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Tracheitis

Tracheitis is an inflammation of the trachea, the cartilaginous tube that connects the larynx to the bronchi and serves as the primary conduit for air to the lungs, most commonly resulting from infectious agents such as viruses or bacteria.^[1] This condition predominantly affects young children due to their narrower tracheal diameter, which predisposes them to airway obstruction, though it can occur in adults as well, often in association with underlying risk factors like intubation or immunosuppression.^[2] Acute infectious tracheitis typically presents as a self-limited process in viral cases but can become life-threatening in bacterial forms, requiring prompt medical intervention to prevent complications such as respiratory failure.^[3] Bacterial tracheitis, the more severe variant, usually develops as a secondary infection following an initial viral upper respiratory tract infection, with Staphylococcus aureus being the most frequent pathogen, alongside Streptococcus pneumoniae and methicillin-resistant Staphylococcus aureus (MRSA).^[2] Symptoms often include a high fever, stridor (a high-pitched breathing sound), a deep barking cough resembling croup, and progressive respiratory distress due to the accumulation of thick, purulent secretions in the trachea.^[3] Viral tracheitis, by contrast, tends to be milder and typically self-resolving within a few days to a week, commonly linked to pathogens like influenza or respiratory syncytial virus (RSV), though it may still cause significant inflammation extending to adjacent airways.^[1] Diagnosis relies on clinical evaluation, including history of recent viral illness and physical signs like intercostal retractions, supported by imaging such as neck X-rays showing subglottic narrowing (the "steeple sign") and direct visualization via laryngoscopy or bronchoscopy to identify exudates.^[2] Treatment for bacterial cases involves urgent airway management, potentially including endotracheal intubation in up to 75% of pediatric patients, along with broad-spectrum intravenous antibiotics such as ceftriaxone combined with vancomycin for 7 to 14 days.^[2] With early intervention, the prognosis is favorable, though untreated cases carry a mortality risk of 2-3% due to potential complications like pneumonia, sepsis, or tracheal stenosis.^[2]

Background

Definition and Classification

Tracheitis refers to inflammation of the trachea, the cartilaginous tube that connects the larynx to the bronchi and serves as the primary conduit for air to the lungs. This condition often arises from infectious agents, leading to mucosal edema, exudative secretions, and potential airway obstruction that compromises breathing. While it can affect individuals of any age, tracheitis is particularly concerning in children due to the narrower diameter of their airways.^[2] Tracheitis is broadly classified based on etiology into infectious and non-infectious forms, with infectious types further subdivided by causative pathogen. Bacterial tracheitis represents one of the most severe variants, also termed pseudomembranous or exudative tracheitis, characterized by thick, adherent mucopurulent membranes lining the tracheal walls, often as a secondary complication following a viral upper respiratory infection. Viral tracheitis, in contrast, is typically milder and more common, manifesting as part of broader acute viral respiratory illnesses, such as those caused by influenza or respiratory syncytial virus, without the formation of dense pseudomembranes. Non-infectious tracheitis encompasses cases triggered by mechanical or chemical insults, including endotracheal intubation, inhalational trauma from irritants like smoke, or direct injury to the tracheal mucosa.^[4]^[5] The recognition of bacterial tracheitis as a distinct clinical entity dates to 1979, when it was described in detail as a life-threatening airway infection separate from conditions like croup or epiglottitis, with which it was previously conflated due to overlapping symptoms of stridor and respiratory distress. Prior reports of similar presentations existed in the early 20th century, but the 1979 characterization highlighted its bacterial etiology and need for prompt intervention.^[6] Anatomically, tracheitis predominantly involves the subglottic region of the trachea—the area just below the vocal cords—in pediatric patients, where inflammation and exudate accumulation can rapidly narrow the already limited airway space. In more extensive cases, the process may extend superiorly to the larynx or inferiorly to the bronchi, exacerbating obstruction and complicating management.^[2]

