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Aspiration Pneumonia in Dogs

Aspiration pneumonia is unfortunately a frequent occurrence in veterinary patients, and is recognized far more commonly in dogs than in cats. The initial injury (aspiration pneumonitis) actually occurs due to chemical irritation from stomach acid, with high risk for subsequent bacterial infection due to altered microenvironment and potentially aspiration of contaminated liquid and/or pathogenic bacteria in the oropharynx. While minor aspiration events probably occur relatively frequently, normal defense mechanisms (coughing, mucociliary clearance, and the immune system) protect against the development of clinical pneumonia. When these systems are impaired or overwhelmed, infection occurs. In some cases, acute respiratory distress syndrome (ARDS) can develop, with a worsening prognosis and often a need for ventilator support.

Risk Factors

Factors shown to predispose aspiration pneumonia in veterinary patients include gastrointestinal disease, esophageal disease, neurologic disease, upper airway disease, and recent anesthesia. Male large-breed dogs appear to be predisposed. A recent retrospective multicenter study showed a post-anesthetic aspiration pneumonia incidence of ~0.17%, with significant association with patients that had a regurgitation episode, and those that received hydromorphone at induction (Ovbey 2014). The aspiration event is often unwitnessed and initial clinical signs can be delayed for hours to days. Physical examination findings can include fever, weakness, lethargy, increased respiratory rate and effort, coughing, abnormal lung sounds on auscultation (including crackles and/or dull regions), and nasal discharge. Interestingly, in a recent retrospective study, only about 50% of the patients presented with signs of aspiration pneumonia and 26% actually had normal lung sounds on thoracic auscultation (Tart 2010), so it is important to keep aspiration pneumonia in mind for patients even without specific signs of this disease.


The diagnosis of aspiration pneumonia is usually made on the basis of radiographic findings, most commonly a dependent alveolar lung pattern. Other differentials to consider should include infectious bronchopneumonia, hemorrhage, neoplasia, atelectasis, and lung lobe torsion. The right middle lung lobe is the most frequently affected, although the cranial lung lobes are also commonly implicated. When aspiration is suspected, it may be helpful to obtain a left lateral radiograph as this will increase the ability to detect right-sided infiltrates. It is not uncommon for radiographic changes to correlate poorly with the stage and/or severity of disease. Radiographs should also be evaluated for the cause of the aspiration event, including megaesophagus and gastrointestinal obstruction or pancreatitis.

Laboratory Testing

A complete blood count (CBC) and chemistry panel are recommended in patients with aspiration pneumonia, but findings are often non-specific. CBC may reveal neutrophilia with a left shift or less commonly neutropenia. A chemistry panel is primarily useful for identifying concurrent or underlying diseases. Additional diagnostic testing should be recommended as indicated based on the specific patient. Tracheal wash with cytology and culture is useful to confirm the diagnosis and identify the organism(s) responsible, which allows for targeted antibiotic therapy. Samples can be obtained via bronchoscopy (with bronchoalveolar lavage) or more commonly via endotracheal or trans-tracheal wash. Antibiotic administration can decrease the yield of bacterial culture, and culture samples should ideally be obtained prior to initiation of antibiotic therapy.

A variety of bacteria can be found in respiratory cultures, with Escherichia coli and Pasturella typically the most common. Other pathogenic respiratory bacteria include Staphylococcus, Mycoplasma, Klebsiella, Pseudomonas, Enterococcus, and Streptococcus species. Polymicrobial cultures are relatively common, likely due to aspiration of oropharyngeal and/or enteric bacteria. A recent study (Epstein 2010) demonstrated that patients with more severe respiratory signs (respiratory failure requiring ventilator support) had a higher incidence of antimicrobial resistance on bacterial cultures, suggesting that these patients should probably be started on more aggressive antibiotic regimens pending culture results. In this patient population, 98% of the bacteria cultured were susceptible to amikacin and 91% were susceptible to imipenem, as compared to only 35% susceptible to amoxicillin-clavulonate and 48% susceptible to enrofloxacin. Another recent study (Proulx 2014) showed that 26% of patients with bacterial pneumonia that had a respiratory culture performed had at least 1 bacterial isolate that was resistant to the empirically selected antimicrobials. The incidence was even higher (57%) in patients that had received antibiotics over the preceding 4 weeks. This suggests that airway cultures should be routinely recommended, and that care should be taken to select different antibiotics in patients that have recently undergone treatment.

