Aspiration pneumonia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2], Sunny Kumar MD [3]

Aspiration pneumonia is a common pneumonia among patients with risk factors such as neurologic diseases, dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization. Microaspiration and macroaspiration of different materials are the primary cause of aspiration pneumonia. The mechanism behind damage of lung due to aspiration of depends on the content of aspirate and the response of lung tissue to the content. Chemical pneumonitis usually occurs following aspiration of materials that are toxic to pulmonary tissue. In case of oropharyngeal secretions the damage is due to bacteria infecting and inducing inflammation in lung tissues. Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis. Lipoid pneumonia is caused by aspiration of mineral oil when used for constipation treatment. Patients might present with acute chest pain, cough, fever, and sweating. Less common symptoms of aspiration pneumonia include fatigue, nausea and vomiting, diarrhea, and dyspnea. Chemical pneumonitis usually develop after aspiration of gastric acid and might present acutely within two hours. Rapid clinical recovery or worsening of respiratory distress and hypoxemia might happen. Bacterial infection following aspiration is slower that other community-acquired pneumonia and might be acute, subacute, or chronic. Complications of aspiration pneumonia include segmental or lobar pneumonia, bronchopneumonia, bronchiectasis, lung abscess, empyema, respiratory failure, bacteremia, and shock. Diagnosis of aspiration pneumonia is by history and symptoms following aspiration or in patients with risk factors. Chest x-ray is used to diagnose aspiration pneumonia. Bronchoscopy is used to remove foreign body from the respiratory tract. Antibiotic therapy such as ampicillin-sulbactam, amoxicillin-clavulanate, or clindamycin for 7 days is required for chemical pneumonitis and bacterial infection. Supportive ventilation might be required in patients with respiratory failure following chemical pneumonitis. Clearing respiratory tract by suction is helpful to prevent the extent of pulmonary damage. Effective measures for the primary prevention of aspiration pneumonia include dietary habit changes, maintaining oral hygiene, postural maneuvers, and medications such as H2 antagonists, metoclopramide, mosapride, amantadine, or cilostazol.

The literature on aspiration pneumonia came into knowledge of medical society along with the discovery of pneumonia. During 1893, Veillon was first to write about the role of anaerobic bacteria in aspiration pneumonia. The major breakthrough came when x-ray was invented by Roentgen in 1896.

Aspiration pneumonia is a part of aspiration syndrome which is consist of four classes depending on nature of aspirated substance including foreign body aspiration, chemical pneumonitis, bacterial infection, and lipid pneumonia. Aspiration pneumonia depends on the duration of systems might be classified into two groups of acute and chronic. 

Aspiration pneumonia is a common pneumonia among patients with risk factors including neurologic diseases. Microaspiration and macroaspiration of different materials are the main cause of aspiration pneumonia. The mechanism behind damage of lung due to aspiration of depends on the content of aspirate and the response of lung tissue to the content. Host factors including mucociliary clearance, cough reflex, and immune system might be probably impaired. Chemical pneumonitis usually occurs following aspiration of materials that are toxic to pulmonary tissue. There might be no bacterial or viral organisms involved. It is mostly associated with aspiration of gastric acid. In case of oropharyngeal secretions the damage is due to bacteria infecting and inducing inflammation in lung tissues. Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis. Lipoid pneumonia is caused by aspiration of mineral oil when used for constipation treatment. Following oil aspiration there is an inflammatory response with regional edema and acute cough, fever, and dyspnea. Patients with genetic syndromes and paralysis of lower cranial nerves might be prone to aspiration pneumonia. On gross pathology, different aspirated particles might be seen. On microscopic histopathological analysis, aspirated material fragments, inflammation, fibrosis, and skeletal muscle fibers might be seen.

Aspiration pneumonia is caused by aspiration of different particles including secretions, gastric contents or any foreign material which reaches lung parenchyma and damages lung tissue by inflammation. Microorganisms that are responsible for aspiration pneumonia include S. aureus, S. pneumoniae, Enteric bacilli, Hemophilus species, Neisseria species, M. catarrhalis, P. aeruginosa.

Aspiration pneumonia must be differentiated from other diseases that cause productive cough, fever, and dyspnea.

