From WikiLectures

Pneumonia is an acute or chronic inflammation of the lung parenchyma due to infectious, allergic, physical or chemical noxious agents. It usually represents acute inflammation at the level of the respiratory bronchioles, alveolar spaces and interstitium. Globally, pneumonia is the third most common cause of death. The causative agent is recognised in at most 50% of cases. [1] [2] [3] Pneumonia is one of the most common inflammatory diseases.

Epidemiology[edit | edit source]

Pneumonia is particularly common in the first year of life, after which its incidence decreases. Between 80,000 and 150,000 pneumonias are reported annually in the Czech Republic, with a lethality of 10-20%. The lethality is increased by increasing age and associated polymorbidity, resistance agents, new agents (SARS), population migration, AIDS, drug addiction, air conditioning, ...[2]

Pneumonia is most often of infectious origin and is transmitted by droplet infection. They usually start with an upper respiratory tract infection, from where they spread to the bronchi and alveoli. Haematogenous spread occurs rarery[1]

Classification pneumonia[edit | edit source]

By the course of the disease[edit | edit source]

  • Acute,
  • chronic – inflammation lasting more than 3 months,
  • recurrent – repeated inflammation in the same localization,
  • migratory – pulmonary infiltrates migrate, appearing at different times in different parts of the lung.

By etiology[edit | edit source]

  • Infectiousbacterial, viral, mycotic and mycobacterial, parasitic
  • non-infectious (so-called "pneumonitis") – aspiration, inhalation, postradiation, soup, hypersensitive (allergic).

by clinic and epidemology [4][edit | edit source]

Community-acquired pneumonia[edit | edit source]

The most common type of pneumonia, up to 90%, acquired in the normal environment outside a hospital setting. Mostly treated as outpatients, they are well sensitive to common ATBs.

The most common causative agents

Nosocomial pneumonia[edit | edit source]

  1. Early nosocomial pneumonia develops in more than 48 hours after admission to hospital. The most common causative agents:
  1. Late-onset nosocomial pneumonia develops after 4 days, G- causative agents are more common. Therapy should be initiated empirically and as soon as possible, each department knowing at least approximately its epidemiological situation, then adjusted on the basis of culture. In addition to the classical pathogens (Klebsiella, Enterobacteriaceae), opportunistic pathogens also appear (RS virus, CMV, Herpes zoster, Pneumocystis, mycobacteria). These agents cause pneumonia in immunocompromised patients. These are patients treated with cytostatics, radiation, post-transplant, HIV positive.

Pneumonia in immunocompromised patients[edit | edit source]

These are mainly HIV-positive patients, patients treated with cytostatics, immunosuppressants, radiation, after transplantation. Infection can be caused by known potential pathogens - Klebsiella pneumoniae, enterobacteria, Legionella, anaerobes. Opportunistic pathogens are also implicated in immunocompromised patients - CMV, RS virus, herpes zoster virus, Pneumocystis jirovecii, mycobacteria.

Ventilator pneumonia[edit | edit source]

It arises in patients connected to a ventilator. It is a nosocomial pneumonia caused by microaspiration of microorganisms from the oropharynx and stomach. Antibiotic treatment is guided by the current epidemiological situation in intensive care units.

Pneumonia in social care institutions[edit | edit source]

It affects elderly polymorbid patients who frequently visit health care facilities; resistant strains are more common.


By the clinical and radiological picture[edit | edit source]

Pneumonia in the right lower lung field.
X-ray examination of a patient with bronchopneumonia, inflammatory infiltrates evident.

Typické (bacterial)[edit | edit source]

They have the classic clinical symptoms of pneumonia (fever, cough and shortness of breath). They are caused by bacterial pathogens. On X-ray they appear as lobular, lobar, to alary pneumonia or bronchopneumonia, with exudate formation in the lung chambers.

In the blood count there is leukocytosis.

Atypical pneumonia[edit | edit source]

Difference between small-range X-ray and CT findings in Covid 19 They manifest with symptoms not typical for bacterial pneumonia (general "flu-like" symptoms - headache, muscle pain, joint pain, also nausea, vomiting). Radiological findings are consistent with disseminated pulmonary process.

the causative agents are characterized by intracellular parasitism.

The inflammation is interstitial, at the level of the wall of the lung chambers and the interstitium itself.

In the blood count leukopenia with relative lymphocytosis

By the mechanism of formation[edit | edit source]

  • Primary – isolated pulmonary disability,
  • secondary – complications of other systemic diseases.

By the the pathological-anatomical picture[edit | edit source]

  • Alveolar – inflammation mainly affects the lung chambers,
  • 'Interstitial – inflammation is localized in the bound connective tissue of the lung.

