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Pneumonia - Knowledge at AMBOSS
Pneumonia - Knowledge at AMBOSS
Summary
Pneumonia is a respiratory infection characterized by inflammation of the alveolar space and/or the interstitial tissue of the lungs. In industrialized nations, it
is the leading infectious cause of death. Pneumonia is most commonly transmitted via aspiration of airborne pathogens (primarily bacteria, but also viruses
and fungi) but may also result from the aspiration of stomach contents. The most likely causal pathogens can be narrowed down based on patient age, immune
status, and where the infection was acquired (community-acquired or hospital-acquired). Pneumonia is classified based on clinical features as either typical
and atypical; each type has its own spectrum of commonly associated pathogens. Typical pneumonia manifests with sudden onset of malaise, fever, and a
productive cough. On auscultation, crackles and bronchial breath sounds are audible. Atypical pneumonia manifests with gradual onset of unproductive
cough, dyspnea, and extrapulmonary manifestations. Auscultation is usually unremarkable. Some patients may present with elements of both types.
Diagnostics include blood tests for inflammatory parameters and pathogen detection in blood, urine, or sputum samples. Chest x-ray in cases of
typical pneumonia shows opacity restricted to one lobe, while x-ray in atypical pneumonia may show diffuse, often subtle infiltrates. Together with the
characteristic clinical features, newly developed pulmonary infiltrate on chest x-ray confirms the diagnosis. Management consists of
empiric antibiotic treatment and supportive measures (e.g., oxygen administration, antipyretics).
For specific information on the diagnosis and management of pneumonia in pediatric patients, see “Pneumonia in children.”
Etiology
Pathogens
Haemophilus influenzae
Moraxella catarrhalis
Klebsiella pneumoniae
Staphylococcus aureus
Atypical pneumonia
Bacteria
Mycoplasma pneumoniae (most common in the ambulatory setting)
Chlamydophila pneumoniae
Chlamydophila psittaci
Legionella pneumophila → legionellosis
Coxiella burnetii → Q fever
Francisella tularensis → tularemia
Viruses
RSV
Influenza viruses, Parainfluenza viruses
CMV
Adenovirus
Coronaviridae (e.g., SARS-CoV-2)
Enterobacteriaceae
Acinetobacter spp
Staphylococci (Staphylococcus aureus)
Streptococcus pneumoniae
For atypical pneumonia bacterial causes, remember the mnemonic: Atypically, Legions of Clams Mind their P's and Q's!
• Legionella pneumophila
• Chlamydophila pneumoniae
• Mycoplasma pneumoniae
• Psittacosis (Chlamydophila psittaci)
• Q fever (Coxiella burnetii)
Klebsiella
H. influenzae
Bronchopneumonia S. pneumoniae
S. aureus
H. influenzae
Klebsiella
Chlamydophila pneumoniae
Chlamydophila psittaci (primarily transmitted by parrots)
Legionella
Histoplasma capsulatum
Coccidioides immitis
Candida species → candidiasis
Cytomegalovirus (CMV) → CMV pneumonia
S. aureus
Gram-negative bacteria
Anaerobes
Viruses
H. influenzae
Gram-negative bacteria
Anaerobes [6]
Influenza virus
Recurrent pneumonia Uncommon organisms (e.g., Nocardia, Coxiella burnetii, Aspergillus, Pseudomonas aeruginosa)
“Track my respiration: chlassic strep formation”: C. trachomatis, Mycoplasma, Respiratory syncytial virus, Chlamydia pneumoniae, and
Streptococcus pneumoniae are the most common causative agents of pneumonia in children.
Chronic diseases
Acquired or congenital abnormalities of the airways (e.g., bronchiectasis, space-occupying lesions, cystic fibrosis)
Immunosuppression
HIV infection
Diabetes mellitus
Alcoholism
Malnutrition
Dysphagia
Smoking
Environmental factors
Surgical procedures
Chest surgery
Bear in mind immune status and potential exposures when considering potential pathogens in patients with suspected pneumonia.
Consider aspiration pneumonia in patients with altered mental status or other risk factors for aspiration.
Classification
Pneumonia can be classified according to etiology, location acquired, clinical features, and the area of the lung affected by the pathology.
