What every physician needs to know:
Aspiration can lead to any of four distinct syndromes: pneumonitis (which is not discussed further in this chapter), necrotizing pneumonia, lung abscess, and empyema (which almost always overlaps with pneumonia or abscess formation). Pulmonary aspiration and its infectious complications are important causes of serious illness and death in hospitalized patients and residents of chronic care facilities.
As a rule, aspiration pneumonia is polymicrobial. The role of anaerobes is controversial but likely less important than historically suggested. Regardless, these organisms should be assumed to be present in patients with risk factors or suspicious physical exam findings. Serious sequelae can be minimized through prompt recognition of infection, timely initiation of appropriate antibiotic therapy, and strategies to avoid recurrent aspiration. Steroids have no proven benefit in aspiration pneumonia. Ventilator-associated pneumonia, a select example of aspiration pneumonia, highlights the importance of minimizing aspiration. Contrary to popular belief, percutaneous endoscopic gastrostomy (PEG) tubes have not been shown to reduce aspiration compared to nasogastric tubes. However, a recent Cochrane Analysis suggests that post-pyloric feeding tube placement results in a ~30% reduction of aspiration pneumonia when compared to intragastric placement.
Are you sure your patient has aspiration pneumonia or lung abscess? What should you expect to find?
Clinical manifestations of an aspiration event fall along a diverse spectrum, including asymptomatic dry cough, dysphonia, stridor, vomiting after meals, and ARDS. Symptoms of true infection (aspiration pneumonia) are highly variable, and they depend on the point at which the patient is seen during the evolution of the disease process, the pathogens involved, and multiple host-specific factors. Symptoms are similar to that of any acute pneumonia process, but they often develop more slowly–typically over several days or weeks instead of hours.
Manifestations range from mild illness in an ambulatory patient to critical illness with shock and/or respiratory failure. Pneumonia is suggested by fever (or hypothermia in the elderly), dyspnea, pleuritic chest pain, and cough productive of purulent mucus. These patients are generally toxic and have fevers above 39°C, tachycardia, and tachypnea. Patients with aspiration pneumonia almost never have rigors. Physical findings, which are consistent with other forms of pneumonia, include decreased breath sounds, dullness to percussion, rales, egophony, pectoriloquy, pleural friction rub, altered mental status, hypotension and/or hypoxemia.
Features that suggest the presence of an anaerobic infection include poor dentition, foul-smelling breath and/or sputum, and consolidative findings in gravity-dependent lung zones. Without timely recognition and appropriate treatment, anaerobic pneumonia cavitates and/or leads to abscess formation. Abscess symptoms, which develop insidiously over many weeks, have a predominance of fatigue, low-grade fever, weight loss, and productive cough. Half of patients report expectoration of putrid sputum that may or may not be associated with hemoptysis. These patients appear chronically ill and have fevers generally below 39°C. Uncommon but suggestive findings include amphoric breath sounds over the abscess cavity and clubbing of the fingers.
The diagnosis of aspiration pneumonia is suspected on the basis of the clinical presentation and the presence of key features, including aspiration risk factors, periodontal disease, foul-smelling secretions, involvement of dependent lung segments, and cavitation. The diagnosis is confirmed if invasive respiratory secretions show numerous polymorphonuclear leukocytes and an abundance of organisms with varying morphologies and Gram stain characteristics.
Beware: there are other diseases that can mimic aspiration pneumonia or lung abscess:
Non-infectious aspiration pneumonitis (Mendelson’s syndrome) is the major consideration. The possibility of a retained aspirated foreign body should also be entertained. Cavitation of a bronchogenic carcinoma can be assessed with bronchoscopy. Mycoses, hypersensitivity pneumonitis, and vasculitis can appear similar radiographically with cavitations that mimic abscess formation.
How and/or why did the patient develop aspiration pneumonia or lung abscess?
Aspiration is defined as entry of particulate or liquid matter below the level of the true vocal cords. Aspirated substances can be endogenous (oropharyngeal secretions, gastric juice) or exogenous (food, water). There are two forms of aspiration syndrome: large-volume aspiration, which is acutely symptomatic, and chronic, small-volume aspiration with slowly progressive complaints. Notably, the bulk of aspiration events cause chemical pneumonitis, not infection (pneumonia).
