Bronkitis Akut

Risk Factors

Smoking, exposure to air pollutants, winter/fall season, close-contact environments, pre-existing chronic lung disease, immunoscompromised state

Etiology

Viral in over 90% of cases (influenza, parainfluenza, RSV, rhinovirus, adenovirus, human metapneumovirus). Atypical bacteria (Mycoplasma pneumoniae, Chlamydophila pneumoniae, Bordetella pertussis) account for fewer than 10%

Presentation

Acute onset cough (productive or nonproductive) lasting up to 3 weeks, often preceded by upper respiratory symptoms (rhinorrhea, sore throat, malaise). Low-grade fever may be present

Classic Exam

Clear lungs or diffuse rhonchi/wheezing on auscultation. Absence of focal consolidation findings (egophony, dullness to percussion, bronchial breath sounds). Mild pharyngeal erythema. No signs of respiratory distress

Diagnostics

Clinical diagnosis. No routine labs or imaging required. Chest X-ray is normal (ordered only to exclude pneumonia when warning signs are present)

Management

Supportive care only. Antitussives for symptom relief. No antibiotics unless pertussis is suspected. Bronchodilators if wheezing is prominent

Keywords

"Self-limiting cough," "post-URI cough," "productive cough with normal chest X-ray," "no antibiotics needed," "viral URI progressing to cough"

01Pathophysiology

Acute bronchitis is an inflammatory condition of the tracheobronchial tree, almost always triggered by a viral respiratory pathogen. The infection begins in the nasopharynx and descends into the larger airways, where viral replication causes epithelial cell damage and denudation of the bronchial mucosa. This loss of the protective epithelial barrier exposes underlying sensory nerve endings (vagal C-fibers and rapidly adapting stretch receptors), which become hyperresponsive to irritants, cold air, and mucus. This is the primary mechanism behind the persistent cough.

The damaged epithelium also triggers a local inflammatory cascade with neutrophil recruitment and mucus hypersecretion from goblet cells. The resulting mucus can be clear, yellow, or even green. This is a critical teaching point: purulent sputum color reflects neutrophil activity and inflammatory debris, not bacterial infection. Many students and clinicians mistakenly interpret green or yellow sputum as evidence of a bacterial process, which it is not.

Additionally, the inflammatory mediators cause transient bronchial hyperreactivity, which explains why some patients develop wheezing and chest tightness that mimic asthma. This hyperreactivity can persist for weeks after the acute infection has resolved, explaining why cough may linger for 3 to 6 weeks even in an otherwise healthy individual.

Because the inflammation is confined to the bronchial walls and does not extend into the alveolar parenchyma, gas exchange is preserved. This is the fundamental pathologic distinction between acute bronchitis (airway disease) and pneumonia (alveolar disease). Patients with acute bronchitis maintain normal oxygen saturation and do not develop the signs of alveolar consolidation seen in pneumonia.

02Clinical Manifestation

Prodromal (URI) Phase

Timing: Days 1 to 3
Manifestations: Rhinorrhea, nasal congestion, sore throat, malaise, low-grade fever, myalgias

Bronchitic (Cough) Phase

Timing: Days 3 to 10 onward
Manifestations: Cough becomes the dominant symptom (initially dry, then productive). Substernal chest soreness from forceful coughing. May develop wheezing or rhonchi. Fever, if present, typically resolves within the first 3 to 5 days

Prolonged Cough Phase

Timing: Weeks 2 to 6
Manifestations: Cough gradually diminishes. Due to persistent bronchial hyperreactivity and slow epithelial regeneration. No systemic symptoms

Phase	Timing	Manifestations
Prodromal (URI) Phase	Days 1 to 3	Rhinorrhea, nasal congestion, sore throat, malaise, low-grade fever, myalgias
Bronchitic (Cough) Phase	Days 3 to 10 onward	Cough becomes the dominant symptom (initially dry, then productive). Substernal chest soreness from forceful coughing. May develop wheezing or rhonchi. Fever, if present, typically resolves within the first 3 to 5 days
Prolonged Cough Phase	Weeks 2 to 6	Cough gradually diminishes. Due to persistent bronchial hyperreactivity and slow epithelial regeneration. No systemic symptoms

