TITLE: Management of the Stridulous Child<=
br>
SOURCE: Grand Rounds Presentation, UTMB, Dept. of Otolaryngology
DATE: April 30, 2009
RESIDENT PHYSICIANS: Ryan Ridley, MD
FACULTY PHYSICIANS: Harold Pine, MD and Shraddha Mukerji, MD
SERIES EDITORS: Francis B. Quinn, Jr., MD
ARCHIVIST: Melinda Stoner Qui=
nn, MS(<=
span
style=3D'mso-bookmark:OLE_LINK2'>ICS)
&q=
uot;This
material was prepared by resident physicians in partial fulfillment of
educational requirements established for the Postgraduate Training Program =
of
the UTMB Department of Otolaryngology/Head and Neck Surgery and was not
intended for clinical use in its present form. It was prepared for the purp=
ose
of stimulating group discussion in a conference setting. No warranties,
either express or implied, are made with respect to its accuracy, completen=
ess,
or timeliness. The material does not necessarily reflect the current or past
opinions of members of the UTMB faculty and should not be used for purposes=
of
diagnosis or treatment without consulting appropriate literature sources and
informed professional opinion."
Introduction
Stridor is a clinical sign that is routinely encountered by pediatricians, primary care and ER physicians. Children with stridor or often ref= erred to the “airway specialists” and it is the otolaryngologist̵= 7;s task to identify the etiology of this “noisy breathing” that ea= sily and understandably causes alarm for parents and = other physicians. This chapter and = the accompanying power point presentation will provide a methodical approach and framework for tackling this physical exam finding as well as a brief overvi= ew of some of the more prevalent causes of stridor.
Definitions
Stridor is a harsh sound produced by turbulent a= irflow through a partial obstruction. The nature of the sounds may be soft and tun= eful;musical in quality. Important to remember is that str= idor is characteristic of certain pathology but never diagnostic. Stertor, another term used to desc= ribe upper airway sounds is a snoring type of noise often made by nasopharyngeal= or oropharyngeal obstruction, but may occasionally be created by the supraglot= tic larynx. Bearing these definitions in mind, it is clear to see that there is= not a true separation between these two definitions therefore a wide differenti= al diagnosis must be kept in mind.
Pathophysiology
In terms of physics, stridor can be explained as=
a
combination of the Bernoulli principle and the law of conservation of
energy. This, in essenc=
e, is
how the Venturi principle is derived. This law can be applied to fluids and
gases. The Venturi effect is the reduction in fluid pressure that results w=
hen
a fluid flows through a constricted section of pipe. To satisfy the law of conservation=
of
energy, the liquid/gas velocity must increase upon reaching the constriction
while the pressure decreases. The
decrease in pressure causes the narrowed, flexible airway of the child to c=
lose
momentarily to obstruct airflow and cause stridor. In clinical terms, the
“pipe” is the pediatric airway, while the “gas” is
oxygen. An alternative way to
comprehend this is the fact that gases normally produce equal pressure in a=
ll
directions when no movement is in effect.&=
nbsp;
However, as gas moves forward (linear) in a tube, it produces pressu=
re
in the forward vector while decreasing lateral pressure. When a narrowed
section is encountered, the pressure in the forward vector increases while
precipitously dropping in the lateral direction. Again, this drop in
pressure causes the pliable pediatric airway to intermittently close yieldi=
ng
airway obstruction/stridor. <=
/p>
Anatomy There are a number of anatomical differences bet=
ween
the pediatric and adult airway that render them vulnerable to compromise.
Functionally, anatomic differences associated wi= th the infant airway create a separation between the airway and digestive tract wi= th air movement being predominantly transnasal. As child grows the larynx descends= , the pharynx becomes larger to facilitate speech production and produces a common conduit for food and air passage. In turn, this increases risk for foreign bodies, food, and gastric contents to enter the airway.