Indiscriminate use of antibiotics in aspiration pneumonitis selects resistant pathogens and predisposes the patient to bacterial superinfection. Aspiration causes direct loss of ciliated cells and non-ciliated cells, which takes up to a week for recovery and predisposes the patient to establishment of active infection. Aspirated gastric contents can also introduce viable endogenous flora into the lower airways.
Conditions that increase the volume of aspirated material and/or the bacterial burden of secretions in a person with impaired defenses promote aspiration pneumonia. Widespread use of proton pump inhibitors (PPIs), which is particularly common in the population at risk for aspiration, alters pH and increases the risk of colonization.
It is increasingly clear that the majority of aspiration pneumonia cases are polymicrobial. In one classic series, patients averaged 3.2 isolates, of which 2.6 were anaerobes and 0.6 were non-anaerobes. Early bacteriology studies routinely implicated anaerobic species (Bacteroides, Prevotella, Fusobacterium, Peptostreptococcus) in community-acquired aspiration pneumonia, but subsequent evaluations have suggested that admixed aerobic Gram negatives (particularly Pseudomonas aeruginosa, Klebsiella pneumoniae and Escherichia coli) and Gram positives (particularly Staphylococcus aureus and Streptococcus pneumoniae) are increasingly important. Two more recent and rigorously designed trials that used protected specimen brush samples and anaerobic culturing in patients with acute, witnessed aspiration failed to recover any anaerobes. These studies imply that anaerobes have a more limited role than traditionally believed.
Changes in the oral flora in the institutionalized elderly, attributable to poor oral hygiene and malnutrition, promote colonization with anaerobic and aerobic Gram-negative organisms. A study that used bronchial sampling in cases of severe aspiration pneumonia in this population suggested that about 50% had Gram-negative bacilli and that only about 15% had anaerobic bacteria. Prior antibiotic exposure is also relevant, as nearly half of culture-positive pneumonia patients who received a single dose of antibiotics before microbiological sampling had Pseudomonas aeruginosa, Staphylococcus aureus, and/or Gram-negative bacilli as causative pathogens. Anaerobic pathogens are particularly likely to induce a fibrosing response, which limits extension of the infectious process, confining the infection to a single lung segment and leading to abscess formation.
Which individuals are at greatest risk of developing aspiration pneumonia or lung abscess?
The true incidence of aspiration pneumonia is unknown, but it is generally accepted as low (5-15% of all community-acquired pneumonia cases). The variability in reported rates in the literature stems from a lack of standardized diagnostic criteria, inherent difficulties in diagnosis, and inability to distinguish pneumonitis from pneumonia. Aspiration pneumonia is seen with increased frequency in elderly patients, particularly residents of nursing homes.
One study of cases with nursing home-acquired pneumonia and controls with community-acquired pneumonia suggested that the prevalence of aspiration pneumonia was 18% in nursing home residents, compared to 5% in CAP patients. A more recent study with a similar design suggested that aspiration pneumonia represented 30% of all nursing home-acquired pneumonia cases, whereas it is 10% of true CAP. The incidence has been reported in 10% of patients admitted to the hospital with drug overdose and in 0.003% of surgical cases where general anesthesia is administered.
Risk factors for aspiration and aspiration pneumonia include advanced age, neurologic disorders (stroke, dementia, neuromuscular disease), altered level of consciousness (coma, seizure, alcohol or sedative/hypnotic use), functional dependence in activities of daily living, and various gastrointestinal conditions (gastroesophageal reflux, esophageal dysmotility, swallowing disorder, delayed gastric emptying).
Obesity is increasingly recognized as a risk factor given increased intra-abdominal pressures, high residual gastric volumes, low pH, delayed gastric emptying and increased rates of reflux. Periodontal disease is also a major risk factor for development of anaerobic pleuropulmonary infections, as bacterial counts in gingival crevices are markedly elevated in patients with a variety of periodontal diseases. The risk of aspiration pneumonia is lower in edentulous patients.
In other select subsets of patients, unique risk factors may apply (e.g., reduced left ventricular ejection fraction is a risk factor for aspiration pneumonia in patients undergoing cardiovascular surgery).
