Pneumonia J18.9

The first descriptions of pneumonia can already be found in Hippocrates (460-370 BC). In 1819 Laennec published a clinical and pathological description of pneumonia and Rokitansky was the first to differentiate between lobar and bronchial pneumonia in 1842.

Pneumonia is an acute or chronic infectious disease with inflammation of the alveoli and/or the interstitium of the lung.

Inflammation of the lungs most frequently caused by bacteria, but also by viruses, mycoplasmas, fungi, parasites, gases, radiotherapy or foreign bodies.

• In ambulatory acquired pneumonia (CAP, see below), Streptococcus pneumoniae is the most common pathogen in all age groups with 40-50 %,
• followed by occasionally occurring (5-10 %) Haemophilus influenzae,
• Mycoplasma pneumoniae,
• Enterobacteriaceae
• Respiratory viruses such as adeno- and influenza viruses
• Adenovirus infection (pneumonia caused by serotypes 1-4,7,14)
• Rarely (< 5 %) are found:
• Respiratory syncytial virus infection
• Coronavirus infections(SARS, MERS, Covid-19)
• Legionella Species(Legionellosis)
• staphylococcus aureus
• chlamydophila pneumoniae infection
• Chlamydophila psittaci(Ornithosis)
• Coxiella burnetii(Q fever)
• Bacillus anthracis(anthrax pneumonia)

Pneumonia caused by primarily non-pneumotropic viruses:

• Cytomegalovirus (CMV)
• Herpes simplex virus (HSV)
• Varicella zoster virus (VZV)

Pneumonia caused by fungi:

Pneumocystis jiroveci (sac fungus: Pneumocystis pneumonia)

Cryptococcus neoformans (Cryptococcosis of the lung)

Mucor, rhizomucor and others(mucor mycoses, zygomycosis)

Fusaria(Fusariosis)

Note: In about 20-30% of the cases the pathogen remains unexplained.

There are different types of classification for pneumonia:

• by place of origin:
  • outpatient: pneumonia acquired at home or in nursing homes (community-acquired pneumonias: CAP)
  • nosocomial: pneumonia acquired in the clinic (hospital-acquired pneumonias: HAP)
  • ventilator-associated pneumonia (Ventilator Associated: VAP)
• by aetiology:
  • infectious (bacteria, viruses, mycoplasmas, fungi, parasites)
  • physical noxae (irradiation, foreign bodies)
  • chemical noxae (irritant gases, aspiration of stomach contents etc.)
  • circulatory problems (congestive or infarct pneumonia)
• Clinical classifications:
  • primary pneumonia: occurrence of pneumonia without previous cardiovascular disease
  • Secondary pneumonia: Occurrence of pneumonia in pulmonary and/or cardiac diseases:
    • Circulation disorders: congestive pneumonia, e.g. in the event of an infarct, left heart failure, pulmonary embolism or bed-ridden
    • due to changes in the bronchus with bronchiectasis, carcinoma, foreign bodies
    • after aspiration of foreign bodies
    • bacterial superinfection in influenza
  • according to its course:
    • acute pneumonia
    • chronic pneumonia
• Pathological-anatomical classification:
  • according to localization
    • alveolar (mostly bacterial)
    • interstitial (mostly viral)
  • after expansion
    • lobar (lobe pneumonia)
    • lobular (focal pneumonia)

Pneumonia is the no. 1 fatal infectious disease in the industrialized countries and the no. 4 worldwide. 500,000 cases/year (for Germany). Nosocomial pneumonia is the third most common hospital-acquired infection (about 0.5 - 1.0% of all hospital patients).

The hospitalization rate for CAP (community-acquired pneumonias) is about 50%. The incidence and also the lethality depend on both age and comorbidity. In particular, alcoholism, asthma, congenital or acquired immunosuppression and increased age play a major role.

In most cases, pneumonia is caused by germs in the nasopharyngeal space. These microorganisms enter the deeper respiratory tract in different ways:

• through nightly aspiration of small amounts of saliva (especially in the elderly) or through clouding of consciousness (e.g. alcohol); most common cause
• inhalation: by inhalation of pathogens (droplet infection)
• haematogenic: rarely pathogens reach the lungs via the bloodstream (e.g. in endocarditis, pleural infection or inflammatory changes in the mediastinum)

Note: The bronchial system has various defence mechanisms to prevent the penetration of pathogens. Cilia and nasal conchae already trap larger particles in the upper airways. Through mucociliary clearance, the majority of the pathogens in the upper airways are transported back to the larynx; coughing and sneezing further support this process. If particles nevertheless enter the alveoli, they are phagocytized by alveolar macrophages and transported to the lymphatic system. In addition, the surfactant lining of the alveoli forms a local immune barrier. However, these defence mechanisms can be impaired by various factors. Smoking, intubation, etc. impair the mechanical defence, whereas changes in the local flora can be caused by the intake of antibiotics, systemic diseases, malnutrition, etc.

