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Laryngotracheobronchitis and epiglottitis.

Upper airway disorders are common causes of illness among the pediatric population. Two such pulmonary conditions frequently seen among this group of patients are epiglottitis and laryngotracheobronchitis. In this article, the etiology, pathophysiology, signs and symptoms, diagnosis, and treatment of these two upper airway disorders will be presented.

Epiglottitis -- The prefix "epi-" means upon or over. The word glottis refers to the opening between the vocal cords in the larynx. Therefore, the meaning of the term epiglottis is upon or over the glottis. The epiglottis, one of the nine cartilaginous structures that comprise the larynx, serves to protect the laryngeal inlet by folding over the glottis during swallowing. This action prevents the aspiration of solid food and liquid. Epiglottitis, occasionally called acute supraglottitis, essentially results from a swollen and distorted epiglottis, producing some degree of upper airway obstruction.

Etiology -- Epiglottitis is most commonly caused by the bacterium Hemophilus influenzae, type b. This infection tends to occur among children ranging from 2-6 years of age. Occasionally, streptococci bacteria are involved when epiglottitis affects older children and adults. Children less than 2 rarely are afflicted with this disorder. Males appear to contract this upper respiratory infectious disease four times greater than females. The overall incidence of epiglottitis has progressively declined since the 1980s because of the availability of the Hemophilus influenzae, type b vaccine.

Pathophysiology -- Epiglottitis is an inflammation of the epiglottis. However, other structures of the laryngeal inlet become inflamed as well. These structures include the aryepiglottic folds and the loose connective tissues in the pre-epiglottic and para-epiglottic spaces; hence, the alternate term acute supraglottitis.


The edema and hyperemia in this supraglottic region produce airway obstruction which can be partial or complete. As the airway obstruction becomes more severe, the respiratory distress becomes greater. Because of the proximity of the supraglottic region to the esophagus, the inflamed epiglottis and the surrounding structures cause the patient to experience difficulty swallowing, i.e., dysphagia. When the inflammation becomes extensive, the epiglottis and the aryepiglottic folds sometimes invaginate through the glottic opening, as the patient generates greater negative pressures with more forceful inspiratory efforts. The onset of these events is sudden and their progression is rapid. Epiglottitis quickly becomes life-threatening. Therefore, epiglottitis is a respiratory emergency requiring swift action to establish a patent airway.

Signs & Symptoms -- The patient will present with a high fever (38[degrees] to 40[degrees]C), severe sore throat, hoarseness, and dysphagia. Because of the difficulty swallowing, the child will drool. When seated, the patient will often assume an erect, forward-leaning posture with the neck craned in an attempt to gain a mechanical advantage to overcome dyspnea. This posture is called the tripod position. The airway obstruction results in forceful inspiratory efforts which, in turn, sometimes produce stridor. However, stridor is a rare presentation in epiglottitis. Observation of the child's thorax may demonstrate suprasternal retractions, while the nose may reveal nasal flaring. When the airway obstruction is severe, cyanosis will develop.

Diagnosis -- Epiglottitis is diagnosed via history, signs and symptoms, and radiography of the neck. When epiglottitis is present, a lateral neck radiography will show an enlarged epiglottis (described as the "thumb sign") and a ballooning hypopharynx. However, treatment of epiglottitis must not be delayed for the sake of obtaining a lateral neck x-ray. Even though an x-ray confirms this condition, a patient experiencing respiratory failure must receive an artificial airway immediately. Intubation must not be postponed.

Treatment -- Before an artificial airway is inserted, the child must be given humidified oxygen. The patient may undergo either nasal or oral endotracheal intubation. However, if neither of these airways can be inserted, a tracheostomy must be performed.

Visualization of the glottic area via direct laryngoscopy is highly hazardous; therefore, this course of action should only be performed as part of the intubation procedure. Probing or manipulating the epiglottis with a tongue depressor or laryngoscope can cause the obstruction to worsen, and possibly close the airway. Endotracheal intubation must be performed by the most skilled person available because the supraglottic edema creates an extremely narrow airway. So, inserting an endotracheal tube through such a small opening and under such emergent circumstances, demands the most accomplished intubator.