By Etiology

Etiology	Distinguishing Features
Influenza	Abrupt onset of high fever, severe myalgias, headache, dry cough. Seasonal (winter). Rapid antigen or PCR confirms
RSV / Parainfluenza	More common in children and elderly. Prominent wheezing, may mimic bronchiolitis in infants
Rhinovirus / Adenovirus	Prominent URI symptoms preceding the cough. Adenovirus may cause pharyngoconjunctival fever
*Mycoplasma pneumoniae*	Younger adults (ages 5 to 40). Gradual onset, dry hacking cough. "Walking pneumonia" if it progresses to involve the parenchyma
*Bordetella pertussis*	Paroxysmal cough with post-tussive emesis or inspiratory whoop. Cough lasting more than 2 weeks. History of incomplete vaccination

03Diagnostic Workup

None (clinical diagnosis)

Role: First-line approach
When to Order: All uncomplicated cases

Chest X-ray

Role: Exclusion of pneumonia
When to Order: Fever >38.5 C lasting beyond 5 days, tachycardia, tachypnea ( $R R > 24$ ), hypoxia ( $SpO_2 < 95\%$ ), focal lung findings on exam

Rapid influenza or PCR

Role: Identifies treatable viral cause
When to Order: During influenza season, within 48 hours of symptom onset (window for antiviral therapy)

Pertussis PCR / culture

Role: Confirms Bordetella pertussis
When to Order: Paroxysmal cough > 2 weeks, post-tussive vomiting, known pertussis exposure

Procalcitonin

Role: Guides antibiotic decision
When to Order: Diagnostic uncertainty between bronchitis and early pneumonia. Low procalcitonin ( $< 0.25\ \mu g/L$ ) supports withholding antibiotics

Sputum culture

Role: Not indicated
When to Order: Sputum culture has no role in routine acute bronchitis workup

Test	Role	When to Order
None (clinical diagnosis)	First-line approach	All uncomplicated cases
Chest X-ray	Exclusion of pneumonia	Fever >38.5 C lasting beyond 5 days, tachycardia, tachypnea ( $R R > 24$ ), hypoxia ( $SpO_2 < 95\%$ ), focal lung findings on exam
Rapid influenza or PCR	Identifies treatable viral cause	During influenza season, within 48 hours of symptom onset (window for antiviral therapy)
Pertussis PCR / culture	Confirms Bordetella pertussis	Paroxysmal cough > 2 weeks, post-tussive vomiting, known pertussis exposure
Procalcitonin	Guides antibiotic decision	Diagnostic uncertainty between bronchitis and early pneumonia. Low procalcitonin ( $< 0.25\ \mu g/L$ ) supports withholding antibiotics
Sputum culture	Not indicated	Sputum culture has no role in routine acute bronchitis workup

The best initial step is a focused history and physical examination. In a patient with acute cough following upper respiratory symptoms, clear lungs or diffuse rhonchi, and no signs of systemic toxicity, the diagnosis of acute bronchitis is made clinically. No labs and no imaging are needed.

Chest X-ray is ordered only when the clinical picture raises concern for pneumonia. The red flags that prompt imaging include: persistent high fever, heart rate above 100, respiratory rate above 24, oxygen saturation below 95%, and focal auscultatory findings such as crackles, egophony, or dullness to percussion. A normal chest X-ray in a coughing patient effectively confirms acute bronchitis and rules out pneumonia.

Rapid influenza testing (or influenza PCR) is relevant during influenza season because it identifies patients who may benefit from oseltamivir. This test is time-sensitive: antivirals are most effective when started within 48 hours of symptom onset.

Pertussis testing should be considered in any patient with cough lasting more than 2 weeks, particularly if the cough is paroxysmal, associated with post-tussive emesis, or the patient has incomplete vaccination. PCR of a nasopharyngeal swab is the preferred confirmatory method.

Procalcitonin is emerging as a useful biomarker in cases of diagnostic uncertainty. A level below $0.25\ \mu g/L$ has strong negative predictive value for bacterial lower respiratory tract infection and supports a decision to withhold antibiotics.

