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Pneumonia Last updated: May 2, 2023

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

Pneumonia pathogens according to the source of infection

Type of pneumonia Common pathogens

Community-acquired pneumonia Typical pneumonia


Streptococcus pneumoniae (most common)
Also the most common pathogen in nursing home residents

Most common cause of pneumonia in persons who inject drugs [1]

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)

Hospital-acquired pneumonia Gram-negative pathogens


Pseudomonas aeruginosa

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)

Pneumonia pathogens according to location

Type of pneumonia Common pathogens

Lobar pneumonia Most common: S. pneumoniae


Less common
Legionella

Klebsiella
H. influenzae

Bronchopneumonia S. pneumoniae
S. aureus

H. influenzae
Klebsiella

Interstitial pneumonia Atypical pathogens


Mycoplasma pneumoniae

Chlamydophila pneumoniae
Chlamydophila psittaci (primarily transmitted by parrots)
Legionella

Viruses (e.g., RSV, CMV, influenza, adenovirus)


Coxiella burnetii

Cryptogenic organizing pneumonia Noninfectious

Pneumonia pathogens according to affected population

Type of pneumonia Common pathogens

Pneumonia in immunocompromised patients Encapsulated bacteria


Pneumocystis jirovecii → Pneumocystis jirovecii pneumonia
Aspergillus fumigatus → aspergillosis

Histoplasma capsulatum
Coccidioides immitis
Candida species → candidiasis
Cytomegalovirus (CMV) → CMV pneumonia

S. aureus
Gram-negative bacteria

Pneumonia in newborns Escherichia coli

Streptococcus agalactiae (Group B streptococcus)


Streptococcus pneumoniae
Haemophilus influenzae

Pneumonia in children (4 weeks –18 years) C. trachomatis (in infants) [2][3]

C. pneumoniae (in young children and adolescents) [4]


S. pneumoniae

Respiratory syncytial virus (RSV)


Mycoplasma
See also “Pneumonia in children.”

Pneumonia in young adults (18–40 years) Mycoplasma


Influenza virus
C. pneumoniae
S. pneumoniae

Pneumonia in adults (40–65 years) S. pneumoniae


H. influenzae
Mycoplasma

Anaerobes
Viruses

Pneumonia in elderly individuals S. pneumoniae [5]

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.

Risk factors [7]

Old age and immobility of any cause

Chronic diseases

Preexisting cardiopulmonary conditions (e.g., bronchial asthma, COPD, heart failure)

Acquired or congenital abnormalities of the airways (e.g., bronchiectasis, space-occupying lesions, cystic fibrosis)

Immunosuppression

HIV infection

Diabetes mellitus

Cytostatic and immunosuppressive therapy

Alcoholism

Malnutrition

Impaired airway protection

Alteration in consciousness (e.g., due to stroke, seizure, anesthesia, drugs, alcohol)

Dysphagia

Smoking

Environmental factors

Crowded living conditions (e.g., prisons, homeless shelters)

Toxins (e.g., solvents, gasoline)

Endemic exposures (e.g., areas of high Coccidioides and Histoplasma endemicity)

Contaminated water systems (e.g., in hotels, on cruise ships)

Zoonotic exposures (e.g., birds, farm animals)

Cryptogenic organizing pneumonia

Specific medications; (e.g., amiodarone, bleomycin) [8]

Chronic inflammatory disorders (e.g., rheumatoid arthritis)

Surgical procedures

Upper abdominal surgery

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.

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Classification

Pneumonia can be classified according to etiology, location acquired, clinical features, and the area of the lung affected by the pathology.
Etiology

Primary pneumonia: no apparent preexisting conditions that may predispose to pneumonia

Secondary pneumonia

Bronchial asthma, COPD, heart failure, cystic fibrosis

Viral upper respiratory tract infections with bacterial superinfection

Anatomical abnormalities such as tubercular caverns, bronchial tumors, or stenosis (postobstructive pneumonia) [9]

Aspiration pneumonia

Location acquired

Community-acquired pneumonia (CAP): pneumonia that is acquired outside of a healthcare establishment

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

Pneumonia featuring classic symptoms (typical findings on auscultation and percussion)

Manifests as lobar pneumonia or bronchopneumonia

Atypical pneumonia

Pneumonia with less distinct classical symptoms and often unremarkable findings on auscultation and percussion

Manifests as interstitial pneumonia

Area of lung affected by the pathology

Lobar pneumonia: pneumonia affecting one lobe of a lung

Multilobar pneumonia refers to the involvement of multiple lobes in a single lung or both lungs.