Evaluation
It is easy to become overwhelmed when presented = with stridor, therefore the following pneumonic may prove u= seful as an initial starting point to gather important details from the his= tory:
SPECS-R
· Severity
· Progression
· Eating difficulties
· Cyanosis
· Sleep disturbance
· Radiologic findings
· Inquire about birth history, maternal STD, a= nd history of intubation.
In terms of physical assessment, f= irst assess the need for emergent airway intervention (ABC’s). Initial evaluation should be nonin= vasive as the pediatric airway can be quite tenuous and compromise must be avoided= . Indicators of severity include respiratory rate, level of consciousness/mental status,= and accessory muscle use. Be cogn= izant of the fact that a child who stops using accessory muscles to breathe (or is not using them when you arrive at bedside) does not signify that all is well. On the contrary, this c= ould be an ominous sign that the patient’s condition is about to plummet. During auscultation, pay attention to not only the lungs, but the neck, mou= th, and nasal airway. If cyanosis is encountered in the absence of stridor, fur= ther investigation is warranted as cardiovascular, CNS, pulmonary or gastrointestinal factors may be culprits.&= nbsp; (A brief algorithm to approaching an infant in respiratory distress = is located in the power point presentation of this chapter.)
Once you’ve determined the patient is not = facing imminent respiratory compromise, a more detailed and comprehensive examinat= ion may ensue. This exam should i= nclude a general assessment (weight, growth percentile, develo= pment), the nasal cavity, oral cavity and oropharynx. A heart and lung exam should alway= s be performed. Finally, flexible fiberoptic laryngoscopy can be performed. This simple test is often the most helpful in trying to narrow down the differential diagnosis.
A formal airway evaluation in the OR is not nece= ssary in every case. For example, in children with a history and exam (including fiberoptic), consistent with mi= ld laryngomalacia, watchful waiting is probably all that is required. However, it is important to realiz= e that children can have more than 1 airway issue. The flexible scope rarely allows an adequate exam of the subglottic region. In unusual or difficult cases, the = ENT surgeon should have a low threshold for recommending a formal airway evaluation.
In= the OR, all of the equipment (laryngoscopes, Hopkins rod-lens telescopes, and bronchoscop= es) must be checked before the patient arrives to ensure they are in working condition. As a rule of thumb= , a tracheostomy tray should be in room just in case an emergent surgical airway is needed.<= span style=3D'mso-spacerun:yes'> Most importantly, good communicati= on and rapport between endoscopist and anesthesiologist is a must.
Various Etiologies of Stridor
Now, a brief review of some common causes of ped= iatric stridor will be examined. This approach will begin at the nose and end in t= he trachea. This is by no means = an all inclusive list and details regarding surgical procedures of these various conditions are beyond the scope of this chapter.
Choanal Atresia (CA)
This rare disorder occurs 1
in 10,000 births with females affected more than males. There is roughly a 50/50 split
Clinical Signs/Symptoms include respiratory distess/paradoxical cyanosis (i.e. cyanosis and respiratory distess that is relieved with crying), feeding difficulty and association with CHARGE syndr= ome:
· C- Coloboma
· H- Heart anomaly
· A- Atresia of choana
· R- Retarded growth
· G- Genital hypoplasia
· E- Ear anomalies and/or deafness
Clues to diagnosis include inability to pass 8 f=
rench
catheter beyond 3.5 cm from nasal vestibule, and a mirror under nares that
fails to fog on expiration. The flexible scope can also be quite helpful.
Initially, management is conservative with the u= se of an oral airway or a McGovern nipple. Surgical approaches are utilized once the conservative measures fail. Each method has its pro= s and cons. The transpalatal approach gives better visualizat= ion, and a high success rate although this can damage the palate growth plate resulting in cross bite deformities. The transnasal method has less blood loss, and requires less procedu= re time; however, there is increased CSF leak and meningitis risk. Lastly, the laser (CO2, KTP, Holmi= um:YAG) is being utilized with good success in combinati= on with endoscopic techniques. T= he operating microscope with the CO2 laser is also being employed.<= /p>
=
Congenital
Nasal Pyriform Aperture Stenosis (CNPAS)
This condition is caused by premature fusion and overgrowth of the medial nasal processes.&= nbsp; Some believe this could represent a microform of holoprosencephaly.<= span style=3D'mso-spacerun:yes'> Associated abnormalities include a central megaincisor (60% of cases) and concomitant malfunction of pituitary/adrenal axis.