04Management and Treatment

Supportive care

Details: Oral hydration, rest, humidified air
Duration: Until symptoms resolve

Antipyretics / Analgesics

Details: Acetaminophen 500 to 1000 mg every 6 hours, or ibuprofen 400 mg every 6 hours
Duration: As needed for fever and myalgias

Antitussives

Details: Dextromethorphan 10 to 20 mg every 4 hours (if cough is disruptive to sleep). Benzonatate 100 to 200 mg three times daily as alternative
Duration: Symptomatic relief only, typically less than 2 weeks

Bronchodilators

Details: Albuterol inhaler 2 puffs every 4 to 6 hours as needed
Duration: Only if wheezing is present on exam

Oseltamivir

Details: 75 mg orally twice daily
Duration: 5 days. Start within 48 hours of influenza symptom onset

Macrolide (pertussis only)

Details: Azithromycin 500 mg day 1, then 250 mg days 2 through 5
Duration: 5 days total. Primarily to reduce transmission, not to shorten illness if cough is already established

Antibiotics for typical bacteria

Details: NOT indicated
Duration: N/A

Intervention	Details	Duration
Supportive care	Oral hydration, rest, humidified air	Until symptoms resolve
Antipyretics / Analgesics	Acetaminophen 500 to 1000 mg every 6 hours, or ibuprofen 400 mg every 6 hours	As needed for fever and myalgias
Antitussives	Dextromethorphan 10 to 20 mg every 4 hours (if cough is disruptive to sleep). Benzonatate 100 to 200 mg three times daily as alternative	Symptomatic relief only, typically less than 2 weeks
Bronchodilators	Albuterol inhaler 2 puffs every 4 to 6 hours as needed	Only if wheezing is present on exam
Oseltamivir	75 mg orally twice daily	5 days. Start within 48 hours of influenza symptom onset
Macrolide (pertussis only)	Azithromycin 500 mg day 1, then 250 mg days 2 through 5	5 days total. Primarily to reduce transmission, not to shorten illness if cough is already established
Antibiotics for typical bacteria	NOT indicated	N/A

Acute stabilization is rarely needed because acute bronchitis is a self-limiting illness. The cornerstone of management is reassurance and symptomatic treatment. Patients should be explicitly informed that cough may persist for 2 to 3 weeks and that this prolonged course is normal.

The single most tested treatment principle is that antibiotics are not indicated for acute bronchitis. This is the highest-yield takeaway from this entire topic. Despite widespread practice of prescribing antibiotics for purulent cough, evidence consistently shows no meaningful benefit. Guidelines from the American College of Physicians, the CDC, and the Infectious Diseases Society of America all recommend against routine antibiotic use. Students must resist the temptation to select an antibiotic answer choice just because the sputum is described as "yellowish-green" or "purulent."

Antitussive agents such as dextromethorphan can be used for symptomatic relief, especially when the cough disrupts sleep. Codeine-containing cough suppressants should be avoided due to limited evidence of efficacy and risk of dependence. Benzonatate is an alternative that works by anesthetizing stretch receptors in the airway.

Inhaled bronchodilators (albuterol) are appropriate only in patients who demonstrate wheezing on examination. Routine use of bronchodilators for all bronchitis patients is not supported by evidence.

Oseltamivir should be started within the 48-hour window if influenza is confirmed or strongly suspected, particularly in high-risk patients (elderly, pregnant, immunocompromised, chronic cardiopulmonary disease).

Azithromycin is reserved for confirmed or highly suspected pertussis. Importantly, macrolide therapy for pertussis is primarily aimed at reducing transmission to close contacts rather than shortening the clinical course, especially when initiated after the paroxysmal stage has begun.

Contraindications and cautions: Dextromethorphan should be used cautiously in patients taking SSRIs or MAOIs due to serotonin syndrome risk. NSAIDs should be avoided in patients with renal insufficiency, active peptic ulcer disease, or third-trimester pregnancy.

05Differential Diagnosis and Distractors

Community-acquired pneumonia

Why It Looks Similar: Cough, fever, and productive sputum overlap significantly
Key Discriminator: Pneumonia produces focal findings on exam (crackles, egophony, dullness to percussion) and an infiltrate on chest X-ray. Acute bronchitis has diffuse or absent lung findings and a normal chest X-ray

Asthma exacerbation

Why It Looks Similar: Wheezing and cough that worsen at night
Key Discriminator: Asthma has a history of recurrent episodes, known triggers, and reversible airflow obstruction on spirometry. Acute bronchitis is a single self-limited episode in a previously healthy patient