The incidence and prevalence of aspiration pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonias from each other. The incidence of aspiration pneumonia is approximately 300,000 to 600,000 individuals annually in the United States. The prevalence of aspiration pneumonia is approximately 5,000 to 15,000 per 100,000 individuals admitted in the hospital due to community acquired pneumonia. The mortality rateof aspiration pneumonia is approximately 10.6-21%. The incidence of aspiration pneumonia increases with age; the median age at diagnosis is 70-80 years. Males are more commonly affected by aspiration pneumonia than females. There is no racial predilection to aspiration pneumonia.

Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization. Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.

There is insufficient evidence to recommend routine screening for aspiration pneumonia.

Aspiration pneumonia occurs following aspiration of different materials and particles. Natural history, complications, and prognosis are different for each category. Chemical pneumonitis usually develop after aspiration of gastric acid and might present acutely within two hours. Rapid clinical recovery or worsening of respiratory distress and hypoxemia might happen. Bacterial infection following aspiration is slower that other community-acquired pneumonia and might be acute, subacute, or chronic. Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis. Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs. Complications of aspiration pneumonia include segmental or lobar pneumonia, bronchopneumonia, bronchiectasis, lung abscess, empyema, respiratory failure, bacteremia, and shock.

Aspiration pneumonia is mainly diagnosed based on clinical presentation. The CURB-65 and the eCURB scoring systems are used to evaluate and predict mortality in patients with pneumonia. However, they are not helpful in aspiration pneumonia.

Patients with aspiration pneumonia may have a positive history of predisposing condition or altered level of consciousness. The most common symptoms of aspiration pneumonia include chest pain, cough, fever, and sweating. Less common symptoms of aspiration pneumonia include fatigue, nausea and vomiting, diarrhea, and dyspnea.

Patients with aspiration might appear normal or toxic. Physical examination of patients with aspiration pneumonia is usually remarkable for fever, tachypnea, hypotension, crackles, decreased breath sounds, and increased tactile fremitus.

Different laboratory tests might be used in patients with aspiration pneumonia. Sputum analysis including gram stain and culture must be done in patients with cough. ABG may show acute hypoxemia and decreased mixed venous oxygen saturation. CBC shows leukocytosis with left shift or leukopenia, anemia, or thrombocytopenia.

There are some non-specific findings on ECG of a patient with chronic aspiration pneumonia which include sinus tachycardia, minor nonspecific ST-segment or T-wave changes, right atrial enlargement, QRS abnormalities like right axis deviation, and presence of S1S2S3.

Chest x-rays may be helpful in the diagnosis of aspiration pneumonia. Findings on an chest x-ray suggestive of aspiration pneumonia include lobar pneumonia, areas of opacity, unilateral consolidation, air bronchogram, or cavitation.

In some cases, ultrasound is used for the diagnosis and follow-up of a patient with aspiration pneumonia, for a guided thoracocentesis and to quantify the amount of pleural effusion.

A chest CT scan might be used in patients with aspiration pneumonia if a chest x-ray is not conclusive. CT findings may include lobar consolidation, ground-glass opacities, bronchiectasis, atelectasis, pleural effusion, and consolidation. A chest CT can also help to assess reasons for therapy failure and complications, such as lung abscess, and pleural effusions.

Chest MRI may be helpful in the diagnosis of aspiration pneumonia. Findings on MRI suggestive of aspiration pneumonia include defining the nature of aspirated particle and extend of lung injury, atelectasis, consolidation and opacities.

Bronchoscopy with bronchoalveolar lavage is useful to obtain samples for gram stain and culture in patients with certain conditions, such as immunocompromised patients, ICU admission, or antibiotic failure.

Videofluoroscopic swallow study (VFSS) might be used to evaluate swallowing difficulties.

There are different approaches for different classes of aspiration pneumonia. Pneumonitis and bacterial infection require antibiotic therapy, while foreign body aspiration and mechanical obstruction may need invasive interventions. Chemical pneumonitis must be treated supportively. Immediate clearing the respiratory tract from aspirated material and fluid by suction must be the first step if the diagnosis of aspiration is definite. Pharmacologic medical therapy for aspiration pneumonia includes antibiotics such as ampicillin-sulbactam, amoxicillin-clavulanate, or clindamycin for 7 days. Alternative regimens include combination of metronidazole with penicillin G, amoxicillin, ceftriaxone, or cefotaxime. Positive pressure ventilation with 100% oxygen to support pulmonary function is sometimes required.