After an airway has been inserted, the child should be sedated to reduce anxiety and to avoid inadvertent extubation. Depending on the degree of sedation required, the patient may need mechanical ventilation. Generally, mechanical ventilation of children with epiglottitis entails low inflation pressures, low ventilatory rates, and low FIO2s because these patients seldom have any complicating lung disease. During this time, the patient receives appropriate antibiotic therapy to eradicate the offending microorganism. The antibiotics ampicillin and chloramphenicol are frequently administered because they are effective against Hemophilus influenzae.

Mechanical ventilation is usually needed for only 24 to 48 hours. The decision to extubate is made when the supraglottic edema has resolved. Following extubation, the child continues with the course of antibiotics already instituted.


In contrast to epiglottitis, laryngotracheobronchitis (LTB) is classified as subglottic airway obstruction. LTB involves the larynx (below the glottis), trachea, and bronchi. The inflammation associated with this condition produces varying degrees of airway obstruction. LTB is also call croup, viral croup, and spasmodic croup. LTB generally results from an infection with parainfluenza viruses. Other viruses involved include either influenza viruses, respiratory syncytial virus (RSV), or paramyxovirus. The most common cause of LTB is parainfluenza virus type 1. The only bacterium known to cause LTB is Hemophilus influenzae. These viral infections tend to occur during the late fall and winter, affecting children six months to three years old. Males seem to experience LTB twice as much as females.

The subglottic region of the larynx becomes inflamed. This is problematic in young children particularly because the area of the larynx in the vicinity of the cricoid cartilage is the narrowest portion of the airway. At the same time, the trachea and bronchi are similarly involved. The mucosal edema and hyperemia present in these areas contribute to the respiratory distress experienced by children with LTB, as the airway resistance through these airways increases.

LTB characteristically develops slowly. The patient usually presents with what appears to be a common cold, i.e., cough, nasal discharge, and low-grade fever. Then, approximately two to three days later, the patient develops a dry, brassy, barking cough. Stridor is likewise audible. This typical feature of LTB results from forceful inspiratory efforts generated by the patient to move air passed the inflamed larynx, trachea, and bronchi. An accumulation of mucus caused by the airway narrowing in this region is believed to contribute to the development of the stridor.

Other clinical manifestations include hoarseness, restlessness, rapid ventilatory rate, use of accessory muscles of ventilation, intercostal and suprasternal retractions, and nasal flaring. In more severe cases the child will appear cyanotic because of marked desaturation.

Diagnosis -- The diagnosis is based on the patient's history, signs, symptoms, and x-ray findings. An A-P or lateral radiograph of the neck classically demonstrates subglottic narrowing. Ordinarily, the subglottic region reveals a more rounded air column. However, in LTB the air column in the subglottic area assumes a pointed, or cone-shaped, configuration. This radiographic presentation is called the "steeple sign." Direct laryngoscopy is appropriate to perform if the patient is not experiencing acute respiratory distress.

Treatment -- Because LTB patients tend to be restless, efforts must be made to calm the patient. Anxiety and distress will produce an increased work of breathing and increase oxygen demand. Supplemental oxygen must be administered to relieve hypoxemia.

In mild cases of LTB humidification (cool mist) may reduce the airway narrowing. Sometimes exposure to the cold night air may diminish symptoms as well. Hearing accounts from parents, who brought their child out of the house and into the cold night for a trip to the emergency room only to witness their child improve en route, is not that uncommon.

In addition to the administration of unheated aerosol therapy with supplemental oxygen, nebulized racemic epinepherine is often provided. Racemic epinepherine is a potent alpha adrenergic medication, causing vasoconstriction of the respiratory mucosa and decreasing the subglottic edema. Corticosteroids are given to also help reduce the subglottic edema. Their action is directed toward suppressing local inflammation. The anti-inflammatory effect of corticosteroids is based on their suppressing the migration of polymorphonuclear leukocytes and reducing capillary permeability.

Hydration with I-V fluids is an important consideration because some of the patients have had preceding illness for a few days.

Many children having LTB respond favorably to the prescribed regimen, and may be discharged from the hospital after two to four hours of observation following treatment. The need for intubation and mechanical ventilation in LTB is infrequent, and is reserved for those patients who develop respiratory failure despite treatment.

by Bill Wojciechowski, MS, RRT
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Author:Wojciechowski, Bill
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Geographic Code:1USA
Date:Jan 1, 2004
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