Panlobar pneumonia involves all the lobes of a single lung.

Bronchial pneumonia: pneumonia affecting the tissue around the bronchi and/or bronchioles

Interstitial pneumonia: pneumonia affecting the tissue between the alveoli

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

Most common: microaspiration (droplet infection) of airborne pathogens or oropharyngeal secretions

Aspiration of gastric acid (aspiration pneumonitis) , food, or liquids

Hematogenous dissemination (rare)

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)

4. Hypoxia due to increased alveolar-arterial oxygen gradient

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

Classic (typical) pneumonia of an entire lobe; primarily caused by pneumococci

Characterized by inflammatory intra-alveolar exudate, resulting in consolidation

Can involve the entire lobe or the whole lung

Stages of lobar pneumonia

Stages Macroscopic findings Microscopic findings

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)

Liver–like consistency Erythrocytes and most bacteria have been degraded.


Alveolar walls thickening

Resolution (day 8 to week 4) Gradual aeration of the affected segment Enzymatic fibrinolysis

Macrophages remove the suppurative exudate.

Bronchopneumonia: mostly commonly a descending infection that affects the bronchioles and adjacent alveoli

Primarily caused by pneumococci and/or other streptococci

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

Manifests as typical pneumonia

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

Bilateral multifocal opacities are classically found on chest x-ray.

Manifests as atypical pneumonia

Often has an indolent course (walking pneumonia)

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

High fever and chills

Productive cough with purulent sputum (yellow-greenish)

Crackles and bronchial breath sounds on auscultation

Decreased breath sounds

Enhanced bronchophony, egophony, and tactile fremitus

Dullness on percussion

Tachypnea and dyspnea (nasal flaring, thoracic retractions)

Pleuritic chest pain when breathing, often accompanying pleural effusion

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.

Nonproductive, dry cough

Dyspnea

Auscultation often unremarkable

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

CBC, inflammatory markers: ↑ CRP, ↑ ESR, leukocytosis


[11]
↑ Serum procalcitonin (PCT): Procalcitonin is an acute phase reactant that can help to diagnose bacterial lower respiratory tract infections. ;

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]

Decrease of PCT to ≤ 80% of peak level

Decrease of PCT to < 0.25 mcg/L


[13]
ABG: ↓ PaO2

BMP, LFTs

Do not rely on laboratory markers like CRP or procalcitonin to determine the need for antibiotic therapy. [11][18]

Microbiological studies

Indication Microbiological studies to consider [10][11][13]

Any admitted patient MRSA nares swab (PCR and/or culture)

Any patient being treated empirically for MRSA or P. aeruginosa Blood cultures (2 sets)

Sputum culture and Gram stain

Severe CAP Blood cultures (2 sets)

HAP Sputum culture and Gram stain


VAP Pneumococcal urinary antigen
Legionella pneumophila urinary antigen
Consider Chlamydia pneumoniae respiratory PCR.

Influenza season Influenza nasal swab (NAAT)

Consider respiratory virus panel nasal swab (NAAT).

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

Chest x-ray (posteroanterior and lateral)

Indications: all patients suspected of having pneumonia

X-ray findings in pneumonia

Lobar pneumonia

Opacity of one or more pulmonary lobes

Presence of air bronchograms: appearance of translucent bronchi inside opaque areas of alveolar consolidation

Bronchopneumonia

Poorly defined patchy infiltrates scattered throughout the lungs

Presence of air bronchograms

Atypical or interstitial pneumonia

Diffuse reticular opacity

Absent (or minimal) consolidation

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]

Chest CT (usually without contrast)

Indications

Inconclusive chest x-ray

Recurrent pneumonia

Poor response to treatment

Advantages: more reliable evaluation of circumscribed opacities, pleural empyema, or sites of consolidation
[22]
Findings:

Localized areas of consolidation (hyperdense)

Air bronchograms

Ground-glass opacities

Pleural effusion/empyema

Hyperdense fluid collection

Split pleura sign

Nodules

Large (e.g., in tuberculosis or fungal pneumonia)

Peribronchial (e.g., bronchopneumonia)

Disseminated (e.g., septic emboli or varicella-zoster pneumonia)

CT is more sensitive and specific than CXR for the diagnosis of pneumonia.