What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
Routine studies include a complete blood count to assess the degree of leukocytosis, a basic metabolic panel to look for electrolyte disorders and estimate kidney function for antibiotic dosing, arterial blood gases to assess the pH and oxygenation, and sputum for Gram stain, culture, and microbiology.
The diagnostic utility of sputum cultures has been criticized, as anaerobes are difficult to isolate reliably using routine culture methods. Accurate results require anaerobic processing and transport to preserve anaerobes and fastidious strains. Definitive diagnosis of an anaerobic infection typically requires an invasive procedure. However, clinicians are generally hesitant to subject acutely ill patients to the majority of these procedures. Accordingly, the diagnosis is typically based on clinical features.
Routine blood cultures are not recommended given their low yield in uncomplicated cases (no evidence of sepsis or shock).
Confirmation of aspiration does not definitively establish that the observed pneumonia resulted directly from the aspirated material, as 45% of healthy adults aspirate during sleep without clinical sequelae. These events are believed to be asymptomatic given the small volumes aspirated, the low pathogen burden in the aspirated material, the presence of efficient clearance mechanisms, and intact immunity. Although many entities have been evaluated (pepsin, lipid-laden macrophages, soluble triggering receptor expressed on myeloid cells, C-reactive protein, procalcitonin, various cytokines, exhaled breath condensate), there are no reliable biomarkers with which to diagnose aspiration pneumonia definitively.
What imaging studies will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
Radiographic findings are variable, but dense infiltrates typically develop in the pulmonary segments that were dependent when the aspiration occurred. Classically, this is seen in posterior upper lobe and superior lower lobe segments when the patient is supine and in basilar segments of the lower lobes when the patient is upright. Swallowing studies in conjunction with a speech pathology consultation can be used to reliably assess for dysphagia in appropriate cases. Lucency within the infiltrate suggests a necrotizing pneumonia. Costophrenic angle blunting and the presence of a meniscus are signs of parapneumonic pleural effusion. Pleural effusions and/or progression to necrosis with cavitation are common with anaerobic infection. Empyema is reported to develop in up to a third of cases.
What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
A recent study suggests that a simple bedside water swallowing test is an inexpensive and sufficiently reliable test to evaluate for aspiration. Clinical utility requires serial sipping maneuvers of large volumes as a screening maneuver followed by small volume single sips to confirm aspiration.
What diagnostic procedures will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
Bronchoscopic visualization of foreign material below the cords establishes the diagnosis of aspiration but not the diagnosis of pneumonia. Protected specimen brush sampling via bronchoscopy avoids oral contamination but requires conscious sedation, which is an established risk factor for further aspiration. A handful of observational studies suggest that early bronchoscopy favorably affects clinical outcomes in aspiration pneumonia in mechanically ventilated patients – a finding that should be confirmed prospectively before widespread adoption in clinical practice. Transtracheal aspiration, once believed to be the gold standard for diagnosis, is rarely pursued given its invasive nature and concerns that recovered organisms present oropharyngeal flora aspirated during the procedure or colonizers of the trachea. Percutaneous lung biopsy is reliable but rarely performed as it is invasive.
If a swallowing disorder is suspected, confirmatory tests may include pH probes, dye visualization tests, radioactive tracer administration, video fluoroscopy, and endoscopy. None of these studies are sufficiently reliable and/or reproducible to be the uniformly accepted standard.
What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
If you decide the patient has aspiration pneumonia or lung abscess, how should the patient be managed?
Antibiotics are always indicated for microbiology-confirmed aspiration pneumonia. Although penicillin was historically the drug of choice for aspiration pneumonia, more recent data suggest its role is limited given a reduced focus on anaerobes as causative pathogens and the increasing frequency of beta-lactamase-producing species. Empiric aspiration pneumonia therapy should have activity against beta-lactamase-producing strains. Two studies have demonstrated that clinical cure rates were superior for clindamycin compared to penicillin. Clindamycin has also been shown to be as effective as ampicillin-sulbactam and imipenem with significantly less expense and fewer MRSA superinfections.