Pertussis

Why It Looks Similar: Prolonged cough after URI symptoms
Key Discriminator: Paroxysmal cough with post-tussive emesis or inspiratory whoop, lasting more than 2 weeks. Lymphocytosis on CBC may be present. PCR confirms

GERD-related cough

Why It Looks Similar: Chronic cough, may worsen when lying down
Key Discriminator: No preceding URI. Symptoms include heartburn, regurgitation, and cough worsening after meals or in the supine position. Empiric PPI trial is diagnostic

Upper airway cough syndrome (postnasal drip)

Why It Looks Similar: Cough with nasal congestion and throat clearing
Key Discriminator: Chronic course. Cobblestoning of the posterior pharynx. Responds to antihistamines or intranasal corticosteroids

Acute exacerbation of COPD

Why It Looks Similar: Cough with increased sputum production and dyspnea
Key Discriminator: Occurs in a patient with known smoking history and baseline chronic cough/dyspnea. Spirometry shows irreversible obstruction ( $F E V_{1} / F V C < 0.70$ )

Post-infectious cough

Why It Looks Similar: Lingering cough for weeks after a respiratory infection
Key Discriminator: No active infection signs. This is essentially the tail end of acute bronchitis. The distinction is academic, but the management remains the same: no antibiotics

Differential	Why It Looks Similar	Key Discriminator
Community-acquired pneumonia	Cough, fever, and productive sputum overlap significantly	Pneumonia produces focal findings on exam (crackles, egophony, dullness to percussion) and an infiltrate on chest X-ray. Acute bronchitis has diffuse or absent lung findings and a normal chest X-ray
Asthma exacerbation	Wheezing and cough that worsen at night	Asthma has a history of recurrent episodes, known triggers, and reversible airflow obstruction on spirometry. Acute bronchitis is a single self-limited episode in a previously healthy patient
Pertussis	Prolonged cough after URI symptoms	Paroxysmal cough with post-tussive emesis or inspiratory whoop, lasting more than 2 weeks. Lymphocytosis on CBC may be present. PCR confirms
GERD-related cough	Chronic cough, may worsen when lying down	No preceding URI. Symptoms include heartburn, regurgitation, and cough worsening after meals or in the supine position. Empiric PPI trial is diagnostic
Upper airway cough syndrome (postnasal drip)	Cough with nasal congestion and throat clearing	Chronic course. Cobblestoning of the posterior pharynx. Responds to antihistamines or intranasal corticosteroids
Acute exacerbation of COPD	Cough with increased sputum production and dyspnea	Occurs in a patient with known smoking history and baseline chronic cough/dyspnea. Spirometry shows irreversible obstruction ( $F E V_{1} / F V C < 0.70$ )
Post-infectious cough	Lingering cough for weeks after a respiratory infection	No active infection signs. This is essentially the tail end of acute bronchitis. The distinction is academic, but the management remains the same: no antibiotics

06Traps and High-Yield Pearls

The most common mistake on this topic is straightforward: choosing antibiotics as the answer for a patient with acute cough and purulent sputum. This is the trap that test-writers rely on most heavily. The vignette will describe a patient with 5 to 7 days of productive cough, yellow or green sputum, low-grade fever, and diffuse rhonchi. One answer choice will be azithromycin or amoxicillin-clavulanate. The correct answer is supportive care. Sputum color does not indicate bacterial infection, and antibiotics do not change outcomes in acute bronchitis.

A second common trap involves failing to order a chest X-ray when it is actually indicated. While the teaching point is "no routine imaging for bronchitis," a vignette that includes persistent high fever, tachycardia, focal crackles, or hypoxia is testing whether you recognize pneumonia warning signs. In that context, the correct next step is a chest X-ray, not reassurance.

A third trap involves pertussis masquerading as prolonged bronchitis. If the vignette describes a cough lasting more than 2 weeks with paroxysmal episodes and post-tussive vomiting, especially in a young adult or someone with lapsed vaccination, the answer is pertussis testing and treatment with azithromycin. This is the one scenario where an antibiotic is correct for what initially appears to be bronchitis.

The core competency being tested across all these questions is the ability to distinguish a self-limiting viral airway infection from conditions that require intervention (pneumonia, pertussis, asthma), and to resist the pressure to prescribe unnecessary antibiotics when the clinical picture is benign.

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