Epidemiology

Tracheitis, particularly its bacterial form, is a rare condition with an estimated annual incidence of 0.1 to 1 case per 100,000 children in developed countries.^[2] The bacterial variant accounts for approximately 0.4 cases per 1,000 pediatric hospital admissions.^[7] This low overall prevalence underscores its status as an uncommon but potentially life-threatening complication of upper respiratory infections. Demographically, bacterial tracheitis predominantly affects young children, with most cases occurring between 1 month and 12 years of age, though the peak incidence is observed in those aged 3 to 8 years, with a mean age at diagnosis of around 5 years.^[2]^[8] It is rare in adults, typically arising only in the context of immunocompromise, intubation, or underlying chronic conditions.^[4] There is no significant gender bias in its occurrence.^[4] Seasonally, cases are more frequent during the fall and winter months, aligning with peaks in viral epidemics such as those caused by influenza or respiratory syncytial virus, which may predispose to secondary bacterial involvement.^[9] Geographically, incidence varies by region.^[2] Historically, the incidence of bacterial tracheitis has declined since the introduction of the Haemophilus influenzae type b (Hib) vaccine in the 1980s, which reduced cases previously misdiagnosed or conflated with epiglottitis.^[9]^[10]

Pathophysiology and Etiology

Pathophysiological Mechanisms

Tracheitis typically begins as a secondary bacterial infection following a viral upper respiratory tract infection that damages the tracheal epithelium, impairing its protective barrier and facilitating opportunistic bacterial invasion.^[2]^[7] This initial epithelial disruption allows pathogens to adhere and proliferate, triggering an intense local inflammatory response characterized by the release of bacterial toxins and exotoxins. These mediators induce significant mucosal edema and the formation of thick, purulent exudate, often manifesting as a pseudomembrane within the trachea, which contributes to partial or complete airway obstruction.^[2]^[11] As the infection progresses, neutrophil infiltration dominates the inflammatory cascade, leading to mucosal ulceration and sloughing of the tracheal lining, with microscopic evidence of neutrophilia in secretions confirming the acute immune activation.^[7] In severe cases, this process extends beyond the trachea to involve the bronchi, resulting in tracheobronchitis, or upward to the larynx, exacerbating the inflammatory burden.^[2]^[11] The resultant reduction in tracheal diameter from swelling and exudate accumulation markedly increases airway resistance, promoting turbulent airflow and the characteristic stridor observed in affected patients.^[2] Unique to the bacterial form of tracheitis, adherent bacterial biofilms and tenacious pus plugs form within the airway, resisting clearance by mucociliary action or coughing and thereby perpetuating obstruction and inflammation.^[11]

Causes and Risk Factors

Tracheitis is primarily an infectious condition, with bacterial infections being the most common etiology in acute cases, particularly in children. The predominant bacterial pathogen is Staphylococcus aureus, including methicillin-resistant strains (MRSA), followed by Streptococcus pneumoniae, Streptococcus pyogenes, Moraxella catarrhalis, and Haemophilus influenzae (both type B and non-typeable strains).^[2]^[7] Viral infections often serve as precursors, with parainfluenza viruses (types 1 and 2), influenza A and B, and respiratory syncytial virus (RSV) damaging the tracheal mucosa and facilitating secondary bacterial invasion; in one study, viral co-infections were identified in 72% of cases.^[2]^[7]^[11] Non-infectious causes are less common but include mechanical trauma from prolonged endotracheal intubation or tracheostomy, which can lead to mucosal injury and colonization by pathogens.^[2]^[12] In adults, radiation therapy for malignancies, often in patients undergoing concurrent chemotherapy, can induce pseudomembranous tracheobronchitis through direct tissue damage.^[13] Key risk factors for tracheitis include a recent viral upper respiratory infection, which precedes the majority of bacterial cases by altering local immunity.^[2]^[7] Young age, particularly under 6 years with peak incidence at 3–8 years, increases susceptibility due to the narrower tracheal diameter.^[2]^[7] Immunocompromised states, such as HIV infection or ongoing chemotherapy, heighten the risk of severe or opportunistic infections, including fungal etiologies like Aspergillus species.^[11] Lack of vaccination against Haemophilus influenzae type B (Hib) also contributes, as immunization has reduced incidence of this pathogen.^[7] Tracheitis itself is not directly contagious, but the bacterial form often arises from community-acquired viral spread during winter epidemics, with nosocomial transmission possible in ventilated patients via colonized equipment.^[11]