Surgical intervention is not recommended for the management of aspiration pneumonia. However, interventional techniques are used to remove foreign body from the respiratory tract. Flexible or rigid bronchoscopy is indicated in patients with observed aspiration or chronic wheezing.

Effective measures for the primary prevention of aspiration pneumonia include dietary habit changes, maintaining oral hygiene, postural maneuvers, and medications such as H2 antagonists, metoclopramide, mosapride, amantadine, or cilostazol.

There are no established measures for the secondary prevention of aspiration pneumonia.

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2], Sadaf Sharfaei M.D.[3]

The literature on aspiration pneumonia came into knowledge of medical society along with the discovery of pneumonia. During 1893, Veillon was first to write about the role of anaerobic bacteria in aspiration pneumonia. The major breakthrough came when x-ray was invented by Roentgen in 1896.

Following are important land mark events that shows how aspiration pneumonia became an important entity of critical care:^{[1][2][3][4][5][6]}

Year	Events
460 BC–380 BC	Hippocrates described pneumonia.
1138–1204 AD	Maimonides wrote about pneumonia as “The basic symptoms which occur in pneumonia and which are never lacking are as follows: acute fever, sticking pleuritic pain in the side, short rapid breaths, serrated pulse, and cough.”
1875	Edwin Klebs identified bacteria in the airways of individuals who died from pneumonia.
1848	Carl Friedländer identified the two common bacteria such as Streptococcus pneumoniae and Klebsiella pneumoniae that cause pneumonia.
1893	Veillon was first to write about the role of anaerobic bacteria in aspiration pneumonia.
1896	Roentgen described x-rays.
1918	Sir William Osler, known as “the father of modern medicine,” appreciated the morbidity and mortality of pneumonia, describing it as the “captain of the men of death.”
1927	Smith was first to clearly show anaerobic bacterial growth in animal models suffered from aspiration pneumonia.
1929	Drinker and Shaw announced the invention of the iron lung during the polio epidemic.
1985	Specimen collected from patients with aspiration pneumonia were vastly cultured and it was called anaerobic bandwagon.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2], Sadaf Sharfaei M.D.[3], Priyamvada Singh, M.D. [4]

Aspiration pneumonia is a part of aspiration syndrome which is consist of four classes depending on nature of aspirated substance including foreign body aspiration, chemical pneumonitis, bacterial infection, and lipid pneumonia. Aspiration pneumonia, depending on the duration of systems might be classified into two groups of acute and chronic.

• Aspiration pneumonia is one class of aspiration syndrome.
• Aspiration syndrome consists of four classes depending on nature of aspirated substance. Following are the four classes of aspiration syndrome:^[1][2]

Classification of aspiration syndrome
Classes	Substance involved	Risk factor	Mechanism of damdage
Mechanical obstruction	Foreign body	Childhood	Traumatic
Chemical pneumonitis	Gastric contents	Decreased level of consciousness	Corrosive effect of acid on respiratory tract
Bacterial infection	Oral cavity bacterial flora	Dysphagia, elderly age	Similar to community acquired pneumonia
Lipid pneumonia	Oil	Childhood	Macrophages engulf lipid substances lining pulmonary tree

• Aspiration pneumonia, depending on the duration of systems might be classified into two groups:
  • Acute aspiration pneumonitis
  • Chronic aspiration pneumonia

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2], Sadaf Sharfaei M.D.[3]

Aspiration pneumonia is a common pneumonia among patients with risk factors including neurologic diseases. Microaspiration and macroaspiration of different materials are the primary cause of aspiration pneumonia. The mechanism behind damage of lung due to aspiration depends on the content of aspirate and the response of lung tissue to the content. Host factors including mucociliary clearance, cough reflex, and immune system might be impaired. Chemical pneumonitis usually occurs following aspiration of materials that are toxic to pulmonary tissue. There might be no bacterial or viral organisms involved. It is mostly associated with aspiration of gastric acid. In case of oropharyngeal secretions the damage is due to bacteria infecting and inducing inflammation in lung tissues. Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis. Lipoid pneumonia is caused by aspiration of mineral oil when used for constipation treatment. Following oil aspiration there is an inflammatory response with regional edema, acute cough, fever, and dyspnea. Patients with genetic syndromes and paralysis of lower cranial nerves might be prone to aspiration pneumonia. On gross pathology, different aspirated particles might be seen. On microscopic histopathological analysis, aspirated material fragments, inflammation, fibrosis, and skeletal muscle fibers might be seen.