Etiology
Secondary pneumonia
Anatomical abnormalities such as tubercular caverns, bronchial tumors, or stenosis (postobstructive pneumonia) [9]
Aspiration pneumonia
Location acquired
Hospital-acquired pneumonia (HAP): nosocomial pneumonia, with onset > 48 hours after admission
Ventilator-associated pneumonia (VAP): pneumonia occurring in patients who are on mechanical ventilation breathing machines in hospitals (typically in
the intensive care unit)
Healthcare-associated pneumonia (HCAP): pneumonia that is acquired in healthcare facilities (e.g., hospital, nursing homes, hemodialysis centers, and
[10][11]
outpatient clinics); this terminology is no longer recommended but is included for historical purposes.
Clinical features
Typical pneumonia
Atypical pneumonia
Pneumonia with less distinct classical symptoms and often unremarkable findings on auscultation and percussion
Multilobar pneumonia refers to the involvement of multiple lobes in a single lung or both lungs.
Bronchial pneumonia: pneumonia affecting the tissue around the bronchi and/or bronchioles
Cryptogenic organizing pneumonia (formerly known as bronchiolitis obliterans organizing pneumonia): a noninfectious pneumonia of unknown etiology
characterized by the involvement of the bronchioles, alveoli, and surrounding tissue
Pathophysiology
Routes of infection
Pathogenesis
1. Failure of protective pulmonary mechanisms; (e.g., cough reflex, mucociliary clearance , alveolar macrophages )
2. Infiltration of the pulmonary parenchyma by the pathogen → interstitial and alveolar inflammation
3. Impaired alveolar ventilation → ventilation/perfusion (V/Q) mismatch with intrapulmonary shunting (right to left)
Hypoxia is worsened when the affected lung is in the dependent position, as perfusion to the dependent lung is better compared to the nondependent
lung.
In the case of a large unilateral pulmonary abscess, it may be helpful to position the patient so that the affected lung is in the dependent position in order
to prevent the pus from filling the unaffected lung.
Pattern of involvement
Lobar pneumonia
Congestion (day 1–2) Parenchymal partial consolidation Alveolar lumens with serous exudate, bacteria, and rare inflammatory cells
Red-purple
Red hepatization (day 3–4) Parenchymal consolidation Alveolar lumens with exudate rich in fibrin, bacteria, erythrocytes, and inflammatory cells
Red-brown Alveolar walls thickening
Dry and firm
Liver–like consistency
Reversible
Gray hepatization (day 5–7) Uniformly gray Alveolar lumens with suppurative exudate (neutrophils and macrophages)
Resolution (day 8 to week 4) Gradual aeration of the affected segment Enzymatic fibrinolysis
Bronchopneumonia: mostly commonly a descending infection that affects the bronchioles and adjacent alveoli
Characterized by acute inflammatory infiltrates that fill the bronchioles and the adjacent alveoli (patchy distribution)
Usually involves the lower lobes or right middle lobe and affects ≥ 1 lobe
Necrotizing bronchopneumonia and pneumatocele are caused by Staphylococcus aureus and are often preceded by an influenza infection. [12]
Interstitial pneumonia: interstitial inflammation, typically caused by Mycoplasma and viral infections
Characterized by a diffuse patchy inflammation that mainly involves the alveolar interstitial cells
Miliary pneumonia: multiple small infiltrations caused by hematogenous dissemination (e.g., of tuberculosis)
Cryptogenic organizing pneumonia: characterized by inflammation of the bronchioles and surrounding structures
Clinical features
Typical pneumonia
Typical pneumonia is characterized by a sudden onset of symptoms caused by lobar infiltration.
Severe malaise
Dullness on percussion
Pain that radiates to the abdomen and epigastric region (particularly in children; see also “Pneumonia in children”)
Suspect bacterial pneumonia in immunocompromised patients with acute high fever and pleural effusion.
Atypical pneumonia
Atypical pneumonia typically has an indolent course (slow onset) and commonly manifests with extrapulmonary symptoms.
Dyspnea
Common extrapulmonary features include fatigue, headaches, sore throat, myalgias, and malaise.
This classification does not have a major impact on patient management because it is not always possible to clearly distinguish between typical
and atypical pneumonia.