The clinical picture is very similar to CA: respiratory distress, feeding difficulty, cyclical cyanosis. The exam reveals bony obstruction = of the vestibule and inability to pass a catheter/scope into the nose. A thin cut CT with emphasis on the pyriform aperture is the image modality of choice.
As with CA, management is initially conservative= with use of the McGovern nipple, topical decongestants, and corticosteroids. Once conservative measures have fa= iled, surgery is the next option. Briefly, the aperture is widened via a superior gingivolabial incision/premaxillary degloving approach to preserve the mucosa. Nasal stents are left in place 1-4 weeks.
In terms of prognosis, mild cases may resolve as= the child grows but if conservative measures fail excellent long term results a= re usually achieved with surgery.
Retropharyngeal Abscess (RPA)
Retropharyngeal abscesses secondary to their oropharyngeal location can present as an emergent situation causing stridor. Expedient diagnosis = and management are necessary.
Anatomically, the retropharyngeal space has it’s superior border at the skull base and exten= ds inferiorly to as far as T6. It’s posterior and anterior boundaries are the prevertebral fa= scia and the buccopharyngeal fascia, pharyngobasilar fascia and the esophagus respectively. Laterally, the = space is bordered by the carotid sheath. Importantly, there is an anterolateral communication with the parapharyngeal space.
This entity is more prevalent in childhood with = 70% of cases being in patients 6 years old or younger. The retropharyngeal space has two paramedian chains that drain the adenoids, nasopharynx, oropharynx, paranas= al sinuses and possibly the middle ear. These lymph nodes are prominent in childhood but atrophy as the child approaches adolescence. When = these lymph nodes suppurate, a retropharyngeal abscess may develop.
Fever, sore throat, progressive dysphagia, and drooling are all symptoms representative of retropharyngeal abscess. Patients may also present with neck stiffness and mild torticollis. In younger children, stridor may be present, the degree of which can be correl= ated with the size of the abscess. On physical exam, asymmetrical posterolateral pharyngeal swelling is present a= nd may be accompanied by cervical adenopathy.
When retropharyngeal abscess is suspected CBC wi=
th
differential and lateral neck films should be ordered. Lateral neck films can be up to 90%
sensitive for RPA. The gold
standard, however, is CT scan with contrast as this can make clarification
between retropharyngeal cellulitis or abscess.
When imaging suggests cellulitis, a trial of IV antibiotics, preferably clindam= ycin or ampicillin-sulbactam, is a reasonable option. However, if an abscess is initiall= y revealed on CT scan or after repeat scanning 48 hrs after antibiotics has been initiated, incision and drainage should be performed in the OR.
Laryngomalacia
This entity is the most common cause of congenit= al stridor. It may manifest days= /weeks after birth but symptoms usually resolve by 12-18months. The stridor in laryngomalacia is believed to be caused by prolapse of supraglottic structures into laryngeal inlet.
Signs and symptoms typical of laryngomalacia inc= lude low pitched, fluttering inspiratory stridor that peaks at 6-9months of age,= has positional variations, and can be exacerbated by activity (i.e. feeding, exertion). Cyanosis is rarely produced by laryngomalacia and if it is observed, suspicion for other patho= logy should be high.
Physical exam with awake fiberoptic laryngoscopy is needed to confirm the diagnosis. Direct laryngoscopy/bronchoscopy i= s sometimes needed to rule out synchronous lesions.
Management is conservative and based on the fact= that this condition is self-limited. Surgical treatment (~10% of cases) comes in the form of a supraglottoplasty which is indicated for cases with severe stridor, failure to thrive, apneas, cor pulmonale, or pulmonary HTN.