To understand the pathogenesis we have to review following physiological facts regarding aspiration pneumonia:^{[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]}

Inhalation of aerosolized droplets of 0.5 to 1 micrometer is the most common pathway of acquiring pneumonia. A few bacterial and viral infections are transmitted in this fashion. The lung can normally filter out particles between 0.5 to 2 micrometer by recruiting the alveolar macrophages.

Aspiration of oropharyngeal contents containing pathogenic microorganisms is one of the mechanisms of acquiring pneumonia. It most commonly occurs in normal persons during sleep, in unconscious persons due to gastroesophageal reflux or impaired gag reflex and cough reflex.

Several strategies are evolved to evade host defense mechanisms and facilitate spreading before establishing an infection.

• Influenza virus possesses neuraminidases for cleavage of sialic acid residues on the cell surface and viral proteins, which prevent aggregation and facilitate propagation of viral particles.

• Chlamydophila pneumoniae induces complete abortion of cilia motions which assists colonization at the respiratory epithelium.

• Mycoplasma pneumoniae produces a virulence factor with ADP-ribosylating activity which is responsible for airway cellular damage and mucociliary dysfunction.

• Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis produce proteases that split mucosal IgA.

• Streptococcus pneumoniae possesses pneumolysin that aid the bacteria during colonization, by facilitating adherence to the host, during an invasion by damaging host cells, and during infection by interfering with the host immune response.

• The lungs can normally filter out large droplets of aerosols.
• Smaller droplets of the size of 0.5 to 2 micrometer are deposited on the alveoli and then engulfed by alveolar macrophages.
• These macrophages release cytokines and chemokines, which also includes tumor necrosis factor-alpha, interleukin-8 and LTB4.
• The neutrophils are recruited by these cells to eliminate these microorganisms.

• The cilia lining the respiratory epithelium serve to move secreted mucus containing trapped foreign particles including pathogens towards the oropharynx for either expectoration or swallowing.
• Elevated incidence of pneumonia in patients with genetic defects affecting mucociliary clearance such as primary ciliary dyskinesia suggests its role in the pathogenesis of community-acquired pneumonia.

• Cough, together with mucociliary clearance, prevent pathogens from entering the lower respiratory tract.
• Cough suppression or cough reflex inhibition seen in patients with cerebrovascular accidents and drug overdosages is associated with an enhanced risk for aspiration pneumonia.
• Another relation to cough is genetic polymorphisms in the angiotensin-converting enzyme (ACE) gene.
• The role of cough in preventing pneumonia may be explained by a higher risk for developing pneumonia in homozygotes carrying deletion/deletion (DD) genotype who are found to have lower levels of bradykinin and tachykinins such as substance P.

• Pathogen-associated molecular patterns (PAMPs) are initially recognized by Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) of the innate immune system.
• Effectors in the acquired immune system are involved in elimination of microorganisms and generation of immunological memory.
• Other components in the immune system such as complement system, cytokines, and collectins, also mediate the defense against microorganisms causing pneumonia.

• Chemical pneumonitis usually occurs following aspiration of materials that are toxic to pulmonary tissue. There might be no bacterial or viral organisms involved. It is mostly associated with aspiration of gastric acid. 
• Following aspiration, there is onset of respiratory distress and cyanosis within 2 hours.
• In animal and autopsy studies, following gastric acid aspiration, atelectasis, peribronchial hemorrhage, pulmonary edema, and degeneration of bronchial epithelial cells initiates within three minutes. Release of proinflammatory cytokines, especially tumor necrosis factor-alpha (TNF) and interleukin-8 causes polymorphonuclear leukocytes and fibrin to fill the alveolar spaces after four hours. The lung become edematous and hemorrhagic with alveolar consolidation.

• Another form of aspiration pneumonia is caused by less virulent oral bacteria that normally colonized in the upper airways or stomach.
• Anaerobic bacteria are more involved in aspiration pneumonia.
• Peptostreptococcus, Fusobacterium nucleatum, Prevotella, Bacteroides melaninogenicus, and other Bacteroides spp are the major pathogens that cause pulmonary infections following aspiration. However, the majority have mixed aerobe and anaerobe infections.

• Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis.
• Foreign body aspiration is more common in children from one to three years of age.