Recommendations for optimal therapy are challenging given the lack of consensus on the pathogens of most concern and the limited prospective comparisons of clinical outcomes with various antibiotic regimens. When anaerobic bacteria are likely pathogens in aspiration pneumonia, clindamycin is typically used as first-line therapy. Alternative regimens include amoxicillin-clavulanate monotherapy and a combination therapy consisting of either amoxicillin or penicillin G plus metronidazole.
For nosocomial and nursing-home-acquired aspiration pneumonia, companion aerobic organisms are increasingly important. In these patients, consider piperacillin-tazobactam or imipenem monotherapy, or combination therapy with levofloxacin, ciprofloxacin, or ceftazidime plus either clindamycin or metronidazole. Metronidazole monotherapy should not be used, as it is associated with a failure rate approaching 50%, presumably because of its lack of effect on microaerophilic and aerobic streptococci.
Convincing data are lacking for the use of moxifloxacin, macrolides, cefotaxime, and tigecycline in aspiration pneumonia and lung abscess. Trimethoprim-sulfamethoxazole shows poor in vitro activity against several pathogens of concern and should be avoided. Regardless of the regimen, therapy is usually given intravenously until the white blood cell count and fever curve show sustained improvement.
The duration of therapy is arbitrary, as there are no prospective studies on the optimal length of treatment. Normalization of fever, resolution of leukocytosis, and return of sputum production to baseline suggest resolution of pneumonia. Antibiotic courses of 7-10 days are often used for an uncomplicated pneumonia (no cavitation, abscess, or empyema) that demonstrates prompt clinical improvement. Shorter courses of therapy are likely to be effective, but they have not been adequately studied. Patients with antibiotic-resistant pathogens, multi-lobar disease, malnutrition or necrotizing infection are typically treated for 14 days or longer. Lung abscesses are often treated with IV therapy for 4-8 weeks, followed by extended courses of oral therapy. Patients with abscesses require serial imaging, as the ultimate duration of therapy is heavily influenced by resolution of the abscess cavity.
Patients with documented swallowing dysfunction require efforts to prevent repeat aspiration events. Prophylactic strategies should combine behavioral, dietary, and medical interventions. Tube feedings are recommended for patients who continue to aspirate despite these interventions and this nutrition should be delivered post-pylorically if feasible. Prophylactic antibiotics have not proven effective in at-risk patients and are not recommended.
What is the prognosis for patients managed in the recommended ways?
The variable time course for improvement appears to be directly related to the extent of infection, the causative pathogen(s), and the timeliness and adequacy of prescribed antibiotic therapy. Case series suggest that fevers should resolve in 1-3 weeks, although it may take many months for abscess cavities to close.
Reported mortality rates are ~19% for community-acquired aspiration pneumonia and ~28% for nursing-home-acquired aspiration pneumonia. Prognosis is heavily determined by underlying comorbid disease, complications of infection, and the overall functional status of the host. Some populations are particularly at risk for poor outcomes. For example, aspiration pneumonia is the most common cause of death in patients with dysphagia due to neurologic disorders.
What other considerations exist for patients with aspiration pneumonia or lung abscess?
Surgical isolation of the esophagus from the trachea – laryngotracheal separation, also known as the Lindeman Procedure – is a potential option for aphasic patients with refractory disease. These are typically institutionalized individuals with severe intellectual disabilities or who are post-stroke. Data from case series suggest that while this is an effective modality to reduce the frequency of acute hospitalization in appropriately selected patients, delayed complications occur in 2-5% of patients.
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- What every physician needs to know:
- Are you sure your patient has aspiration pneumonia or lung abscess? What should you expect to find?
- Beware: there are other diseases that can mimic aspiration pneumonia or lung abscess:
- How and/or why did the patient develop aspiration pneumonia or lung abscess?
- Which individuals are at greatest risk of developing aspiration pneumonia or lung abscess?
- What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?
- What imaging studies will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
- What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
- What diagnostic procedures will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
- What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of aspiration pneumonia or lung abscess?
- If you decide the patient has aspiration pneumonia or lung abscess, how should the patient be managed?
- What is the prognosis for patients managed in the recommended ways?
- What other considerations exist for patients with aspiration pneumonia or lung abscess?