By the the X-ray findings[edit | edit source]

  • Alar – the entire pulmonary wing is affected,
  • lobar – one lobe affected,,
  • Segmental – segment disability,
  • bronchopneumonia – the infiltrate does not respect the anatomical arrangement of the lungs (lobe and segment boundaries).[2][5]

Diagnosis[edit | edit source]

CT image of pneumonia with two abscesses in the left lung bordered by pyogenic membrane

  • 'physical finding – consolidation of lung tissue,
  • 'Lung X-ray,
  • microbiological examination of sputum (preferably before ATB treatment, good quality sample) - Gram staining, culture, detection of antigens of S. pneumoniae, H. infuenzae, (only some serotypes), L. pneumophila, amplification methods (L. pneumophila),
  • hemoculture – 2× before starting ATB treatment,
  • examination of an effusion – biochemistry, cytology, Gram staining, culture, BK, MTD, detection of S. pneumoniae antigens,
  • urine examination – detection of S. pneumoniae, L. pneumophila antigens,
  • serology – in the acute phase only IgM, IgA antibodies,
  • blood count, FW, CRP, ABR, …

Treatment[edit | edit source]

Antibiotics[edit | edit source]

Penicillin antibiotics , Tetracyclines and Macrolides group (at least 10 days for typical pneumonias, 14 days to 3 weeks for atypical pneumonias; 2 to 5 days intravenously). U nozokomiálních infekcí Cephalosporins III., IV. generation (cefotaxim, ceftazidim, cefepim), higher generation penicillin antibiotics (ticarcilin, piperacilin/ tazobaktam atd.), fluorochinolons, Carbapenems (imipenem, meropenem) or in combination with e.g. Aminoglycosides.

Symptomatic treatment[edit | edit source]

  • Expectorants, mucolytics, in irritating dry cough antitussives,
  • antipyretics,
  • analgesics for pleural pain,
  • oxygen therapy in respiratory insufficiency.

Nebulization therapy[edit | edit source]

Regime measures[edit | edit source]

  • Sufficient intake of fluids, calories, vitamins;
  • respiratory rehabilitation;
  • orthopaedic position (in a slight prone position the patient puts less strain on the respiratory muscles and breathes better).

A pulmonary function test is indicated 6 weeks after resolution of pneumonia.[3]

Complications[edit | edit source]

Comparison table for typical and atypical pneumonia[edit | edit source]

Parametr Typical pneumonia Atypical pneumonia
Základní charakteristika výrazný fyzikální nález chudý fyzikální nález
Agens (extracelulární)

Streptococcus pneumoniae, Haemophilus influenzae Haemophilus parainfluenzae, Staphylococcus aureus, Klebsiella pneumoniae, Escherichia coli a Pseudomonas aeruginosa


Mycoplasma pneumoniae, Chlamydophila pneumoniae, Chlamydophila psittaci, Legionella pneumophila Coxiella burnetii, viry – RSV, influenzy, Pneumocystis carinii

Onset Sudden after HDC infection, slow
Ectopic symptoms insipid frequent - headache and muscle pain, vomiting, diarrhoea
Fever septic febrilia subfebrilia
Tremors present rarely
Cough productive dry, irritating
Heart rate possible tachycardia normal
The patient looks Sick 'normal'
Physically crepitus, tubular breathing, chrysalises isolated chrysoprines
X-Ray segmental/lobar opacification (alveolar involvement) intestinal reticulonodulation (interstitial involvement)
Sedimentation High slightly elevated
Inflammatory markers High slightly elevated
Blood count leukocytosis Lymphocytosis
Treatment Penicillin Macrolides

Odkazy[edit | edit source]

Related articles[edit | edit source]

External links[edit | edit source]

Sources[edit | edit source]

  1. a b MUNTAU, Ania Carolina. Pediatrie. 4. edition. Praha : Grada, 2009. 348-349 pp. ISBN 978-80-247-2525-3.
  2. a b c KLENER, Pavel, et al. Vnitřní lékařství. 3. edition. Praha : Galén, 2006. pp. 370. ISBN 80-7262-430-X.
  3. a b c BABÁČKOVÁ, P. Zdravotnické noviny [online]. Mladá fronta a.s, ©2007. [cit. 2011-02-03]. <>.
  4. ČEŠKA, Richard, et al. Interna. 1. edition. Praha : Triton, 2010. 855 pp. pp. 473-474. ISBN 978-80-7387-423-0.
  5. KRÁKOROVÁ, G – FERDA, J – KREUZBERG, B. Atypické pneumonie. Postgraduální medicína [online]2001, vol. 9, p. -, Available from <>. ISSN 1214-7664. 

Bibliography[edit | edit source]

  • KLENER, Pavel, et al. Vnitřní lékařství. 3. edition. Praha : Galén, 2006. 370 pp. ISBN 80-7262-430-X.
  • ČEŠKA, Richard, et al. Interna. 1. edition. Praha : Triton, 2010. 855 pp. pp. 473-480. ISBN 978-80-7387-423-0.