helpful in assessing the vascular anatomy and its relationship to
the trachea and 3D reconstructions allow better surgical planning

61. • Mild cases with minimal symptoms may require no intervention after
the diagnostic endoscopy,
• Very narrow, short segments can be excised with end-to-end
anastomosis , Augmentation tracheoplasty with costal cartilage
grafting or a pericardial flap or free patch can be tried
• Successful endoscopic balloon dilatation
• Absorbable PDS stents offer an advantage over metallic stents and are
used to treat malacia, particularly bronchomalacia

62. Tracheomalacia and bronchomalacia
• Tracheomalacia is a condition in which there is reduced stiffness of
the tracheal wall, resulting in abnormal collapse of the trachea during
expiration
• produce symptoms of airway obstruction
• Pathologically, the striking finding is an
increased muscle- to-cartilage ratio
seen on the transverse section of the
trachea

63. • Tracheomalacia is traditionally classified as primary (idiopathic), due to an
intrinsic abnormality in the wall of the airway, or
secondary, due to another associated anomaly or to external compression.
• high-pitched expiratory noise stridor becomes apparent during the first few
weeks of life with a harsh, barking cough
• Characteristically, the stridor becomes much worse when the child is active,
feeding, upset, coughing or crying,
• it may be associated with cyanotic attacks which are sometimes sufficiently
severe to be termed ‘dying spells’.

64. • There may be a prolonged expiratory phase to respiration, possibly with faint
expiratory stridor
• A barium swallow may identify a TOF and can also demonstrate the airway
collapse on lateral screening
• CT angiogram is extremely useful for identifying the cause of extrinsic
compression of the trachea by normal or abnormal vessels, including vascular
rings.
• Contrast bronchography may be the most useful radiological investigation:

65. Treatment :
• Mild tracheobronchomalacia (less than 75% collapse) requires no
intervention, and the stridor can be expected to resolve
spontaneously by around the age of 2 years.
• If it is secondary to a vascular anomaly, this should be corrected an
extended tracheostomy tube will effectively support a midtracheal
malacic segment, but this is not a satisfactory solution for lower-end
tracheal or for bronchial collapse include internal or external stenting
of the trachea, segmental resection and cartilage grafting

66. Anomalous bifurcations
• The right upper lobe bronchus may take origin from the right lateral
wall of the trachea above the carina
• is termed a tracheal bronchus or
suis bronchus(PIG BRONCHUS)
• asymptomatic, incidental finding,
but may sometimes be associated
with tracheal stenosis

67. Tracheo-oesophageal fistula
• It is a fairly common congenital malformation of the neonatal air and food
passages, which usually occurs in association with oesophageal atresia.
• Eighty-seven per cent of cases have oesophageal atresia with a TOF
communicating between the distal oesophagus and the mid- to lower trachea or
a main bronchus
• m/c present to intensivist TOF without atresia (‘H-type fistula’)
the least symptomatic of the group, with no swallowing difficulty, but small
amounts of fluid pass through the fistula into the trachea and produce symptoms
and signs of recurrent minor aspiration.
barium swallow confirms the diagnosis
treatment by ligation and division of fistula

68. Vascular compressions
• Vascular ring :
• common is double aortic arch mostly involving ascending aorta
• Presents earlier in life with airway obstructions
• Barium swallow shows double impression upon the column of
contrast
• Surgical treatment involves diving the lesser component of the ring
• Post op tracheomalacia will persists for few monthds

69. • Vascular sling :
• Common is aberrant innominate artery crosses the anterior surface of trachea
above the carina
• Presents with less severe airway obstruction
• Expiratory stridor , cough ,recurrent URTI
• Bronchoscopy shows sloping pulsatile compression of the trachea 2 cm above the
carina
• Upward compression with bronchoscopes compress the artery against the
sternum thus obliterating the radial pulse
• Treatment by aortopexy