Diagnostics
Pneumonia is a clinical diagnosis based on history, physical examination, laboratory findings, and CXR findings. Consider microbiological studies and advanced
[13]
diagnostics based on patient history, comorbidities, severity, and entity of pneumonia.
In ambulatory settings, the combination of normal vital signs and an unremarkable lung examination indicates a very low likelihood of CAP. [14]
[15]
Laboratory studies
Routine
PCT can be used to guide antibiotic treatment but should not be used to decide if antibiotic therapy is necessary on its own. [11][16][17]
PCT levels ≥ 0.25 mcg/L correlate with an increased probability of a bacterial infection.
Low PCT level after 2–3 days of antibiotic therapy can help facilitate the decision to discontinue antibiotics. [17]
BMP, LFTs
Do not rely on laboratory markers like CRP or procalcitonin to determine the need for antibiotic therapy. [11][18]
Microbiological studies
Any patient being treated empirically for MRSA or P. aeruginosa Blood cultures (2 sets)
All patients in pandemic or epidemic settings Testing for specific pathogens: e.g., COVID-19 testing with SARS-CoV-2 PCR [19]
In pandemic or epidemic settings, rule out the prevalent respiratory pathogen (e.g., COVID-19) in all patients with suspected pneumonia. [19]
Avoid routine blood cultures and sputum Gram stain in patients with CAP, except if severe or there is concern for MRSA or Pseudomonas
infection. [11]
Imaging
Lobar pneumonia
Presence of air bronchograms: appearance of translucent bronchi inside opaque areas of alveolar consolidation
Bronchopneumonia
Parapneumonic effusion
A new pulmonary infiltrate on chest x-ray in a patient with classic symptoms of pneumonia confirms the diagnosis.
Typical pneumonia usually appears as lobar pneumonia on x-ray, while atypical pneumonia tends to appear as interstitial pneumonia. However,
the underlying pathogen cannot be conclusively identified based on imaging results alone.
Consider chest CT or empiric treatment if clinical suspicion for CAP remains high despite a negative CXR, as the initial CXR may be
falsely negative. [20][21]
Indications
Recurrent pneumonia
Advantages: more reliable evaluation of circumscribed opacities, pleural empyema, or sites of consolidation
[22]
Findings:
Air bronchograms
Ground-glass opacities
Pleural effusion/empyema
Nodules
CT is more sensitive and specific than CXR for the diagnosis of pneumonia.
Point-of-care ultrasound (POCUS) has high sensitivity and specificity for the diagnosis of pneumonia. [23][24]
Indications
Consolidation
Air bronchograms
Unilateral B-lines
Pleural effusion
In the emergency department, consider POCUS to quickly confirm pneumonia and assess for other causes of dyspnea.
Bronchoscopy
Indications
Need for pathohistological diagnosis (e.g., biopsy of a central mass discovered on CT)
Inconclusive results on CT
Diagnostic thoracentesis
[13][28]
Indications: consider if pleural effusion > 10 mm is present to evaluate for pleural empyema
Consider therapeutic thoracentesis in large effusions (≥ half of the hemithorax) or if the effusion is suspected of causing dyspnea [28]
Consider tube thoracostomy if pleural empyema (e.g., echogenic debris on lung ultrasound) or complicated effusion (e.g.,pH < 7.20, glucose < 60 mg/dL, LDH
[28]
above three times the upper limit of serum LDH, positive culture) is suspected
Treatment
Approach
Evaluate all patients for hypoxemia and/or sepsis and manage as indicated.
Assess the need for hospitalization with the CURB-65 score or the pneumonia severity index (PSI/PORT score).
Determine the appropriate level of care using clinical judgment and the IDSA/ATS criteria for severe CAP.
Begin empiric antibiotic therapy based on severity and patient risk factors (e.g., VAP vs. CAP).
Re-evaluate therapy after 48 hours (earlier if the patient's condition deteriorates or new information becomes available).
Age ≥ 65 years
Interpretation
Patients are assigned to one of five risk classes based on a more complex point system than in CURB-65.
Points are distributed based on patient age, comorbidities, and lab results.
The CURB-65 score and PSI are tools for evaluating the risk of mortality. They have not been validated for determining the necessity for ICU
admission.
