Internal Diseases and Therapy · MU Sofia

1. Acute bronchitis, tracheobronchitis, broncheolitis

Covers three acute inflammations of the airways, named by the level they affect: acute bronchitis, tracheobronchitis and bronchiolitis. It takes each in turn through definition, causes, pathogenesis, presentation, diagnosis and treatment, with a comparison table of conditions that can mimic an acute cough and a closing section on infant viral bronchiolitis and the several forms of bronchiolitis seen in adults.

Inside: 4 sections · 1 labelled picture · 1 table · 16 flashcards · 8 min

Topic 1 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 4 sections, about 1,167 words (8 min of reading), with 16 flashcards.

In this note

  1. Introduction
  2. Acute bronchitis
  3. Acute tracheobronchitis
  4. Bronchiolitis

Introduction

Three acute inflammations of the conducting airways, named by the level they affect: tracheobronchitis (trachea and large bronchi), acute bronchitis (bronchi) and bronchiolitis (bronchioles, < 2 mm). All three are mostly viral and self-limiting; the main clinical task is to exclude pneumonia and to avoid unnecessary antibiotics.

Acute bronchitis

Definition

An acute, self-limiting inflammation of the large airways (bronchi) without evidence of pneumonia, whose main symptom is cough lasting more than 5 days and up to 3 weeks. One of the most common reasons for visiting a GP.

Etiology

  • About 90% viral: rhinoviruses, coronaviruses, influenza A and B, parainfluenza, RSV, adenovirus, human metapneumovirus.
  • Bacteria in < 10%: Bordetella pertussis (in adults too, waning immunity), Mycoplasma pneumoniae, Chlamydophila pneumoniae. Streptococcus pneumoniae, H. influenzae and M. catarrhalis matter mainly in smokers and patients with COPD (as exacerbations).
  • Non-infectious: inhaled irritants (smoke, gases, dusts, chlorine, ammonia).
  • Risk factors: smoking, cold season, crowding, chronic lung disease, immunosuppression, young children and the elderly.

Pathogenesis

  • Infection of the bronchial epithelium → inflammatory response → oedema and thickening of the mucosa, hyperaemia, increased mucus.
  • Shedding of ciliated epithelial cells and release of inflammatory mediators → transient bronchial hyperresponsiveness and bronchospasm with a fall in FEV1 that recovers within about 5–6 weeks; this explains the prolonged cough.
  • The spread of the pathogen and the inflammatory response correlate with the symptoms.

Clinical presentation

  • Often starts as an upper respiratory infection: runny nose, sore throat, headache, malaise, myalgia.
  • Cough is the dominant symptom: dry at first, later productive; typical duration 10–20 days, up to 3 weeks. Coughing fits are often worse at night → fatigue.
  • Sputum: mucoid or purulent. Purulent (yellow-green) sputum does not mean bacterial infection: it reflects shed cells and peroxidase from white cells.
  • Retrosternal burning on coughing (tracheal involvement), mild dyspnoea, wheeze.
  • Fever is uncommon or low-grade; a high or persistent fever suggests influenza or pneumonia.
  • Examination: usually normal; possibly scattered rhonchi (change after coughing), wheezes, coarse crackles. No signs of consolidation.

Diagnosis

  • Clinical diagnosis. Routine tests (X-ray, sputum culture, blood tests) are not needed.
  • Suspect pneumonia and do a chest X-ray when any of these are present: heart rate > 100/min, respiratory rate > 24/min, temperature > 38 °C, focal chest signs (crackles, dullness, bronchial breathing, egophony), SpO2 < 95%, confusion, or in the elderly with fewer signs. CRP < 20 mg/L argues against pneumonia; > 100 mg/L makes it likely.

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