Empiric antibiotic therapy should be started pending bacterial culture results, or when airway sampling is not feasible due to patient stability or finances. Cytology can be evaluated quickly in hospital, and can help guide selection. In stable patients with mild clinical signs, monotherapy with amoxicillin-clavulanic acid may be adequate. Patients that are more clinically compromised should be treated with combination therapy (such as a potentiated penicillin along with either a fluoroquinolone or an aminoglycoside). Alternative antibiotic strategies may be necessary in patients that are not showing a good clinical response, patients that have been on recent antibacterial therapy, or based on known hospital bacterial populations and resistance patterns.

Some patients with aspiration pneumonia do not require hospitalization, and can be managed with oral antibiotics. Radiographs should be monitored serially to help determine response to therapy, and duration of antibiotic treatment should ideally continue for 2 weeks past clinical and radiographic resolution of disease. Many patients are sick enough that they require hospitalization for supportive care. Fluid therapy should be used as needed to maintain hydration and perfusion, and febrile patients in particular can have increased losses and easily become dehydrated. However, excessive administration of intravenous fluids should be avoided as pulmonary capillaries may have increased permeability due to the acute inflammatory response; this can lead to interstitial edema and worsening hypoxemia. This risk is higher in patients with cardiac disease. Patients with sepsis may require vasopressor support to help maintain perfusion.

The need for oxygen supplementation is determined by both subjective and objective means. Pulse oximetry (SpO2) measurements assess the percentage of hemoglobin saturation with oxygen and can be obtained non-invasively, but can be difficult to measure in non-compliant patients, those with pigmented mucous membranes, and those with arrhythmias. In general, patients with SpO2 <95% will benefit from supplementation oxygen. Arterial blood gas measurement is a more accurate assessment of oxygenation, but is also more invasive and requires specialized equipment. Subjective evaluation of the respiratory status of the patient can also be useful, and includes monitoring respiratory rate and effort, as well as observing appetite and ability to rest. Oxygen supplementation can be provided in a variety of ways, including an oxygen cage, oxygen mask, nasal prongs or tubes, an oxygen “hood” constructed from a covered E-collar, and via endotracheal tube. Oxygen supplementation is typically at ~40% initially, but can be provided at higher concentrations depending on the method and patient requirements. Oxygen supplementation at high concentrations (60% or above) can cause toxicity due to free radical accumulation, and use should ideally be limited to 24 hours or less. Patients with severe respiratory impairment may require mechanical ventilation.

Bronchodilators such as terbutaline or theophylline are sometimes used in patients with aspiration pneumonia, and can be theoretically useful in ameliorating the bronchospasm that can accompany chemical injury to the airways. However, bronchodilators can potentially impede the cough reflex and also worsen hypoxemia by opening airways that lead to diseased alveoli and increasing dead-space ventilation. Recent human ARDS trials have not shown any improvement with bronchodilator therapy. While glucocorticoids could theoretically be beneficial to reduce pulmonary inflammation, they are also immunosuppressive which can be deleterious in the face of bacterial infection. Glucocorticoids are likely only indicated in the presence of concurrent inflammatory lung disease, with upper airway swelling, and with hypoadrenocorticism or other concurrent steroid-responsive conditions. Cough suppressants are generally contraindicated in aspiration pneumonia as they can impair clearance of respiratory secretions. In some cases, oral or intravenous N-acetylcysteine (mucomyst) may be useful as a mucolytic, but this medication should not be nebulized due to airway irritation and bronchospasm. Furosemide should not be used as it can result in drying and trapping of infectious debris in the lower airways.

Preventive measures are very important, especially in patients that have known risk factors for aspiration.

With rapid recognition and treatment, the prognosis for aspiration pneumonia is relatively good. A recent retrospective study (Tart 2010) showed a survival rate of approximately 82% in patients treated for aspiration pneumonia. A statistically significant association was documented between number of lung lobes affected radiographically, and survival. No prognostic difference was found among patients based on signalment, culture results or specific treatment protocol.


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