The decision of whether to admit a patient to the ICU should be based on clinical judgment.
The IDSA/ATS criteria for severe CAP can be used to help triage patients with CAP and guide empiric antibiotic treatment decisions. [11]
Mechanical ventilation
Multilobar infiltrates
Interpretation
Outpatient
Previously healthy patients without comorbidities or risk factors for resistant pathogens Monotherapy with one of the following:
Amoxicillin
Doxycycline
A macrolide (only in areas with a pneumococcal macrolide resistance < 25%)
Azithromycin
Clarithromycin
Patients with comorbidities or risk factors for resistant pathogens Combination therapy
An antipneumococcal β-lactam:
Amoxicillin-clavulanate
Cefuroxime
Cefpodoxime
PLUS one of the following:
A macrolide
Azithromycin
Clarithromycin
Doxycycline
Monotherapy: with a respiratory fluoroquinolone
Gemifloxacin
Moxifloxacin
Levofloxacin
Duration of treatment
5 days of therapy is usually sufficient for CAP that is treated in the outpatient setting.
Any patient being treated in a primary care setting should be re-examined after 48–72 hours to evaluate the efficacy of the prescribed antibiotic.
Additional considerations: Knowing local resistance patterns of S. pneumoniae to macrolides is critical when deciding on an empiric antibiotic regimen.
Inpatient
Ceftriaxone
Cefotaxime
PLUS one of the following:
A macrolide
Azithromycin
Clarithromycin
Doxycycline
Monotherapy: with a respiratory fluoroquinolone
Gemifloxacin
Moxifloxacin
Levofloxacin
Ceftriaxone
Cefotaxime
PLUS one of the following:
A macrolide
Azithromycin
Clarithromycin
Doxycycline
A respiratory fluoroquinolone
Moxifloxacin
Levofloxacin
Alternative for patients with a penicillin allergy:
Aztreonam
PLUS a respiratory fluoroquinolone
Moxifloxacin
Levofloxacin )
Meropenem
Imipenem-cilastatin
PLUS one of the following:
A macrolide
Azithromycin
Clarithromycin
Doxycycline
A respiratory fluoroquinolone
Levofloxacin
Moxifloxacin
Alternative for patients with a penicillin allergy:
Aztreonam
PLUS a respiratory fluoroquinolone
Moxifloxacin
Levofloxacin
Risk factors for MRSA Addition of one of the following antibiotics with MRSA activity
Vancomycin
Linezolid
Duration of therapy
Concurrent meningitis
Additional considerations
If aztreonam is used instead of a β-lactam antibiotic (e.g., for penicillin allergy), the addition of MSSA coverage (e.g., a fluoroquinolone) is necessary.
Anaerobic coverage is not routinely recommended for suspected aspiration pneumonia (unless lung abscess or empyema is suspected). [11]
If aztreonam is used as an alternative to other β-lactam antibiotics, additional coverage for MSSA must be included (e.g., a fluoroquinolone).
Patients not at high risk for mortality and without risk factors for MRSA infection Monotherapy
An antipneumococcal, antipseudomonal β-lactam
Imipenem
Meropenem
Cefepime
Piperacillin-tazobactam
OR levofloxacin
Patients not at high risk for mortality but with risk factors for MRSA infection Combination therapy
One of the following antibiotics with MRSA activity:
Linezolid
Vancomycin
Meropenem
Imipenem
A fluoroquinolone
Levofloxacin
Ciprofloxacin )
Aztreonam
Meropenem
Imipenem
A fluoroquinolone
Levofloxacin
Ciprofloxacin
An aminoglycoside
Amikacin
Gentamicin
Tobramycin
Aztreonam
Duration of treatment
Additional considerations: Resistance patterns can vary widely; local antibiograms should be considered when starting empiric treatment.
Patients with structural lung disease and/or at high risk for mortality should receive double antipseudomonal coverage!