Laryngeal Cysts
Laryngeal cysts are a rare form of stridor in infants. Typical symptoms inc= lude stridor, feeding difficulty, and cyanosis.=
There are two types of laryngeal cysts: ductal a= nd saccular. Ductal cysts are th= e most common type. The etiology of = this type is obstruction of submucous glands and they can be located anywhere in larynx but most commonly in supraglottis.&= nbsp; Saccular cysts are the least common. They are usually congenital in inf= ants and located in the laryngeal ventricle without communication with the laryn= geal lumen.
Management of laryngeal cysts is comprised of endoscopic excision or unroofing.
Congenital Laryngeal Web
Congenital laryngeal webs arise from failure of recanalization of the larynx in the embryo. They are predominantly in the ante= rior glottis and associated with subglottic stenosis in cases of severe webbing. Common presenting sy= mptoms include abnormal cry and stridor.
Diagnostic endoscopy is required for diagnosis a= s well as ruling out other abnormalities. There appears to be and association between anterior glottic webs and velocardiofacial syndrome. Th= ere is ample evidence to support investigating for a 22q11 deletion in any child f= ound to have a laryngeal web. Trea= tment ranges from simple incision for small webs to laryngofissure with stenting = for severe webbing. Endoscopic la= ser treatment is also an option.
Posterior Laryngeal Cleft
Laryngeal clefts
arise from failure of the posterior larynx to fuse (may involve trachea).
Type I-Interarytenoid cleft; superior to the glottis
Type II-Partial cricoid cleft; extends infer= ior to the glottis and partially through the
= posterior lamina of the cricoid.
Type III- Total cricoid cleft, with or witho= ut extension into the cervical
= tracheoesophageal wall.
Type IV- Laryngotracheoesophageal cleft exte= nding beyond the thoracic inlet.
Diagnosis is made by demonstration of laryngeal penetration on contrast swallow, but the confirmation, as with most larynge= al pathology, is made at endoscopy.
Surgical intervention may be avoided with mild c= lefts and the only intervention needed may be to thicken feeds. If aspiration continues despite conservative measures then consideration of endoscopic closure is reasonable. Surgical closure utilizing lateral pharyngotomy or laryngofissure approach may be necessary = in cases of extensive clefts.
Vocal Cord Paralysis
Vocal Cord Paralysis comprises 10% of congenital laryngeal lesions. It may be congenital or acquired but most often the caus= e is idiopathic. Various etiologie= s are as follows:
Vocal cord paralysis can exist unilaterally or bilaterally. The key differen= ces are briefly summarized below:
Unilateral
Bilateral
Evaluation of vocal cord paralysis can be seen w= ith fiberoptic laryngoscopy while pt is awake.= Despite this, laryngotracheobronchoscopy must be performed to palpate the arytenoids and rule out congenital arytenoid fixation and exclude synchronous lesions. As furth= er work-up, an MRI of the brain,= brain stem, neck and chest are reasonable if the cause is not obvious (delineate course of vagus). FEES/MBS may be utilized in cases of aspiration.
When considering management options it is import= ant to know that vocal cord paralysis in infants usually resolves in 6-18mos, so scheduled monitoring is reasonable for the first 2 yrs. During this time, a temporary tracheotomy may be necessary. &= nbsp; If the cord paralysis does not resolve various surgical methods are being employed such as CO2 transverse partial cordotomy, costal cartilage grafting, and arytenoidopexy w/wo arytenoidectomy (CO2 laser or external approach).
Recurrent Respiratory Papillomatosis
Recurrent respiratory papill=
omatosis
although rare overall, is the most common neoplasm of the larynx in childre=
n.
The incidence of newly diagnosed RRP in children <15yo is 4.3/100,000.
The etiology is linked to HPV types 6 & 11 via maternal-fetal transmission.
Commonly seen is the hallmark triad of progre= ssive hoarseness, stridor, and respiratory distress. Patients most often present with dysphonia and stridor is usually the 2nd symptom to manifest as the conditi= on worsens.