Since the clinical picture depends on the pathogen, a historical distinction was made between typical lobar pneumonia and atypical bronchopneumonia. However, this classification is not important for both diagnosis and therapy; clinical picture of bacterial lobar pneumonia (mostly caused by pneumococci):

• sudden onset of the disease due to a feeling of well-being with high fever and chills coughing, nasal respiration, in case of involvement of the pleura breath-dependent pain in the thorax
• unspecific symptoms such as fatigue, headaches, myalgia, arthralgia
• in approx. 20 % also gastrointestinal symptoms such as nausea, vomiting, diarrhoea
• reddish-brown sputum from the 2nd day (contains plenty of granulocytes)
• X-rays: sharp shading limited to one lobe

The lobar pneumonia runs in 4 stages:

1. Stage: (approx. 24 h long) so called knock-on; the alveoli fill with exudate; there is a crepitatio inducx (due to lack of consolidation of the infiltrate)
2. Stage: (2nd-3rd day) so-called red hepatization; fibrin threads and erythrocytes stain the lungs dark red and give them a liver-like consistency (hepatization)
3. Stage: (4th-6th/8th day) so-called greyish-yellow hepatisation by leukocyte infiltration; peak of the disease
4. Stage:(after the 8th day) so-called lysis; dissolution of the exudate by granulocyte decay; expectoration of purulent sputum; auscultatory crepitatio redux (alveoli are again aerated)

Picture of atypical pneumonia (often caused by viruses, but also by chlamydia, legionella, mycoplasma):

• slow onset
• moderate fever
• chesty cough
• Leukocytes in the normal range (!)
• X-rays: large difference between low auscultation findings and the X-ray image (blurred, coarse-spotted foci over all lung fields)

Frequently, during a febrile pneumonia a reactivation of herpes simplex viruses occurs in the form of herpes blisters on the lips, the so-called "cold sores".

Chest radiograph: To confirm the diagnosis of community-acquired pneumonia, evidence of a new-onset infiltrate is required in a lung imaging radiograph. Performing radiography <4 h after admission is associated with faster case finding, shortened access to antimicrobial therapy, and shorter length of stay. Radiographic findings are used to record:

• the extent of the findings (mono-multilobar, uni-bilateral)
• concomitant diseases (e.g. cardiac insufficiency)
• complications (pleural effusion, abscess).

It also provides guidance for differential diagnostic considerations(pulmonary tuberculosis, lung carcinoma) and baseline findings if monitoring is indicated during the course of the disease. Sensitivity and specificity as well as reliability of infiltrate detection in chest radiography (infiltrate formation not infrequently only in the course of the disease); in mild to moderate pneumonias, there is considerable examiner dependence with regard to the assessment of infiltrates.

Lobar and segmental pneumonia: homogeneous shadowing of the corresponding anatomic unit;

Alveolar pneumonia: positive bronchopneumogram.

Bronchopneumonia: focal confluent infiltrates.

Interstitial pneumonia: interstitial or reticular drawing proliferation.

Thoracic ultrasound: Sonographic diagnosis of pneumonia is possible with a high sensitivity and specificity and has a very good predictive value in conjunction with clinical examination (especially auscultation). The procedure allows pleural processes to be detected (pleural effusion, empyema) and assessed during the course of the disease. The advantages of thoracic sonography are its wide availability, lack of radiation exposure, and arbitrary repeatability. Disadvantages include the limited penetration depth of the sound in the thorax (central infiltrations cannot be detected). Negative thoracic sonography does not rule out pneumonia (performance of thoracic sonography can therefore only be used as an alternative to radiography).

The diagnosis is made on the basis of main and secondary criteria.

Main criterion:

• New onset or progressive infiltrate on radiograph in 2 planes.

Secondary criteria:

• Pneumonia-typical auscultation findings, positive bronchophony/vocal fremitus.
• fever > 38.5°C (measured rectally) or hypothermia
• purulent sputum
• leukocytosis or leukopenia
• Pathogen detection (sputum, bronchial secretions, pleural punctate, blood culture).
• Note: There must be 1 major criterion plus 2 minor criteria to make the diagnosis of pneumonia.

Further Diagnostics:

• ABG
• Pulse oximetry
• Procalcitonin determination (if HAP is suspected of pneumogenic sepsis)
• CRB-65 score or CURB-65 score
• PSI (Pneumonia Severity Index, favored in the USA)
• Auscultation: fine-bubble sounding rales, "bronchial breathing" also auscultable in the periphery, increased bronchophony/vocal fremitus (in atypical pneumonia often no pathological auscultation findings)

• Percussion: muffled tapping sound

C(U)RB-65 score: quantification of severity of illness:

• Confusion(degree of confusion)
• Urea> 7 mmol/l
• Respiratoryrate > 30/min
• Blood pressure: systolic < 90mmHg or diastolic <60mmHg
• Age 65 years or older

From 2 out of a maximum of 4 (5) points, patients should be hospitalized in any case.

• 0 points: lethality 1-2%
• 1-2 points: lethality 13
• 3-4 (5)points: lethality > 31 %
• cave: in multimorbid patients not always reliable, because despite low score the prognosis is
• is often unfavorable

The mortality of patients who were initially treated in the normal ward and transferred to the intensive care unit because of a deterioration in their condition is higher than that of patients who received immediate intensive care. The evaluation required for this reason should be performed by recording the minor criteria of the modified ATS score.