Clinical Presentation

Signs and Symptoms

Tracheitis typically presents with an acute onset of high fever, often exceeding 39°C (102°F), accompanied by a deep, barking cough that is productive and painful, distinguishing it from the typically non-productive cough in viral croup.^[2]^[14] Hoarseness and a high-pitched inspiratory stridor are prominent, reflecting inflammation and narrowing of the trachea, with progressive respiratory distress manifesting as tachypnea, retractions, and dyspnea.^[3]^[1] However, atypical presentations have been reported, particularly in recent cases as of 2024, where patients exhibit primarily stridor and rapidly worsening respiratory distress without high fever or a toxic appearance.^[10] Systemic signs include a toxic or septic appearance, marked by lethargy and irritability, particularly in children who may refuse to lie flat due to worsening distress and exhibit dehydration from poor oral intake secondary to painful swallowing.^[2] Symptoms often worsen 2-5 days following an initial viral upper respiratory illness, with biphasic stridor in severe cases signaling subglottic extension of the inflammation.^[14]^[1] In adults, presentations vary with more chronic, productive cough and wheezing, while stridor is less common owing to the larger airway diameter, though respiratory distress can still progress rapidly in immunocompromised individuals.^[1] Red flags for imminent airway compromise include rapid deterioration to cyanosis or apnea, often within hours of acute worsening.^[2] These manifestations overlap with but are more toxic than those of croup or epiglottitis.^[14]

Differential Diagnosis

The differential diagnosis of tracheitis primarily involves other causes of upper airway obstruction and inflammation, particularly in children where the condition is most common. Key mimics include croup (viral laryngotracheobronchitis), which presents with a milder course, barking cough, and stridor that typically responds to corticosteroids and nebulized epinephrine, unlike the high fever, toxic appearance, and purulent tracheal secretions observed in bacterial tracheitis.^[15]^[16] Epiglottitis, often historically linked to Haemophilus influenzae type b, is distinguished by rapid progression, drooling, dysphagia, absence of cough, and a preference for sitting forward, with involvement of the supraglottic structures rather than the subglottic trachea.^[15]^[2] Foreign body aspiration should be considered in cases of sudden onset respiratory distress, unilateral wheezing, or asymmetric breath sounds, often with a history of choking, contrasting the more gradual progression and bilateral symptoms of tracheitis.^[15]^[16] Other differentials encompass retropharyngeal abscess, characterized by neck swelling, stiffness, and trismus due to deep neck infection; anaphylaxis, marked by urticaria, angioedema, and a clear history of allergen exposure; and asthma exacerbation, featuring prominent wheezing, reversible airflow obstruction, and a personal or family history of atopy without high fever or systemic toxicity.^[15]^[2] Distinguishing tracheitis relies on clinical features such as persistent high fever (>39°C), leukocytosis, and visualization of thick purulent secretions via laryngoscopy, which are absent in viral croup and epiglottitis.^[15] Age-specific considerations are important: in neonates, congenital anomalies like tracheal stenosis or laryngomalacia may present with stridor and respiratory distress from birth, necessitating imaging to differentiate from infectious tracheitis.^[2]^[17] In adults, where tracheitis is rarer and often secondary to intubation or immunosuppression, differentials include gastroesophageal reflux disease (GERD), which can cause chronic tracheal inflammation, cough, stridor, and dyspnea through microaspiration without infectious signs, as well as tracheal tumors such as squamous cell carcinoma or adenoid cystic carcinoma leading to obstructive symptoms.^[2]^[18]

