Except in patients with a tracheostomy or an endotracheal tube, bacterial tracheitis is an uncommon infectious cause of acute upper airway obstruction. It is more prevalent than acute epiglottitis among children who have received Haemophilus influenzae type b (Hib) vaccine.
Patients may present with crouplike symptoms, such as barking cough, stridor, and fever; however, patients with bacterial tracheitis do not respond to standard croup therapy (racemic epinephrine) and instead require treatment with antibiotics and may experience acute respiratory decompensation.[1, 2, 3, 4] Radiographs may reveal subglottic narrowing on anteroposterior views (Steeple sign). See the image below.
View Image
Steeple sign.
Signs and symptoms
In the classic presentation, patients present acutely with fevers, toxic appearance, stridor, tachypnea, and respiratory distress. Cough is frequent and not painful.
See Presentation for more detail.
Diagnosis
Laboratory studies
Obtain bacterial culture and Gram staining of tracheal secretions and blood cultures in patients with suspected bacterial tracheitis.
Imaging studies
Radiography of the neck may be indicated.
See Workup for more detail.
Management
Maintenance of an adequate airway is of primary importance. Once the airway is stabilized, obtain intravenous access for initiation of antibiotics.
Tracheostomy is rarely necessary unless injury or trauma to the airway has caused scarring and documented narrowing of the airway.
See Treatment and Medication for more detail.
Patient education
Advise patients and their family to keep immunizations up-to-date.
Bacterial tracheitis is a diffuse inflammatory process of the larynx, trachea, and bronchi with adherent or semiadherent mucopurulent membranes within the trachea. The major site of disease is at the cricoid cartilage level, the narrowest part of the trachea. Acute airway obstruction may develop secondary to subglottic edema and sloughing of epithelial lining or accumulation of mucopurulent membrane within the trachea. Signs and symptoms are usually intermediate between those of epiglottitis and croup.[5, 6]
Bacterial tracheitis may be more common in the pediatric patient because of the size and shape of the subglottic airway. The subglottis is the narrowest portion of the pediatric airway, assuming a funnel-shaped internal dimension. In this smaller airway, relatively little edema can significantly reduce the diameter of the pediatric airway, increasing resistance to airflow and work of breathing. With appropriate airway support and antibiotics, most patients improve within 5 days.
Although the pathogenesis of bacterial tracheitis is unclear, mucosal damage or impairment of local immune mechanisms due to a preceding viral infection, an injury to the trachea from recent intubation, or trauma may predispose the airway to invasive infection with common pyogenic organisms.
S aureus: Community-associated methicillin-resistant S aureus (CA-MRSA) has emerged as an important agent in the United States; this could result in a greater frequency of MRSA strains that cause tracheitis.
S pyogenes, Streptococcus pneumoniae, and other alpha hemolytic streptococcal species
Moraxella catarrhalis: Reports suggest it is a leading cause of bacterial tracheitis and associated with increased intubation.
Haemophilus influenzae type b (Hib): This cause is less common since the introduction of the Hib vaccine.
Tan and Manoukian reported that 500 children were hospitalized for croup at one pediatric hospital over a 32-month period.[10] Approximately 98% had viral croup, and 2% had bacterial tracheitis. Cases usually occur in the fall or winter months, mimicking the epidemiology of viral croup.
A study that described the frequency and severity of complications in hospitalized children younger than 18 years with seasonal influenza (during 2003-2009) and 2009 pandemic influenza A(H1N1) (during 2009-2010) reported that out of 7293 children hospitalized with influenza, less than 2% had complications from tracheitis. However, along with other rare complications, tracheitis was associated with a median hospitalization duration of more than 6 days, with 48%-70% of children requiring intensive care.[11]
International statistics
Bacterial tracheitis remains a rare condition, with an estimated incidence of approximately 0.1 cases per 100,000 children per year.[12]
Sex- and age-related demographics
In most epidemiologic studies, male cases are preponderant. Gallagher et al reported a male-to-female predominance of 2:1.[13]
Bacterial tracheitis may occur in any pediatric age group. Gallagher et al reported 161 cases of patients younger than 16 years.[13] The age range was from 3 weeks to 16 years, with a mean age of 4 years. This is in contrast to viral laryngotracheobronchitis, which occurs in patients aged 6 months to 3 years.
Once the patient is past the acute phase, complete recovery is expected.
Morbidity/mortality
The predominant morbidity and mortality is related to the potential for acute upper airway obstruction and induced hypoxic insults. The mortality rate has been estimated at 4-20%. In the acute phase, patients generally do well if the airway is adequately managed and if antibiotic therapy is promptly initiated.
Complications
The following complications have been reported:
Pneumonia - Reported in 19-60% of cases (guidelines for avoiding healthcare-associated pneumonia have been established[14] )
Septicemia
Toxic shock
Adult respiratory distress syndrome (ARDS)
Endotracheal tube complications
Plugging, accidental extubation
Postextubation stridor, subglottic stenosis
Anoxic encephalopathy
Cardiorespiratory arrest
A retrospective study by Gross et al, in which four patients who received antibiotic treatment for bacterial laryngotracheitis showed improvement in presumed iatrogenic laryngotracheal stenosis, suggested that airway bacterial growth is significantly involved in adult postintubation airway injury. The patients had a history of intubation and/or tracheostomy, with complete resolution of upper airway obstruction seen in three of the patients after laryngotracheitis treatment and significant improvement of airway status seen in the fourth.[15]
Symptoms of bacterial tracheitis may be intermediately between those of epiglottitis and croup. Presentation is either acute or subacute.