Modified ATS score:

- Major criteria:

1. Need for intubation and mechanical ventilation.
2. Need for administration of vasopressors > 4 hours (septic shock).

- Minor criteria:

1. severe acute respiratory failure (paO2 / FiO2 <250)
2. multilobular infiltrates on chest x-ray
3. systolic blood pressure < 90 mmHg
4. impaired consciousness
5. respiratory rate > 30/min
6. acute renal failure
7. leukopenia
8. thrombocytopenia
9. Hypothermia

If at least 1 major criterion or 2 minor criteria are positive, immediate intensive care treatment is recommended. Note: Sensitivity is 69%, specificity is 97%, predictive value is 94%.

• Bronchial carcinoma (bronchoscopy and biopsy)
• Pulmonary tuberculosis (pathogen detection)
• Sarcoidosis (biiliary lymphadenopathy, BAL, transbronchial lung biopsy)
• Lung mycosis (detection of pathogens, lung biopsy, antigen or antibody antigens)
• Pulmonary embolism - Infarct pneumonia (perfusion scintigraphy)
• Pulmonary fibrosis (HR-CT, bronchoscopy, biopsy)
• Chronic eosinophilic pneumonia
• Allergic bronchopulmonary aspergillosis

Complications:

• Lung abscess
• Pleuritis
• Pleural effusion (puncture required for diagnostic and therapeutic reasons)
• Pleural empyema (drainage)
• Sepsis
• Shock
• Multiorgan Failure
• Acute aggressive lung failure (ARDS)

General measures:

• Physical protection (if necessary heparinization and / or antithrombosis stockings)
• adequate fluid intake (important in case of fever and for secretolysis)
• NaCl inhalations
• in case of hypoxia oxygen by nasal probe

After decrease of bronchial secretion and blood cultures (in 30-50 % positive!) untargeted immediate treatment, which should be adjusted after receiving the antibiogram.

Therapy for outpatients1
. For patients without concomitant diseases, who
havenot received antibiosis within the last 3 months
, aminopenicillin e.g.
amoxicillin 3x1g/d p.o. is the drug of choice.
Alternative: Macrolides such as Azithromycin 1x500 mg/d p.o. on the 1st day,
then 250 mg/d p.o.
(10% of pneumococci are resistant to macrolides
) or tetracycline such as doxycycline 2x100 mg/d p.o.

2. patients with concomitant diseases or previous antibiosis: betalactams as a middle
choice e.g.
amoxicillin/clavulanic acid 2 -3x1g/d p.o. or as an alternative fluoroquinolone of
group 3 / 4 e.g. levofloxacin1-2x500 mg/d p.o..

Therapy for in-patients1
. Patients without the risk of Pseudomonas aeruginosa infection should
receive amoxicillin/clavulanic acid
3-4 x 2.2 g/day plus macrolide antibiotic e.
g. azithromycin 1x500 mg/d.

2. patients with the risk of a Pseudomonas aeruginosa infection should

receivea Pseudomonas effective
penicillin plus beta-lactamase inhibitor piperacillin/tazobactam 3-4x4
.5g plus fluoroquinolone e.g. levofloxacin 1-2x500mg/d
In in-patients the antibiosis is usually given intravenously, with the exception of fluoroquinolones.

Therapy for in-patients

1. Patients without the risk of Pseudomonas aeruginosa infection should receive amoxixixillin/clavulanic acid plus macrolide.
2. Patients at risk of Pseudomonas aeruginosa infection should receive a Pseudomonas effective penicillin plus beta-lactamase inhibitor (piperacillin/tazobactam) plus fluoroquinolone (e.g. levofloxacin).

In in-patients, the antibiosis is usually given intravenously.

The most important preventive measure is vaccination against pneumococcus (see d) and influenza.

In otherwise healthy patients, fever and leukocytosis regress a few days after the start of therapy. The physical findings usually last longer.

The radiological changes persist the longest. They only disappear after about 4-12 weeks. Patients who have been treated in the clinic or who are smokers should definitely have a radiological check-up after 4-6 weeks. A radiological control before 28 days has proven to be useless in studies.

Caution: If the control reveals an increase of the infiltrate, a malignoma must be excluded.

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2. Bass et al (2009) Master medicine: General and Systematic Pathology S 138
3. Bauer TT et al (2006) CRB-65 predicts death from community-acquired pneumonia. J Internal Med 260: 93-101 .
4. Blümke et al. (2013) Pathology of the lung S 396 .
5. Ewig S et al. (2004) Validation of predictive rules and indices of severity for community acquiredpneumonia.thorax 59: 421-427.
6. Ewig S et al (2016) Treatment of adult patients with community-acquired pneumonia and prevention - Update 2016 AWMF guideline.
7. Herold G et al (2018) Internal Medicine S 372-380
8. Krams et al (2010) Short Textbook Pathology S 178
9. Mackenzie G (2016)The definition and classification of pneumonia. Pneumonia (Nathan) 8:14.
10. Mandell et al (2015) In: Harrison's 19th Edition, Section 2, Chapter 153 S 803-813