• Lipoid pneumonia is caused by aspiration of mineral oil when used for constipation treatment.
• Patients usually have risk factors for aspiration.
• Following oil aspiration there is an inflammatory response with regional edema and acute cough, fever, and dyspnea.
• Fibrous tissue encapsulates aspirated oils and develop intraalveolar hemorrhage. They will presents with a mass seen on imaging in an asymptomatic patient.

• There are no genetic causes of aspiration pneumonia.
• However, patients with genetic syndromes and paralysis of following lower cranial nerves might be prone to aspiration pneumonia.^[16][17]
  • Cranial nerve 9 (glossopharyngeal)
  • Cranial nerve 10 (vagal)
  • Cranial nerve 11 (accessory)
  • Cranial nerve 12 (hypoglossal)
• Associated genetic syndromes are as follow:
  • Cerebral palsy
  • Amyotrophic lateral sclerosis (ALS)
  • Spinal muscular atrophy
  • Bulbospinal muscular atrophy (BSMA)
  • Unclassified motor neuron diseases such as:
    • Sandhoff disease
    • Triple-A syndrome
    • Brown-Vialetto-Van Lare-syndrome
  • Hereditary neuropathy

• On gross pathology, different aspirated particles might be seen.

• On microscopic histopathological analysis, aspirated material fragments, inflammation, fibrosis, and skeletal muscle fibers might be seen.

{{#ev:youtube|bTqgAfQv0p4}}

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sunny Kumar MD [2], Sadaf Sharfaei M.D.[3]

Aspiration pneumonia is caused by aspiration of different particles including secretions, gastric contents or any foreign material which reaches lung parenchyma and damages lung tissue by inflammation. Microorganisms that are responsible for aspiration pneumonia include S. aureus, S. pneumoniae, Enteric bacilli, Hemophilus species, Neisseria species, M. catarrhalis, P. aeruginosa.

Aspiration pneumonia may be caused by:^[1]

• Inhalation of different particles such as:
  • Food
  • Saliva
  • Liquid
  • Vomit
• Microorganisms that are responsible for aspiration pneumonia include:^[2]
  • S. aureus
  • S. pneumoniae
  • Enteric bacilli
  • Hemophilus species
  • Neisseria species
  • M. catarrhalis
  • P. aeruginosa 

Less common causes of aspiration pneumonia include:

• Inhalation of different particles such as:
  • Foreign body
  • Meconium
  • Oil

Cardiovascular	No underlying causes
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	S. aureus, S. pneumoniae, Enteric bacilli, Hemophilus species, Neisseria species, M. catarrhalis, P. aeruginosa
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	Aspiration of different particles including secretions, gastric contents or foreign body

List the causes of aspiration pneumonia in alphabetical order.

• Aspiration of different particles including secretions, gastric contents or foreign
• Enteric bacilli
• Hemophilus species
• Moraxella catarrhalis
• Neisseria species
• P. aeruginosa
• S. aureus
• S. pneumoniae

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Karina Zavaleta, MD [2], Anmol Pitliya, M.B.B.S. M.D.[3]

Aspiration pneumonia must be differentiated from other diseases that cause productive cough, fever, and dyspnea.