A list of current surgical and adjuvant treatmen= ts for RRP are below:
Surgical
Adjuvant
Subglottic stenosis
Subglottic stenosis may be congenital or acquire= d:
In subglottic stenosis, the degree of stenosis dictates the symptoms. During= cases of severe stenosis, an infant may have stridor at birth whereas mild stenos= is may not manifest until a URI takes place. In acquired SGS, a clue in neonat= es may be a failed extubation trial. Older children may successfully extubate = but present later with progressive worsening respiratory distress.
Subglottic stenosis is quantified using the Myer-Cotton grading system:
· 0-50% obstruction=3D grade I
· 51-70% obstruction =3D grade II
· 71-99% obstruction =3D grade III
· No detectable lumen =3D grade IV
When evaluating SGS, stenotic portions may be vi= sualized on plain films however, direct laryngoscopy/bronchoscopy is needed for conf= irmation and airway staging.
The best way to address SGS is to avoid the occu= rrence altogether. Preventative measures currently being used include the use of uncuffed, polyvinylchloride endotracheal tubes, smaller tubes, and nasotrac= heal intubation. Conservative treatment options have the primary goal of achievi= ng decannulation (if tracheostomy present) or the prevention of a tracheostomy= by means of close observation (grades I-II).&= nbsp; Definitive surgical options include endoscopic methods employing use= of lasers, anterior cricoid split, laryngotracheal reconstruction, cricotrache= al resection.
Subglottic Hemangioma
Subglottic hemangiomas comprise 1.5% of all cong= enital laryngeal anomalies. Female occurrences predominate with a 2:1 female to male ratio. This condition is one of the most c= ommon neoplasm of infant airway.
Clinically, subglottic hemangiomas are usually asymptomatic at birth. The ma= jority of patients present with biphasic stridor in first 6 months and cutaneous hemangiomas are present in 50% of patients at the time of diagnosis. The lesions are characterized by r= apid growth that ceases at 12 months and may resolve by 5 years of age.
When diagnosing subglottic hemangiomas, biopsy i= s unnecessary due to the lesion’s pathognomonic appearance seen during endoscopy described as a compressible, submucosal mass with a reddish or bluish hue t= hat is asymmetric and located in the posterior left subglottis.
The objective of treatment in dealing with subgl= ottic hemangiomas is to preserve a stable airway while mitigating the long term sequelae of the treatment. Current treatment modalities involve tracheotomy= (temporizing measure), steroids, laser excision, surgical excision, and interferon.
Vascular Causes
Congenital vascular anomalies make up 5% of stri= dor cases. Symptoms are caused by tracheal/bronchial external compression by:
A double aortic arch develops as a result of
persistance of the fourth branchial arch and dorsal aortic root
bilaterally. This is the most
common symptomatic vascular ring.
On the other hand, pulmonary artery slings are the most symptomatic =
of
the noncircumferential anomalies.
The right mainstem bronchus is affected in the majority of cases.
The presentation of patients with the above cond= itions may be subtle or present with biphasic stridor/expiratory grunting along wi= th chronic cough, recurrent bronchitis, pneumonia, feeding difficulty, and/or failure to thrive.
Diagnostic imaging of choice is CT with contrast= or MRI, however, barium esophagram may reveal filling defects characteristic of the= se anomalies. Plain films are of limited value. Endoscopy allows greater assessment of the degree of compression.
= Absolute indications for surgery include reflex apnea, 48hrs of failed medical management, and prolonged intubation. Relative indications include recurrent infections, exercise intolerance, dysphagia causing failure to thrive, concomitant SGS, asthma, and cystic fibrosis.
Tracheomalacia
Tracheomalacia is a congenital deformity of the tracheal rings. Patients usua= lly present with expiratory stridor or respiratory distress. Like many airway lesions, the seve= rity of symptoms depends on the extent of the lesion.
Diagnosis is made by flexible bronchoscopy in th= e awake patient. During this exam, collapse of anterior tracheal wall against membran= ous posterior portion of the trachea can be observed.
Treatment is rarely needed as most cases are self-limited although some cases may need temporary tracheotomy. In seconda= ry tracheomalacia, treatment is directed at the underlying cause.