Lung ultrasound in pneumonia

Point-of-care ultrasound (POCUS) has high sensitivity and specificity for the diagnosis of pneumonia. [23][24]

Indications

Evaluation of suspected pneumonia


[25]
Assessment of undifferentiated dyspnea

Characteristic findings [26][27]

Consolidation

Irregular and serrated lung margins

Air bronchograms

Unilateral B-lines

Pleural effusion

In the emergency department, consider POCUS to quickly confirm pneumonia and assess for other causes of dyspnea.

Advanced diagnostics for pneumonia

Bronchoscopy

Indications

Suspected mass (e.g., recurrent pneumonia)

Need for pathohistological diagnosis (e.g., biopsy of a central mass discovered on CT)

Inconclusive results on CT

Poor response to treatment

Diagnostic thoracentesis

[13][28]
Indications: consider if pleural effusion > 10 mm is present to evaluate for pleural empyema

Findings: See “Diagnostics” and “Parapneumonic effusion” in “Pleural effusion”.

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).

Provide supportive care.

Re-evaluate therapy after 48 hours (earlier if the patient's condition deteriorates or new information becomes available).

Initial stabilization [29][30]

Identification and management of sepsis

Fluid resuscitation and management of septic shock as needed

Respiratory support as needed

Supplemental oxygen for hypoxia

HFNC oxygen therapy, NIPPV, or intubation for respiratory failure

Criteria for hospitalization [11][18]


Every patient should be assessed individually and clinical judgment is the most important factor. The pneumonia severity index (PSI) and the CURB-65 score
are tools that can help to determine whether to admit a patient.
[31]
CURB-65 score

Confusion (disorientation, impaired consciousness)

Serum Urea > 7 mmol/L (20 mg/dL)

Respiratory rate ≥ 30/min

Blood pressure: systolic BP ≤ 90 mm Hg or diastolic BP ≤ 60 mm Hg

Age ≥ 65 years

Interpretation

Each finding is assigned 1 point.

CURB-65 score 0 or 1: The patient may be treated as an outpatient.

CURB-65 score ≥ 2: Hospitalization is indicated.

CURB-65 score ≥ 3: Consider ICU level of care.

CRB-65 score (if serum urea is not known or unavailable)

CRB-65 score of 0: The patient may be treated as an outpatient.

CRB-65 score of ≥ 1: Hospitalization is recommended.


[32]
Pneumonia severity index (PSI/PORT score)

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.

Criteria for ICU admission [11][18]

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]

IDSA/ATS criteria for severe CAP [11]

Major criteria Septic shock/need for vasopressors

Mechanical ventilation

Minor criteria Confusion


Body temperature < 36°C

Hypotension requiring fluid resuscitation


Respiratory rate ≥ 30/min
PaO2/FiO2 ≤ 250

Leukopenia (WBC < 4,000/mm3)

Thrombocytopenia (platelet count < 100,000/mm3)


BUN ≥ 20 mg/dL

Multilobar infiltrates

Interpretation

Severe CAP: one major criterion or ≥ 3 minor criteria

Empiric antibiotic therapy for community-acquired pneumonia [11][33]

Outpatient

Empiric antibiotic therapy for community-acquired pneumonia in an outpatient setting

Patient profile Recommended empiric antibiotic regimen [11]

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

Empiric antibiotic therapy for community-acquired pneumonia in an inpatient setting

Patient profile Recommended empiric antibiotic regimen [11]

Nonsevere CAP/non-ICU treatment Combination therapy


An antipneumococcal β-lactam:
Ampicillin-sulbactam
Ceftaroline

Ceftriaxone
Cefotaxime
PLUS one of the following:
A macrolide
Azithromycin
Clarithromycin

Doxycycline
Monotherapy: with a respiratory fluoroquinolone
Gemifloxacin
Moxifloxacin

Levofloxacin

Severe CAP/ICU treatment Combination therapy


An antipneumococcal β-lactam:
Ampicillin-sulbactam
Ceftaroline

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 )

Risk factors for Pseudomonas aeruginosa Combination therapy


An antipneumococcal, antipseudomonal β-lactam:
Piperacillin-tazobactam
Cefepime
Ceftazidime

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

5–7 days is usually sufficient.

