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Differential Diagnosis of Upper Airway Obstruction and Overview Laryngomalacia

Upper airway obstruction is most often a medical emergency requiring rapid evaluation

with simultaneous therapy to ensure adequate ventilation and oxygenation. The etiology varies

from simple nasal blockage in a newborn to near fatal epiglottitis in a child. Any child with

respiratory distress with or without noisy breathing may have airway obstruction. Patients with

upper airway obstruction usually present with inspiratory stridor.1

Based on our history taking, this patient has noisy breathing, hoarseness, and difficulty of

breastfeeding due to shortness of breath since fifteen days prior to admission. According to our

physical examination, there is high pitched and harsh sound that may be heard over the upper

airways without a stethoscope that called stridor. Those symptomps indicating suspicion of

upper airway obstruction in this children. The causes of upper airway obstruction are grouped

into acute and chronic and then further reclassified into infectious and non infectious. Common

causes of upper airway obstructions are laryngomalacia, epiglottitis (supraglottitis), croup

(laryngotracheitis), and bacterial tracheitis.2

Epiglottitis presents more commonly in children ages 2 to 6 years, although it can affect

children and adults of any age. Young children typically present with rapid onset of respiratory

distress, high temperatures, a muffled voice, drooling, dysphagia, and stridor. However, cough

and hoarseness are not characteristically present. Children commonly sit still in the hallmark

“tripod” position to increase the caliber of the supraglottic airway. These patients appear very

uncomfortable and are often anxious.2,3

Laryngotracheitis (Croup) typically presents in children ages 6 to 36 months. Younger

children typically present with hoarseness and a barking cough, whereas signs of lower airway
disease are rarely seen. The characteristic cough is uniformly present, and lack of this symptom

should suggest a different diagnosis. In older children, hoarseness may be significant and may be

the predominant symptom. Stridor may manifest only after significant disease progression

narrows the glottic and subglottic airway significantly. Children with croup rarely exhibit the

marked respiratory failure, fever, and anxiety seen in epiglottitis and bacterial tracheitis.4,5

Bacterial tracheitis is usually seen in otherwise healthy children between the ages of 3

months and 6 years. Children younger than 3 years may have more severe symptoms, in part due

to smaller airway diameter. Children with bacterial tracheitis may present to the emergency

department with recent onset of cough and progressive stridor suggestive of upper airway

obstruction.6

This patient is two months old baby, and based on his age, our history taking, and

physical examination, the suspicion of diagnosis on this patient is laryngomalacia.

Laryngomalacia refers to the prolapse of supraglottic structures into the laryngeal airway on

inspiration. It is the most common congenital laryngeal anomaly and the most frequent

congenital cause of stridor in infants.7 (Level of evidence 3A) Patients typically present with

inspiratory stridor during the first few weeks of life, which usually worsens over the first 6

months of life and peaks in severity at about 6 months of age, followed by gradual improvement

in the symptoms, with most patients being resolved of symptomps by age 18 to 24 months.8

(Level of evidence 2A). The stridor is typically worse with agitation, crying, feeding, and supine

positioning. In addition to stridor, patients with laryngomalacia can have feeding difficulty,

failure to thrive, dysphagia, aspiration, apnea, cyanosis, reflux, obstructive sleep apnea, and

pulmonary hypertension in severe cases. Gastroesophageal reflux disease (GERD) is a well-


established comorbidity of laryngomalacia and many patients with laryngomalacia have

symptoms of and are treated for reflux.2,9 (Level of evidence 2B).

The etiology of laryngomalacia is likely multifactorial, with anatomic, inflammatory, and

neurologic factors all contributing to the disease process. Anatomic factors include abnormal

prolapse of laryngeal tissue, sometimes associated with tissue redundancy, leading to

supraglottic obstruction.The cartilaginous theory suggests that immaturity or weakness of the

laryngeal cartilage contributes to the obstruction.10

Laryngomalacia has a disease spectrum that can be divided into mild, moderate, and

severe categories. These categories are not based on the quantity of stridor but rather by the

associated feeding and obstructive symptoms. Mild laryngomalacia that approximately 40% of

infants present with inspiratory stridor and the occasional feeding-associated symptoms of

cough, choking, and regurgitation. Meanwhile moderate laryngomalacia has presentation up to