Foreign Body Aspiration
The majority of foreign body aspiration occurs in patients less than 3 years old. Aspiration of various foreign bodies are responsible f= or approximately 150 pediatric deaths/year in US. Choking accounts for 40% of accidental deaths in children <1yo.
Coins are the most commonly ingested object whil= e food such as nuts and seeds are the most commonly aspirated. In older children fish and chicken= bones are likely as well.
As stated previously, foreign bodies can be eith= er ingested or aspirated. The cl= inical presentation can help the astute clinician determine whether ingestion or aspiration is more likely:
Esophageal
Airway
Plain films are important in FB assessment. PA and lateral CXR are good for radiopaque objects and can still prove useful despite lack of obvious forei= gn body. Rigid endoscopy is warranted when clinical suspicion is high despite “innocent/negative” films.
Unstable airway foreign bodies should be = dealt with at the time of presentation. &nb= sp; Of course, not all airway foreign bodies are emergencies that warrant operative intervention. When a patient with an airway foreign body presents in stable condition in the mid= dle of the night or “after hours”, it may behoove the endoscopist to postpone going to the OR until the appropriate team and staff is present du= ring the light of day. These perso= nnel are already familiar with the equipment, pediatric anesthesiology is readily available, and the situation becomes less stressful for everyone involved.<= span style=3D'mso-spacerun:yes'> In the case of esophageal foreign bodies, it is possible to closely observe in the hospi= tal in hopes of spontaneous passage (mid/distal esophagus). The exception is when an object su= ch as a disc battery is ingested—this requires prompt removal in the OR.
Inflammatory Causes: Croup & Epiglottitis
Below is a chart briefly summarizing the differe= nces between croup and epiglottitis as these are often confu= sed.
|
|
Croup |
Epiglottis |
|
Onset |
2yo |
1-5yo |
|
Etiology |
Parainfluenza virus type 1 |
H. Influenza Gram + bugs |
|
Symptoms/Signs |
Barking cough, inspiratory stridor |
Odynophagia, “sniff position” with mouth open |
|
Diagnostic |
AP neck film=3D“steeple sign” |
Lateral neck film=3D“thumb sign” |
|
Treatment |
Racemic epi, corticosteroid, humidified O2 |
Airway established in OR, IV abx |
DISCUSSANTS’ REMARKS – Drs. Pine and Muk= erji
Evaluation of Stridor in Children
Faculty Comments by Dr. Pine and Dr. Mukerji=
The vital first step in evaluating any child with stridor is first to decide whether the patient requires urgent airway intervention. This decision is often made quickly and with limited information. A failure = in judgment at this point places the patient at risk and puts the otolaryngolo= gist in an untenable situation, having to later obtain an emergent airway in less than ideal circumstances with little or no equipment. If the clinical situa= tion merits, it is safer to bring the patient to the operating room to secure the airway. Diagnostic and someti= mes therapeutic endoscopy can be performed at the same time.
Fortunately, most children who present for evalu= ation of stridor are stable enough to undergo a complete history and physical exa= m. Additional lab tests and radiographs are ordered as needed. The single best test is probably flexible laryngoscopy.&nb= sp; It allows a quick and usually excellent view of the nasal cavity, the nasopharynx, the hypopharynx and the larynx. There are small scopes (2.2mm)= which can be easily passed thru an infant’s nasal cavity. If such a scope is not available, = the standard sized scope can usually be passed thru the mouth to obtain a view = of the larynx. I only attempt th= is in children with no teeth. This procedure is almost always possible at the bedside with few complications. = It is important to realize that flexible laryngoscopy is not a substitute for a formal airway evaluation in the operating room. There are certainly cases w= here the flexible laryngoscopy exam can be normal in a child with serious airway issues. (= i.e. vascular compression, tracheomalacia) One must also realize that finding one problem like laryngomalacia does not rule out another problem further down = in the airway. In fact, many chi= ldren have more than one airway problem. Otolaryngologists should have a low threshold for recommending a for= mal airway evaluation to include laryngoscopy bronchoscopy and possibly esophagoscopy.