Aztreonam
Imipenem
Meropenem
Ceftazidime
Cefepime
Piperacillin-tazobactam
Vancomycin
Linezolid
A fluoroquinolone
Levofloxacin
Ciprofloxacin
An aminoglycoside
Amikacin
Gentamicin
Tobramycin
A polymyxin
Colistin
Polymyxin B
Additional considerations:
Risk factors for multi-drug resistant organisms (e.g., presence of structural lung disease, recent IV antibiotic therapy, local resistance patterns) should be
considered when deciding on an empiric regimen
Empiric antibiotic therapy for ventilator-associated tracheobronchitis is not routinely recommended. [10]
Incentive spirometer
Calculate the CURB-65 score and/or PSI/PORT score to identify patients who would benefit from admission.
Assess severity of CAP with the IDSA/ATS criteria for severe CAP.
[33]
Consider advanced diagnostic evaluation.
Pathogen-specific pneumonia
Epidemiology
Outbreaks most commonly occur in schools, colleges, prisons, and military facilities.
Clinical features
Erythema multiforme
Diagnostics
Subclinical hemolytic anemia: associated with elevated cold agglutinin titers (IgM)
Chest x-ray can show extensive pulmonary involvement in patients with mild pneumonia.
Treatment
See “Empiric antibiotics for CAP” for dosages and duration of treatment.
Legionnaire disease
Pneumocystis pneumonia
Tuberculosis
Various viral infections (e.g., respiratory syncytial virus, hantavirus, adenovirus, CMV, SARS-CoV, SARS-CoV-2)
Ornithosis
Aspiration pneumonia
Definitions
Aspiration
Most commonly occurs after instrumentation of the upper airways or esophagus (e.g., upper GI endoscopy) or secondary to vomiting and regurgitation of
gastric contents
Aspiration pneumonia: a type of pneumonia that occurs as a result of oropharyngeal secretions and/or gastric contents aspiration
Aspiration pneumonitis
Aspiration of gastric acid that initially causes tracheobronchitis, with rapid progression to chemical pneumonitis
Patients may develop aspiration pneumonitis without pneumonia, aspiration pneumonia without pneumonitis, or aspiration pneumonitis
complicated by pneumonia. [36]
Etiology
Pathogens [11][36]
Gram-positive and gram-negative aerobic bacteria predominate in community-acquired infections (e.g., S. pneumonia, S. aureus, H. influenza,
Enterobacteriaceae).
Mixed infections with anaerobic organisms; may occur (e.g., Fusobacterium, Peptostreptococcus, Bacteroides).
Risk factors for aspiration (predispose individuals to reduced epiglottic gag reflex and dysphagia)
Aspiration pneumonitis and pneumonia are unusual following aspiration of tube feeds or blood, which are typically high-pH and sterile. [36]
Aspiration pneumonitis
Aspiration pneumonia
Diagnostics
Clinical diagnosis supported by characteristic laboratory and imaging findings
Supine position: superior segment of the right lower lobe (most common site of aspiration)
Right lateral decubitus position: posterior segment of the right upper lobe or right middle lobe
Treatment [36]
Choose agents based on site of acquisition, illness severity, and risk factors for resistant organisms (see “Empiric antibiotics for CAP“ and “Empiric
antibiotics for HAP”).
Consider coverage for anaerobic bacteria (e.g., with ampicillin-sulbactam, moxifloxacin) in patients with severe periodontal disease, lung abscess, or
empyema. [11][36][40]
All patients: supportive care for pneumonia, monitoring, consider serial imaging.
Aspiration pneumonia requires antibiotic therapy while aspiration pneumonitis typically self-resolves within 24–48 hours with supportive care
alone. [11][41]
Avoid routine anaerobic coverage for aspiration pneumonia without lung abscess, empyema, or severe periodontal disease. [40]
Complications
Abscess
Prevention [36]
Dysphagia-modified diet
Complications
Parapneumonic pleuritis
Fibrinous pleuritis: inflammation → increased vessel permeability → fibrin-rich exudate deposited on the serosal surface of the pleura →
pleuritic chest pain and friction rub
Pleural empyema
Lung abscess
ARDS
Respiratory failure
Sepsis
Prognosis
The mortality risk can be evaluated with the CURB-65 score. [42]
Score 0: ∼ 1%
Score 3: ∼ 14%
Score 4: ∼ 40%
Prevention
Immunization (see “ACIP immunization schedule” for information on doses and intervals)
Pneumococcal vaccination
Influenza vaccination
Smoking cessation
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