In the classic presentation patients present acutely with fevers, toxic appearance, stridor, tachypnea, respiratory distress, and high WBC counts. Cough is frequent and not painful.
In a study by Salamone et al, a significant subset of older children (mean age, 8 y) did not have severe clinical symptoms.[16]
The prodrome is usually an upper respiratory infection, followed by progression to higher fever, cough, inspiratory stridor, and a variable degree of respiratory distress.[8]
Patients may acutely decompensate with worsening respiratory distress due to airway obstruction from a purulent membrane that has loosened.
Patients have been reported to present with symptoms and signs of bacterial tracheitis and multiorgan failure due to exotoxin-producing strains of Staphylococcus aureus or Streptococcus pyogenes in the trachea.
A high index of suspicion for bacterial tracheitis is needed in children with viral croup–like symptoms who do not respond to standard croup treatment or clinically worsen.
A study by Patnaik et al found that among pediatric patients aged between 5 and 18 years, bacterial tracheitis was one of the most common causes of stridor.[17]
Treatment of bacterial tracheitis consists of the following:
Airway
Maintenance of an adequate airway is of primary importance.[18]
Avoid agitating the child. If the patient's respiratory status deteriorates, it is usually because of movement of the membrane, and bag-valve-mask ventilation should be effective.
If intubation is required, use an endotracheal tube 0.5-1 size smaller than expected in order to minimize trauma in the inflamed subglottic area. Frequent suctioning and high air humidity is necessary to maintain endotracheal tube patency; therefore, use the most appropriate-sized tube (without causing trauma). Most patients (57-100%) require eventual intubation.
Intravenous access and medication
Once the airway is stabilized, obtain intravenous access for initiation of antibiotics.
Antibiotic regimens have traditionally included a third-generation cephalosporin (eg, cefotaxime, ceftriaxone) and a penicillinase-resistant penicillin (eg, oxacillin, nafcillin). More recently, clindamycin (40 mg/kg/d intravenously [IV], divided every 8 h) has been used instead of penicillinase-resistant penicillin against community acquired–methicillin-resistant S aureus (CA-MRSA) in places where resistance rates of CA-MRSA to clindamycin is low.[19]
Vancomycin (45 mg/kg/d IV, divided every 8 h), with or without clindamycin, should be started in patients who appear toxic or have multiorgan involvement or if MRSA is prevalent in the community.
Further outpatient care
Patient should complete an appropriate course (usually 10 d) of oral antibiotics.
Tracheostomy is rarely necessary unless injury or trauma to the airway has caused scarring and documented narrowing of the airway. Tracheostomy is necessary if the patient has failed extubations despite appropriate medical management or if intubation is prolonged. Pulmonary toilet is potentially better with tracheostomy.
Further inpatient care
Consider extubation when bacterial tracheitis appears to be resolving, especially with decreased secretions suctioned from the endotracheal tube.
Transfer
Transfer is required for patients in respiratory distress, patients in need of a pediatric intensive care unit, and patients who need a pediatric-sized bronchoscope.
Clinical Context:
May be used in severe cases or in cases with a history of allergies instead of oxacillin for coverage of gram-positive organisms (eg, S aureus, S pyogenes).
Clinical Context:
Use in combination with chloramphenicol in patients who are allergic to penicillin. Clindamycin in combination with cefuroxime is an acceptable regimen for patients who are not allergic.
Empiric antimicrobial therapy in bacterial tracheitis must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
What is bacterial tracheitis?What is the pathophysiology of bacterial tracheitis?What is the prevalence of bacterial tracheitis in the US?What is the global prevalence of bacterial tracheitis?What is the morbidity of bacterial tracheitis?What is the sexual predilection of bacterial tracheitis?Which age groups have the highest prevalence of bacterial tracheitis?Which clinical history findings are characteristic of bacterial tracheitis?Which physical findings are characteristic of bacterial tracheitis?What causes bacterial tracheitis?What are the differential diagnoses for Bacterial Tracheitis?What is the role of lab testing in the workup of bacterial tracheitis?What is the role of radiography in the workup of bacterial tracheitis?What is the role of laryngotracheobronchoscopy in the workup of bacterial tracheitis?How is bacterial tracheitis treated?What is the role of surgery in the treatment of bacterial tracheitis?Which specialist consultations are beneficial to patients with bacterial tracheitis?Which medications in the drug class Antibiotic agents are used in the treatment of Bacterial Tracheitis?
Sujatha Rajan, MD, Assistant Professor of Pediatrics, Albert Einstein School of Medicine; Consulting Staff, Department of Pediatrics, Division of Pediatric Infectious Diseases, Schneider Children's Hospital, North Shore-Long Island Jewish Health System
Disclosure: Nothing to disclose.
Coauthor(s)
Sunil K Sood, MBBS, , MD, Professor of Clinical Pediatrics, Department of Pediatrics, Albert Einstein College of Medicine; Chief, Pediatric Infectious Diseases, Firm Director, Pediatric Unit, Schneider Children's Hospital at North Shore, North Shore University Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Mary L Windle, PharmD, Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University
Disclosure: Received research grant from: Pfizer;GlaxoSmithKline;AstraZeneca;Merck;American Academy of Pediatrics, Novavax, Regeneron, Diassess, Actelion<br/>Received income in an amount equal to or greater than $250 from: Sanofi Pasteur.
Chief Editor
Russell W Steele, MD, Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation
Disclosure: Nothing to disclose.
Additional Contributors
Kathryn Clark Emery, MD, Associate Professor, Department of Pediatrics, University of Colorado Health Sciences Center; Consulting Staff, Department of Emergency Medicine, Children's Hospital of Denver