Diagnosis

Clinical Evaluation

The clinical evaluation of suspected tracheitis begins with a thorough history to identify predisposing factors and recent exposures that may contribute to the condition. A history of recent viral upper respiratory illness, such as croup, influenza, or parainfluenza infection, is common and often precedes bacterial superinfection in affected children.^[2] Vaccination status should be reviewed, particularly for Haemophilus influenzae type b (Hib) and pneumococcal vaccines, as widespread immunization has significantly reduced the incidence of tracheitis caused by these pathogens.^[7] Inquiries into potential exposures, including contact with ill individuals during winter viral epidemics or environmental irritants, are essential, alongside assessment for underlying immunocompromise or a history of recent intubation, both of which elevate the risk of bacterial tracheitis.^[2] Symptoms such as persistent cough and increasing respiratory distress further direct the focus of this initial assessment.^[19] Physical examination emphasizes careful evaluation of vital signs and airway patency to avoid exacerbating the condition. Vital signs typically reveal fever, tachycardia, and tachypnea, reflecting systemic inflammation and compensatory respiratory effort.^[19] Airway assessment may show inspiratory stridor in 54% to 95% of cases, along with intercostal retractions, nasal flaring, and cyanosis in severe presentations; tracheal tenderness and a toxic appearance are also frequent findings.^[7] To prevent airway spasm, the examination should be conducted calmly, minimizing agitation of the patient, especially in children.^[2] Hoarseness and a productive brassy cough may accompany these signs, helping to distinguish from milder viral etiologies where the cough is typically nonproductive.^[19] Notably, patients with bacterial tracheitis typically show little to no improvement with nebulized racemic epinephrine or systemic corticosteroids, unlike those with viral croup, prompting further diagnostic consideration.^[2] Severity is quantified using adapted clinical scoring tools, such as the Westley Croup Score, to objectively measure airway obstruction and guide immediate management decisions. This score evaluates key features including the degree of stridor at rest, presence of cyanosis, and reduced air entry, with scores greater than 6 indicating moderate to severe obstruction requiring close monitoring.^[20] Higher scores in an ill-appearing child with croup-like symptoms raise suspicion for bacterial tracheitis over viral croup alone.^[21] Initial laboratory studies support the clinical suspicion without delaying care. A complete blood count (CBC) commonly demonstrates leukocytosis with neutrophilia, consistent with bacterial etiology, though findings can be nonspecific.^[19] A basic metabolic panel is performed to evaluate for dehydration, which may arise from fever, poor oral intake, and increased respiratory effort.^[2] This evaluation is conducted emergently in the emergency department (ED) for most cases, with transfer to the intensive care unit (ICU) for high-risk patients exhibiting severe distress or impending respiratory failure.^[2]

Diagnostic Procedures

The gold standard for diagnosing tracheitis involves direct laryngoscopy or bronchoscopy, which allows visualization of purulent exudate, edema, and pseudomembrane formation in the trachea, often extending to the subglottic region or main bronchi.^[2]^[7] This procedure also facilitates obtaining tracheal aspirates or swabs for microbiological analysis, identifying pathogens such as Staphylococcus aureus or Moraxella catarrhalis in 62-87% of cases when performed before antibiotic administration.^[7]^[11] Imaging modalities support the diagnosis but are not definitive. Lateral neck radiographs may reveal the "steeple sign" indicating subglottic narrowing or the "candle-dripping sign" from intratracheal debris, though these findings are less specific for tracheitis compared to croup.^[2]^[7] Computed tomography (CT) of the neck or chest is reserved for cases with suspected extension, such as abscess formation or concurrent pneumonia, providing detailed views of tracheal wall thickening, stenosis, or pseudomembranes.^[2]^[11] Microbiological confirmation relies on throat or nasopharyngeal swabs, tracheal aspirates, or sputum samples subjected to Gram staining, bacterial culture, and sensitivity testing to guide antibiotic therapy.^[2]^[7] Viral PCR testing may be employed if co-infection is suspected, particularly with influenza or parainfluenza viruses.^[7] In septic presentations, blood cultures are obtained to detect bacteremia, though they are positive in only a minority of cases.^[2]^[11] Arterial blood gas analysis assesses for hypoxemia or respiratory acidosis in patients with significant airway compromise.^[2] Diagnostic procedures, particularly endoscopy, should be conducted in a controlled environment such as the operating room or intensive care unit to manage potential airway obstruction and ensure immediate access to intubation or ventilation if needed.^[7]^[11]