Consider longer courses in patients with one of the following:

Patient not responding to treatment

Suspected or concern for MRSA or P. aeruginosa infection

Concurrent meningitis

Unusual pathogens (e.g., Burkholderia pseudomallei, fungal infection)

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]

Corticosteroids are not routinely recommended as adjunct therapy. [11]

If aztreonam is used as an alternative to other β-lactam antibiotics, additional coverage for MSSA must be included (e.g., a fluoroquinolone).

Empiric antibiotic therapy for hospital-acquired pneumonia [10]

Empiric antibiotic therapy for hospital-acquired pneumonia

Patient profile Recommended empiric antibiotic regimen [10]

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

PLUS one of the following:


An antipneumococcal, antipseudomonal β-lactam
Piperacillin-tazobactam
Cefepime
Ceftazidime

Meropenem
Imipenem
A fluoroquinolone
Levofloxacin

Ciprofloxacin )
Aztreonam

Patients at high risk for mortality Combination therapy


One of the following antibiotics with MRSA activity:
Patients with structural lung disease (e.g., cystic fibrosis, bronchiectasis)
Vancomycin
Linezolid

PLUS any two of the following (avoid combining two β-lactams):


An antipneumococcal, antipseudomonal β-lactam
Piperacillin-tazobactam
Cefepime
Ceftazidime

Meropenem
Imipenem
A fluoroquinolone
Levofloxacin

Ciprofloxacin
An aminoglycoside
Amikacin
Gentamicin

Tobramycin
Aztreonam

Duration of treatment

Empiric antibiotic therapy should be narrowed and/or de-escalated as soon as feasible.

Seven days of therapy are usually sufficient. [10]

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!

Empiric antibiotic therapy for ventilator-associated pneumonia [10]

Recommended combination therapy

An antipneumococcal, antipseudomonal β-lactam

Aztreonam

Imipenem

Meropenem

Ceftazidime

Cefepime

Piperacillin-tazobactam

PLUS one of the following antibiotics with MRSA activity:

Vancomycin

Linezolid

PLUS one of the following:

A fluoroquinolone

Levofloxacin

Ciprofloxacin

An aminoglycoside

Amikacin

Gentamicin

Tobramycin

A polymyxin

Colistin

Polymyxin B

Duration of treatment: Seven days of therapy are usually sufficient. [10]

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]

Supportive therapy for pneumonia

Sufficient rest (not absolute bed rest) and physical therapy

Hydration with PO or IV fluids, supplemental oxygen as needed

Incentive spirometer

Antipyretics, analgesics as needed (e.g., acetaminophen )


[34]
Expectorants and mucolytics

Antitussives (e.g., codeine )

Acute management checklist

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.

Order microbiological workup as indicated by patient severity and risk factors.

Community-acquired pneumonia: Start empiric antibiotics for CAP.

Hospital-acquired pneumonia: Start empiric antibiotics for HAP.

Ventilator-associated pneumonia: Start empiric antibiotics for VAP.

Evaluate and treat sepsis if present (see sepsis).

Administer supplemental O2 if patient is hypoxemic.

[33]
Consider advanced diagnostic evaluation.

Provide supportive care for pneumonia (e.g., antipyretics, , IV fluids).

Continuous pulse oximetry

Trend inflammatory markers, procalcitonin.

Narrow antibiotic therapy as soon as feasible.

Pathogen-specific pneumonia

Mycoplasma pneumonia [35]

Epidemiology

One of the most common causes of atypical pneumonia

More common in school-aged children and adolescents

Outbreaks most commonly occur in schools, colleges, prisons, and military facilities.

Clinical features

Generalized papular rash

Erythema multiforme

See “Atypical pneumonia”.