Organ system	Diseases	Clinical manifestations								Diagnosis				Other features
		Symptoms							Physical exam
		Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Foreing body aspiration[1][2][3]	Acute	Variable	+	+	−	+	+	Wheezing Decreased breath sounds	No specific tests	Hyperinflated lungs, atelectasis, and mediastinitis Shift in chest radiograph when the object is radio−opaque CT may be helpful	Not specific	Bronchoscopy	In children <1 year and adults >75 years Organic materials in children Inorganic materials in adults
	Croup[4]	Acute	3−5 days	+	−	−	+	+	Stridor Crackles	Leukopenia	Subglottic narrowing (steeple sign) in postero−anterior radiograph chest	Decresed tidal volume	Clinical diagnosis. Laboratory findings and imaging are not necessary for diagnosis	Barking cough Etiology: Parainfluenza virus type 1 (most common)
	Pertussis[5][6]	Acute	Two weeks	+ Whooping sound	−	+	+	+	Clear chest	Polymerase chain reaction (PCR) shows Bordetella pertussis Serologic testing	Atelectasis may seen on chest imaging Lymphadenopathy	Normal function	Culture	Etiology: Bordetella pertussis Phases: Catarrhal, paroxysmal and convalescent
	Rhinosinusitis[7][8]	Acute, subacute, chronic, recurrent	Acute: Less than 4 weeks Subacute: 4−12 weeks Chronic: More than 12 weeks Recurrent: 4 or more episodes or acute rhinosinusitis per year	+	−	−	+	+	Clear chest	In complicated acute bacterial rhinosinusitis, endoscopic cultures or sinus aspirate is indicated Nasal culture may also be helpful	Air−fluid level, mucosal edema and bony erosion of sinus on CT MRI for distinguish the etiology	Normal function	Clinical diagnosis: Nasal congestion, obstruction, and purulent rhinorrhea	Erythema in periorbital area
Organ system	Diseases	Clinical manifestations								Diagnosis				Other features
		Symptoms							Physical exam
		Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Acute Bronchitis[9]	Acute	From 5 days to 1 or 3 weeks	+	−	−	+/−	+	Wheezing Rhonchi	Sputum culture is not indicated PCR in bacterial infection may be helpful	Chest X−ray to exclude other diseases	FEV1 < 80%	Clinical diagnosis	Majority of cases are caused by respiratory viruses
	Chronic Bronchitis[10][11]	Chronic	Most of the days for three months in the las two years.	+ Clear sputum	−	−	+	+	Wheezing Rhonchi	CBC and ABG may be helpful	Chest X−Ray to exclude other diseases CT may also be helpful	FEV1/FVC ratio < 70% Post bronchodilatador FEV1 > 80% Reduced FVC after bronchodilatador administration Decread vital capacity Increased total lung capacity	Demostration of airflow limitation on spirometry	Smoker’s cough Cigarette smoking Pollution
	Emphysema [12]	Chronic	Months to years	+ Mucoid or purulent sputum	−	−	+	+	Shortness of breath Wheezing Prolonged expiration Crackles	Testing for alpha 1−antitrypsin may be helpful	Chest X−Ray to exclude other diseases CT may also be helpful	FEV1/FVC <70% Post bronchodilator FEV1 >80	Detection of early emphysema in CT of chest	Exposure of tobacco and air pollution
	Bronchiolitis[13][14]	Acute	8−15 days	+	−	−	+	+	Wheezing Crackles Increased respiratory rate	Complete blood count (CBC) may be helpful Urinalysis & urine culture ( in infants)	Chest X−Ray may be helpful	Normal function or obstructive changes (FEV1/FVC <70%) Air trapping in Lung volumes Reduced Diffusing capacity of carbon monoxide ( DLCO)	Clinical diagnosis	Etiology: Respiratory syncytial virus, Rhinovirus Children <2 years
Organ system	Diseases	Clinical manifestations								Diagnosis				Other features
		Symptoms							Physical exam
		Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Respiratory	Pneumonia[15][16]	Acute	Variable	+ Mucopurulent sputum	−	−	+	+	Crackles Egophony Decreased bronchial sounds	Leftward shift leukocytosis Blood culture in hospitalized patients Sputum culture in hospitalized patients	Consolidation, cavitation, and infiltrated interstitial in chest X−ray Anatomical changes observed in chest CT	Not specific	Infiltration observed in chest X−ray	Community−acquired pneumonia Healthcare−associated pneumonia
	Lung cancer[17][18]	Chronic	Years	+	+	+	+/−	+	Hoarseness	The following investigations may be helpful: Complete blood count (CBC) ALT, AST Calcium Alkaline phosphatase LDH Creatinine	Contrast−enhanced CT of chest and upper abdomen	Not specific	Tissue biopsy (sample should be sufficient for molecular testing)	Risk factor: Cigarette smoking Types Small cell lung cancer (SCLC) Non−small cell lung cancer (NSCLC)
	Tuberculosis (TB)[19][20]	Chronic	More than 2 or 3 weeks	+	+	+	+	+	Pleural effusion Crackles Whispered pectoriloquy Decreased fremitus Rhonchi	Sputum acid−fast bacilli (AFB) smear may be positive Mycobacterial culture may be positive Molecular testing may be helpful	Reactivation of TB is observed as infiltration in the upper lobe in chest X−Ray In patients with HIV, Tb is observed as lobar infiltration, adenopathy, lung mass named tuberculoma, small fibronodular lesions, and/or pleural effusion on chest X−Ray CT can detect early nodal process	Decreased FEV1 Reduced FVC	Isolation of Mycobacterium tuberculosis from some secretion	Etiology: Mycobacterium tuberculosis Complications: Pneumothorax, bronchiectasis, pulmonary destruction and chronic pulmonary aspergillosis
	Cystic fibrosis (CF)[21][22]	Chronic	Variable	+	−	+	+/−	+	Barrel−shaped chest Wheezing Tachypnea	Respiratory tract culture may be helpful for diagnosing secondary bacterial infection Bronchoalveolar lavage for cytology may be helpful ≥ 60 mmol/L Sweat chloride test CFTR mutation in molecular testing may be positive	Hyperinflation, atelectasis, and infiltrates on chest X−Ray Severe patients present bronchietasis, “tram tracks” peribronchial cuffing in chest X−Ray The extension of bronchietasis can be defined by CT	RV/TLC ratio increased FEV1/FVC ratio <70% Low levels of FEV1 High levels of TLC RV increased	Sweat chloride test	Evidence of CFTR dysfunction
Organ system	Diseases	Clinical manifestations								Diagnosis				Other features
		Symptoms							Physical exam
		Onset	Duration	Productive cough	Hemoptysis	Weight lost	Fever	Dyspnea	Ascultation	Lab findings	Imaging	PFT	Gold standard
Autoimmune	Wegener’s disease (GPA) [23][24]	Chronic	Months	+	+	+	+	+	Hoarseness Stridor Wheezing	The following investigations may be helpful: ANCA, P−ANCA, C−ANCA BUN Creatinine Complete blood count Urinalysis Lung biopsy	Nodules, pulmonary infiltrates, reticular margins, pleural opacities and cavities in chest X−Ray Nodules, cavities and stellate−shaped peripherial pulmonary in chest CT Bronchoscopy may be helpful	Low levels of DLCO Reduce lung volumes	Tissue biopsy	Nasal crusting, sinus pain, chronic rhinosinusitis, nasal obstruction and discharge in upper airway Saddle nose deformity Purpura in lower extremities
	Microscopic polyangitis (MPA)[25]	Chronic	Variable	+	+	+	+	+	Hoarseness Stridor Wheezing	The following investigations may be helpful: ANCA positive BUN Creatinine Complete blood count Urinalysis	Cavitation, nodules, and alveolar opacities in chest X−ray Head and chest CT may be helpful Electromyography/nerve conduction study may also be helpful	Reduced lung volumes	Tissue biopsy	Nerve damage Rhinosinusitis Purpura involving lower extremities
	Churg−Strauss[26][27]	Chronic	Variable	+	+	+	+	+	Wheezing Rales Rhonchi Expiratory sounds(related to asthma)	Peripherial eosinophilia In active phase CRP and erytrocyte sedimentation rate high Elevated IgE ANCA positive	Infiltrates in chest X−Ray Ground glass opacities, tree−in−bud sign and small nodules in chest CT	Lung volumes decreased FVC reduced FEV1/FVC ratio <70%	Tissue biopsy	Asthma Eosinophilia Rhinosinusitis