Management

Treatment Approaches

Viral tracheitis, being milder and self-limited, is managed supportively with measures such as hydration, humidified air, and analgesics for symptom relief, without the need for antibiotics.^[22] Bacterial tracheitis requires more aggressive intervention. The primary treatment involves intravenous broad-spectrum antibiotics to target common pathogens such as Staphylococcus aureus (including MRSA), Streptococcus species, Moraxella catarrhalis, and Haemophilus influenzae, with selection guided by local resistance patterns and initial gram stain results.^[2] Typical regimens include a third-generation cephalosporin like ceftriaxone combined with vancomycin for MRSA coverage, or alternatives such as clindamycin plus a cephalosporin; therapy is narrowed once culture sensitivities are available.^[23]^[24] Airway management is critical in severe cases, with endotracheal intubation required in 38% to 100% of patients to secure the airway and facilitate suctioning of purulent secretions, often using an endotracheal tube 0.5 to 2 sizes smaller than usual due to subglottic edema.^[2]^[23] Bronchoscopy, either flexible or rigid, is performed in the operating room or intensive care unit for diagnostic confirmation, culture procurement, and mechanical debridement of thick pseudomembranes or pus, particularly when obstruction is significant.^[25] Intubation is typically managed by experienced pediatric airway specialists, with extubation considered once secretions decrease, clinical stability is achieved, and an air leak is present around the endotracheal tube, typically within 3 to 5 days.^[23]^[24]^[2] Anti-inflammatory interventions such as nebulized racemic epinephrine are generally ineffective for relieving airway obstruction caused by bacterial tracheitis, as the pathology involves purulent exudate rather than reversible edema, and are not routinely recommended.^[25] Systemic or inhaled corticosteroids similarly lack proven benefit and are controversial, with no established role in standard management due to insufficient evidence of efficacy.^[2]^[8] Treatment duration consists of 10 to 14 days of antibiotics, starting intravenously until the patient is afebrile for 48 hours and clinically stable, followed by step-down to oral equivalents to complete the course.^[2]^[25] Hospitalization in an intensive care unit is standard for close monitoring with serial clinical examinations, vital sign assessments, and airway suctioning, with hospital stays averaging 3 to 12 days.^[23] In adults, where bacterial tracheitis is rare, mild cases may allow for outpatient management with oral antibiotics if the patient is well-appearing and without significant respiratory distress.^[14]^[2]