Diagnostics

Subclinical hemolytic anemia: associated with elevated cold agglutinin titers (IgM)

Interstitial pneumonia; , often with a reticulonodular pattern on chest x-ray

Chest x-ray can show extensive pulmonary involvement in patients with mild pneumonia.

Treatment

A macrolide, doxycycline, or fluoroquinolones

Beta-lactam antibiotics are not effective

See “Empiric antibiotics for CAP” for dosages and duration of treatment.

Other types of pathogen-specific pneumonia

Legionnaire disease

Pneumocystis pneumonia

Pseudomonas aeruginosa: causes VAP

Tuberculosis

Primary influenza pneumonia

Various viral infections (e.g., respiratory syncytial virus, hantavirus, adenovirus, CMV, SARS-CoV, SARS-CoV-2)

Ornithosis

Aspiration pneumonia

Definitions

Aspiration

The inhalation of foreign material into the respiratory tract

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

May cause ARDS in extreme cases

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).

Gram-negative bacilli predominate in hospital-acquired infections (e.g., P. aeruginosa, Klebsiella spp.).

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)

Altered consciousness: alcohol, sedation, general anesthesia, stroke

Apoplexy and neurodegenerative conditions

Gastroesophageal reflux disease, esophageal motility disorders

Congenital defects (e.g., tracheoesophageal fistula)

Use of a nasogastric feeding tube

Aspiration pneumonitis and pneumonia are unusual following aspiration of tube feeds or blood, which are typically high-pH and sterile. [36]

Clinical features [36][37]

Aspiration pneumonitis

Immediate symptoms: bronchospasms , dyspnea, wheezing and/or crackles, hypoxemia

Late symptoms: fever, shortness of breath, cough

Aspiration pneumonia

Immediate symptoms: often none

Late symptoms: fever, shortness of breath, cough with foul-smelling sputum

Diagnostics
Clinical diagnosis supported by characteristic laboratory and imaging findings

Laboratory and microbiological studies: same as for the diagnosis of pneumonia.

ABG: e.g., ↓ PaO2


[38][39]
Imaging: The lung region in which the infiltrates are seen depends on the patient's position on aspiration.

Supine position: superior segment of the right lower lobe (most common site of aspiration)

Standing/sitting: posterior basal segment of the right lower lobe

Right lateral decubitus position: posterior segment of the right upper lobe or right middle lobe

The initial CXR may be negative in early aspiration pneumonia. [36]

Treatment [36]

Acute aspiration: airway management and respiratory support

Immediate oropharyngeal suctioning

Intubation if there is ongoing risk of aspiration (e.g., post-extubation, ↓ LOC)

O2 therapy and inhaled bronchodilators as needed

Aspiration pneumonitis: typically requires supportive care only


[11]
Antibiotics are usually not required

Consider empiric antibiotics for patients with any of the following :

Respiratory failure or suspected septic shock

Acid suppression medications

Small bowel obstruction

Aspiration pneumonia: antibiotic therapy following standard pneumonia treatment regimens

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

Acute respiratory failure, acute respiratory distress syndrome (ARDS)

Abscess

Prevention [36]

Treatment of underlying causes to reduce the risk of aspiration

NPO status prior to elective procedures with general anesthesia

Formal swallowing evaluation when clinically appropriate

Aspiration precautions for patients with risk factors for aspiration

Regular oral care

Elevation of the head of the bed

Dysphagia-modified diet

One-on-one observation with meals

Suctioning equipment at bedside

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

Analgesics can be used for the relief of symptoms.

Parapneumonic pleural effusion (common)

Pleural empyema

Lung abscess

ARDS

Respiratory failure

Sepsis

We list the most important complications. The selection is not exhaustive.

Prognosis

Mortality increases with age.

The mortality risk can be evaluated with the CURB-65 score. [42]

Score 0: ∼ 1%

Score 1–2: ∼ 10%

Score 3: ∼ 14%

Score 4: ∼ 40%

HAP is associated with a mortality rate of > 20%.

Prevention

Immunization (see “ACIP immunization schedule” for information on doses and intervals)

Pneumococcal vaccination

Influenza vaccination

Smoking cessation

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