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

The incidence and prevalence of aspiration pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonias from each other. The incidence of aspiration pneumonia is approximately 300,000 to 600,000 individuals annually in the United States. The prevalence of aspiration pneumonia is approximately 5,000 to 15,000 per 100,000 individuals admitted in the hospital due to community acquired pneumonia. The mortality rate of aspiration pneumonia is approximately 10.6-21%. The incidence of aspiration pneumonia increases with age; the median age at diagnosis is 70-80 years. Males are more commonly affected by aspiration pneumonia than females. There is no racial predilection to aspiration pneumonia.

• The incidence and prevalence of aspiration pneumonia are underestimated. It is mostly because of similarities between pneumonias from different causes and lack of specific marker to distinguish pneumonia from each other.^[1]
• The incidence of aspiration pneumonia is approximately 300,000 to 600,000 individuals annually in the United States.^[2]

• The prevalence of aspiration pneumonia is estimated to be 5% to 15% of all pneumonias in the hospitalized population.^[3]
• The prevalence of aspiration pneumonia is approximately 5,000 to 15,000 per 100,000 individuals admitted in the hospital due to community acquired pneumonia.^[4]

• The mortality rate of aspiration pneumonia is approximately 10.6-21%.^[1]

• Aspiration pneumonia commonly affects children and elderly.^[5]
• The incidence of aspiration pneumonia increases with age; the median age at diagnosis is 70-80 years.^[1]

• There is no racial predilection to aspiration pneumonia.