Supportive Care and Prevention

Supportive care for bacterial tracheitis focuses on maintaining airway patency, hydration, and comfort while addressing the inflammatory response without suppressing cough mechanisms essential for secretion clearance. Patients often require humidified supplemental oxygen to alleviate respiratory distress and prevent drying of secretions, particularly in cases of subglottic edema.^[2] Intravenous fluids are administered to ensure adequate hydration, with regular monitoring of intake and output due to increased fluid requirements from fever and tachypnea.^[26] Pain management, typically with acetaminophen, is provided to facilitate effective coughing and airway clearance without the use of cough suppressants.^[7] For patients requiring mechanical ventilation, intensive care unit monitoring in a pediatric setting is standard to allow frequent endotracheal suctioning and close observation for signs of airway compromise.^[27] Nutritional support involves nasogastric tube feeding if oral intake is inadequate due to prolonged intubation, aiming to prevent malnutrition during acute illness.^[28] The goal is early extubation, typically within 3 to 5 days, guided by clinical improvement such as reduced fever, decreased secretions, and the presence of an air leak around the endotracheal tube.^[2] Prevention strategies emphasize reducing the risk of predisposing viral upper respiratory infections and bacterial superinfections. Vaccination against Haemophilus influenzae type b (Hib) has significantly decreased the incidence of epiglottitis, which can overlap with or predispose to tracheitis, while influenza vaccination mitigates the primary viral trigger in many cases.^[14] Prompt treatment of viral upper respiratory infections with supportive measures helps limit progression to bacterial involvement. Avoiding exposure to airway irritants such as tobacco smoke and chemicals is recommended to preserve mucosal integrity.^[29] Hand hygiene practices, including regular washing or use of alcohol-based sanitizers, are critical to curb the spread of viral pathogens that precede bacterial tracheitis. In hospital settings, contact and droplet isolation precautions are implemented for patients with symptomatic upper respiratory infections to prevent nosocomial transmission.^[30] Following discharge, patients benefit from follow-up evaluation by an otolaryngologist to assess airway recovery and monitor for residual effects. Caregiver education on recognizing warning signs, such as persistent stridor or fever recurrence, enables timely intervention and reduces readmission risks.^[2]

Prognosis and Complications

Clinical Outcomes

The prognosis for tracheitis varies by etiology. Viral tracheitis is typically mild and self-limited, resolving within 1 to 3 weeks without specific treatment or long-term sequelae.^[1] For bacterial tracheitis, the overall prognosis is excellent with prompt treatment and appropriate airway management, with mortality rates below 1% in modern medical settings where care is readily available.^[24] This represents a dramatic improvement from the pre-antibiotic era, when mortality ranged from 10% to 40% due to limited therapeutic options.^[7] Most affected children, primarily those under 6 years of age, can be extubated within 3 to 5 days of initiating treatment, with full clinical resolution typically occurring in 1 to 2 weeks, though residual cough or wheezing may persist longer.^[24]^[8] Prognosis is influenced by several factors, including the timeliness of diagnosis and intervention, which significantly reduces the risk of complications such as respiratory failure; outcomes are generally worse in infants due to their narrower airways and in cases of delayed care.^[2] Long-term sequelae are uncommon, with recurrence being rare; however, severe cases involving prolonged intubation may result in tracheal stenosis, occasionally necessitating surgical correction.^[2] Recent post-2020 analyses, including updated reviews of pediatric cases, report survival rates exceeding 95% when managed through multidisciplinary approaches involving intensive care and targeted antibiotics.^[2]

Potential Complications

Tracheitis can lead to several acute complications due to the rapid progression of airway inflammation and bacterial overgrowth. Airway obstruction from thick purulent secretions or pseudomembrane formation may result in acute respiratory failure, requiring emergent intubation in up to 100% of severe cases.^[2] Secondary pneumonia develops in approximately 50% of affected children, often exacerbating respiratory distress and necessitating prolonged mechanical ventilation.^[7] Systemic spread of infection can cause sepsis or toxic shock syndrome, particularly when Staphylococcus aureus is the causative pathogen, leading to hemodynamic instability and multi-organ dysfunction.^[2]^[5] In the subacute phase, intubation-related trauma contributes to tracheal stenosis or excessive granulation tissue formation, which may narrow the airway and impair long-term ventilation.^[2] Atelectasis frequently arises from mucus plugging, as copious tracheal secretions obstruct distal bronchi, reducing lung expansion and promoting further infection.^[2]^[5] Rare complications include mediastinitis or empyema if the infection extends beyond the trachea into mediastinal or pleural spaces, though these occur infrequently with timely intervention.^[2] Hypoxia-induced cardiac arrest represents another severe but uncommon outcome, often linked to untreated airway compromise.^[2]^[7] In adults, where bacterial tracheitis is less common and often secondary to intubation or underlying conditions, repeated episodes may predispose to chronic tracheomalacia, characterized by tracheal wall weakening and persistent dyspnea.^[2]

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