There are a host of things that can cause or exacerbate stridor in children. Having a systematic approach to the history and exam can help narrow down the differential diagnosis. Ultimately, direct airway evaluation using both flexible and rigid techniques provide the most useful information and = can often guide further testing if necessary. Even in this modern age with all sorts of fancy equipment, a host of possible tests to order, there is still= no substitute for good clinical judgment.&nbs= p;
References
April MM, Ward RF.&nb= sp; Choanal atresia repair: The use of powered instrumentation.
Oper Tech Otolaryngol Head Neck Surg 1996; 7:248-251
Bailey, B. Head and Neck Surgery-Otolaryngology. 4
Brown OE, Pownell P, Manning SC. Choanal atresia: A new anatomic classification
and clinical management applications. Laryngoscope 1996; 106:97-101.
Coulthard M, Isaacs D: Retrophary= ngeal abscess. Arch Dis Child 1991;&= nbsp;66:1227
Cummings: Otolaryngology: Head & Neck Su= rgery, 4th ed.
De Jong AL, Kuppersmith RB, Sulek M=
, et
al. Update on the pediatric airway: vocal
cord
paralysis in infants and children. Otolaryngol Clin North A=
m 2000;33:131<=
/span>–149
Gonzalez Valdepena H, Wald ER, Rose=
E, et
al. Epiglottitis and
influenza immunization. The Pittsburgh exp=
erience:
a five year review. Pediatrics
1995;96:424–427
Harris J, Robert E, Kallen B. Epidem= iology of choanal atresia with specific reference
to CHARGE association. Pediatrics 1997; 99:363-367
Holinger LD. Evaluation of stridor =
and
wheezing. In: Holinger LD, Lusk RP, Green
CG,
eds. Pediat=
ric laryngology
and bronchoesophagology. Philadelphia: Lippincott-
Raven,
1997:41–48
http://emedicine.medscape.com/artic= le/995267-overview
Josephson GD, Vickery CL, GilesWC, et al. Transnasal endoscopic repair of
congential choanal atresia. Arch Otolaryng= ol Head Neck Surg 1998; 124:537-540.
Journal of Clinical Anesthesia= Volume 12, Issue 5 August 2000, Pages 417-419
Kirse D, Roberson D: Surgical management of retropharyngeal space infections in
children. Laryngoscope = ; 2001; 111:1413
Lusk RP, Kang D, Muntz HR. Auricular
cartilage grafts in laryngotracheal
reconstruction.
Rahbar R, Nicollas R, Roger G, et a=
l. The
biology and management of subglottic
hemangioma: past, present, future. Lar=
yngoscope 2004;114:188=
0–1891
Stern Y. Partial cricotracheal rese=
ction
with primary anastomosis in the pediatric age
group. Ann Otol Rhinol Laryngol=
1997; 106:891–896
Walker P, Crysdale W: Croup, epiglottitis, retropharyngeal abscess, and bacterial
tracheitis: evolving patterns of occurrence and care. = Int Anesth Clin 1992; 30:57
Wetmore R.F., Muntz H.R., McGill T.J. Pediatric Otolaryngolog= y. Thieme Medical
Publishers,= Inc., New York 2000 pgs 453-63.
Yates Philip D, Anari Shahram, "Chapter 32. Stridor in Children" (Chapter). Lalwani
AK: CURRENT Diagnosis & Treatment in Otolaryngology—Head & Neck Surgery,
2nd Edition
<=
span
style=3D'color:black'>Brigger MT, Hartnick CJ. Surgery for pediatric vocal cord paralysis:
a meta-a=
nalysis.
Otolaryngol Head Neck Surg. 2002; 126(4):349.
Goldenberg D, Golz A, Joachims HZ: Retropharyngeal abscess: a clinical review. &nbs= p;
J
Larngol Otol 1997; 111:546
Oto
Head & Neck 2004, 130: 415-17