40%. Those in this category present with the typical stridor but are described by their parents as

fussy and hard to feed. They have frequent feeding-associated symptoms of cough, choking,

regurgitation, and cyanosis during feeding. Twenty percent of infants have severe

laryngomalacia at the time of presentation to a health care provider. They present with

inspiratory stridor and other associated symptoms that include recurrent cyanosis, apneic pauses,

feeding difficulty, aspiration, and failure to thrive. Suprasternal and subcostal retractions can

lead to pectus excavatum. As discussed below those with severe disease will likely require

surgical intervention in addition to acid suppression treatment for management. The mainstay for

surgical intervention is supraglottoplasty whereby the obstructing collapsing tissue is removed

through an endoscope. Tracheotomy is rarely indicated and is reserved for supraglottoplasty

failures and those with multiple medical comorbidities.10–12


This patient has the been diagnosed as failure to thrive due to his weight increment level

was below -2 SD. We assumed that those condition present as the result of difficulty of feeding

due to the anatomy position of the infant’s larynx, which is relatively high in the neck, and lead

the condition of difficulty coordinating his feeding and breathing as of he needs to take frequent

breaks during feeding. Also, there was increased of metabolic demand on coordinating feeding

and breathing against the obstruction results in weight loss and lead to failure to thrive.12

The diagnosis of laryngomalacia is suspected by the typical clinical history but is

confirmed by flexible fiberoptic laryngoscopy in an awake infant to assess for prolapse of

supraglottic structures on inspiration. Plain radiography of the neck can provide information

regarding other potential causes of stridor. In a child with recent onset of stridor, upper airway

radiography may identify inflammatory or infectious causes of upper airway obstruction, such as

croup, epiglottitis, and bacterial tracheitis.2,12

Classifications of the various types of laryngomalacia according to the result of flexible

fiberoptic laryngoscopy have been proposed. Holinger’s classification is indicated below13 :

Type 1: anterior prolapse of the arytenoid and corniculate cartilages

Type 2: tubular epiglottis which curls on itself, often associated with type 1

Type 3: anteromedial collapse of the arytenoids

Type 4: posterior prolapse of the epiglottis

Type 5: short aryepiglottic folds.

1. Mandal A, Kabra SK, Lodha R. Upper Airway Obstruction in Children. 2015;

2. Virbalas J, Smith L. Upper Airway Obstruction. 2019;


3. Depuydt S, Nauwynck M, Bourgeois M, Mulier JP. Acute epiglottitis in children: A

review following an atypical case. Acta Anaesthesiol Belg. 2003;54(3):237–41.

4. SA Child Health Clinical Network. Acute croup in children. 2013;185(15):1–13.

5. Zoorob R, Sidani M, Murray J. Croup : An Overview. Am Fam Physician.

2011;83(9):1067–73.

6. Al-Mutairi B, Kirk V. Bacterial tracheitis in children: Approach to diagnosis and

treatment. Paediatr Child Health (Oxford). 2004;9(1):25–30.

7. Mandour Z, Abdel-fattah HM. Laryngomalacia : Diagnosis and Management. 2011;(May

2015).

8. Isaac A, Zhang H, Soon SR, Campbell S, El-Hakim H. A systematic review of the

evidence on spontaneous resolution of laryngomalacia and its symptoms. Int J Pediatr

Otorhinolaryngol. 2016;83:78–83.

9. Hartl TT, Chadha NK. A Systematic Review of Laryngomalacia and Acid Reflux. 2012;

10. Thompson DM. Laryngomalacia: factors that influence disease severity and outcomes of

management. Curr Opin Otolaryngol Head Neck Surg. 2010 Dec 1;18(6):564–70.

11. Thompson DM. Abnormal Sensorimotor Integrative Function of the Larynx in Congenital

Laryngomalacia : A New Theory of Etiology. 2007;(June):1–33.

12. Landry AM, Thompson DM. Laryngomalacia : Disease Presentation , Spectrum , and

Management. 2012;2012.

13. Ayari S, Aubertin G, Girschig H, Abbeele T Van Den, Mondain M. Pathophysiology and

diagnostic approach to laryngomalacia in infants. Eur Ann Otorhinolaryngol Head Neck

Dis. 2012;129(5):257–63.

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