• Males are more commonly affected by aspiration pneumonia than females.^[3]

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization. Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.

• Common risk factors in the development of aspiration pneumonia include dysphagia, swallowing dysfunction, altered mental status, COPD, and hospitalization.^[1][2][3]
• Less common risk factors in the development of aspiration pneumonia include medications, esophageal motility disorders, vomiting, enteral feeding, oropharyngeal colonization, male sex, and smoking.

• Common risk factors in the development of aspiration pneumonia include:
  • Dysphagia from neurologic diseases such as:
    • Dementia
    • Parkinson disease
    • Multiple sclerosis
    • Post-stroke
  • Swallowing dysfunction
  • Chronic obstructive pulmonary disease (COPD)
  • Hyperinflation
  • Altered mental status
  • Acute alcohol abuse
  • Seizures
  • Hospitalization
  • Nursing home residents

• Less common risk factors in the development of aspiration pneumonia include:
  • Medications such as:
    • Sedatives
    • Antipsychotics
    • Proton pump inhibitors
    • Histamine receptor-2 antagonists
    • Systemic antibiotics
  • Esophageal motility disorders such as
    • Achalasia
    • Esophageal strictures
  • Vomiting
  • Anesthesia induction
  • Enteral feeding
  • Oropharyngeal colonization
  • Poor oral hygiene
  • Male sex
  • Smoking
  • Diabetes mellitus

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

There is insufficient evidence to recommend routine screening for aspiration pneumonia.

There is insufficient evidence to recommend routine screening for aspiration pneumonia.

​

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]

Aspiration pneumonia occurs following aspiration of different materials and particles. Natural history, complications, and prognosis are different for each category. Chemical pneumonitis usually develop after aspiration of gastric acid and might present acutely within two hours. Rapid clinical recovery or worsening of respiratory distress and hypoxemia might happen. Bacterial infection following aspiration is slower that other community-acquired pneumonia and might be acute, subacute, or chronic. Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis. Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs. Complications of aspiration pneumonia include segmental or lobar pneumonia, bronchopneumonia, bronchiectasis, lung abscess, pleural empyema, respiratory failure, bacteremia, and shock.

• Aspiration pneumonia occurs following aspiration of different materials and particles. Natural history, complications, and prognosis are different for each category.^{[1][2][3][4][5][6][7][8][9][10][11]}

• The symptoms of chemical pneumonitis usually develop after aspiration of gastric acid.
• Following aspiration, onset of respiratory distress and cyanosis occurs within 2 hours.
• The clinical course following chemical pneumonitis might be rapid clinical recovery or worsening of respiratory distress and hypoxemia.
• Pulmonary fibrosis might happen even after recovery.

• Bacterial infection following aspiration is slower that other community-acquired pneumonia.
• Cough, fever, purulent sputum, and dyspnea are typical symptoms of aspiration pneumonia.
• Anaerobic infections may last several days or weeks and the patients may present with anemia and weight loss.
• Later, the patients may present with following complications including lung abscess, necrotizing pneumonia, or empyema.

• Foreign body aspiration might present acutely with mechanical obstruction or chemical pneumonitis.
• Foreign body aspiration is more common in children from one to three years of age.
• Foreign body might be visualized on chest radiographs.
• The Heimlich maneuver is recommended to remove foreign body from respiratory tract.

• Lipoid pneumonia might happen following aspiration of oil.
• Patients might present acutely with inflammation and cough, fever, and dyspnea. However, they might be asymptomatic and present with an incidental mass on radiographs.

• Complications of aspiration pneumonia include:
  • Segmental or lobar pneumonia
  • Bronchopneumonia
  • Bronchiectasis
  • Lung abscess
  • Pleural empyema
  • Respiratory failure
  • Bacteremia
  • Shock
  • Death

• Aspiration pneumonia prognosis is generally good, and mortality rate of patients with aspiration pneumonia is approximately 10.6-21%.^[8]
• The presence of underlying neurologic diseases that affect cough reflex is associated with a particularly poor prognosis among patients with aspiration pneumonia.

​