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Compendium December 2012 (Vol. 34, No. 12)

Aspiration Pneumonia in Dogs: Pathophysiology, Prevention, and Diagnosis

by Heidi M. Schulze, DVM, DACVECC, Louisa J. Rahilly, DVM, DACVECC

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    Abstract

    Aspiration pneumonia and aspiration pneumonitis are associated with significant morbidity in veterinary and human medicine. A variety of medical conditions and medications can predispose patients to aspiration, and every precaution should be taken to prevent aspiration from occurring. For dogs that aspirate oral or gastric contents and subsequently develop pneumonia, monitoring and supportive care are imperative. This article discusses the pathophysiology, prevention, and diagnosis of aspiration pneumonia. A companion article describes the treatment options and prognosis.

    Pulmonary aspiration is the inhalation of fluid and/or particulates into the airways. In clinical medicine, aspirated material comes from the contents of the gastric and/or oral cavities. Aspiration pneumonitis is the result of inhalation of these contents into the respiratory tract with subsequent inflammation of the airways and pulmonary parenchyma.1–3 Aspiration pneumonia is a bacterial infection of the pulmonary parenchyma that develops secondary to aspiration. It may occur simultaneously with aspiration pneumonitis if the aspirated contents are contaminated with bacteria. It may also occur when patients with aspiration pneumonitis develop secondary bacterial colonization of the airways.1–4

    Pathophysiology

    Aspiration pneumonia develops in three stages. The first stage occurs immediately after aspiration.1 During this phase, damage to the airways and pulmonary parenchyma is a direct result of the nature of the aspirated fluid (i.e., irritant or acidic).3,5 This caustic tissue damage triggers the activation of cytokines and other inflammatory mediators.2 The inflammation leads to necrosis of type I alveolar cells, bronchiolar constriction, pulmonary hemorrhage, increased mucus production, increased vascular permeability resulting in extravasation of proteins into the pulmonary parenchyma, and pulmonary edema.4,5 Ultimately, alveolar collapse and atelectasis result.4 The second phase of aspiration pneumonia begins 4 to 6 hours after aspiration, lasts for 12 to 48 hours, and is characterized by infiltration of neutrophils into the alveoli and pulmonary interstitium.1,3 This inflammatory phase is characterized by ongoing vascular leakage of proteins with continued development of high-protein pulmonary edema, neutrophil sequestration and activation, and release of further proinflammatory cytokines.3,4 These first two stages constitute aspiration pneumonitis. The third phase, which constitutes the difference between aspiration pneumonitis and aspiration pneumonia, involves bacterial colonization of the airways and pulmonary parenchyma.1,4,5

    Predisposing Etiologies


    Many conditions can increase the risk of aspiration and resultant pneumonia in dogs (BOX 1). Dogs that have recently been heavily sedated or undergone general anesthesia are at risk for aspiration.6–9 Premedication with narcotics can predispose patients to gastric reflux, regurgitation, and possible aspiration.10 Neurologic conditions that affect esophageal or laryngeal function, as well as head trauma and seizures, also predispose patients to aspiration.3,11–14 In a 2009 study of dogs undergoing general anesthesia for diagnosis and/or treatment of intervertebral disk disease, patients that vomited or regurgitated after anesthesia, were tetraparetic, had cervical lesions, or underwent longer anesthetic procedures (4.5 h compared with just under 4 h, on average) or more than one anesthetic procedure were more likely to develop pneumonia.15 In addition, patients with feeding tubes may be at increased risk of aspiration due to gastric distention and atony after feeding.1 Other conditions such as vomiting or regurgitation (for any reason), oropharyngeal or esophageal obstructive lesions, anxiety, and pain may predispose patients to aspiration. Long-term treatment with histamine type 2 (H2) blockers or proton pump inhibitors (PPIs) can lead to alkalinization of the gastric lumen and secondary colonization of the gastric lumen with enteric bacteria.16 Therefore, a greater potential for bacterial aspiration pneumonia may be present in patients receiving these medications.16

    Preventive Measures

    Numerous measures can be taken to prevent aspiration pneumonia in patients with a known risk factor. Preoperative fasting of patients, when possible, is recommended. However, the ideal length of the fast is debatable. Recent studies report that the historical 12- to 18-hour preanesthetic fast is not only unnecessary but also potentially harmful to patients.17,18 Shiun et al17 demonstrated that an 8-hour fast, with water up to 2 hours before anesthesia, is sufficient to minimize reflux during general anesthesia. Another study18 found that fasting for longer periods of time increased the acidity of the gastric environment, which would result in more severe pulmonary damage from reflux and aspiration. Patients at risk for aspiration should have their esophagus and stomach suctioned before extubation. Ensuring intact gag and swallow reflexes before extubation in patients undergoing anesthesia, especially those at risk for reflux or regurgitation, is imperative. If an episode of regurgitation or reflux is witnessed, the oropharyngeal cavity should be suctioned.

    Key Points

    • Many conditions can predispose dogs to aspiration pneumonia.
    • Preliminary diagnosis of aspiration pneumonia is based on history, physical examination, and thoracic radiography.
    • Definitive diagnosis of aspiration pneumonia is based on culture of pulmonary exudate.
    • Causative agents are often oropharyngeal commensal bacteria or enteric bacteria.

    At-risk patients may benefit from prophylactic therapy to reduce the incidence of gastric reflux; however, reviews of this practice in both the human and veterinary literature are mixed. Metoclopramide at high doses was shown to significantly decrease the incidence of gastric reflux in canine patients premedicated with morphine that underwent general anesthesia.19 However, a more recent report20 found that neither ranitidine nor high-dose metoclopramide reduced the incidence of reflux in anesthetized dogs. Patients in the latter study were not premedicated with opioids; thus, the effectiveness of ranitidine and high-dose metoclopramide at minimizing the reflux caused by opioids was not evaluated in this study. The use of omeprazole, a potent PPI, has also been evaluated and shown to reduce gastroesophageal reflux in dogs undergoing anesthetic procedures when administered preoperatively.21 However, another study22 showed that esomeprazole, the S-isomer of omeprazole, failed to reduce the incidence of gastric reflux in dogs premedicated with hydromorphone and maintained with fentanyl infusions during orthopedic procedures, despite increasing the pH of refluxed fluids. Patients that received intravenous cisapride in addition to esomeprazole in this study did have a decreased incidence of reflux.22

    In a meta-analysis of controlled trials in human medicine,23 PPIs were found to be less effective than ranitidine at increasing gastric pH and to possibly increase gastric secretions, making reflux more likely; however, ranitidine has been shown to be ineffective at increasing gastric pH in dogs.24 In these studies, reflux was identified via pH probe placement in the caudal esophagus and/or stomach during anesthesia and was not directly witnessed (i.e., fluid was not seen coming from the mouth or nares).

    Despite the controversy as to the effectiveness of H2 blockers, PPIs, and prokinetics, little morbidity is associated with their use and the potential benefit associated with administration warrants consideration. As these medications are only used in the immediate perioperative period, there should be little risk of enteric bacterial colonization of the gastric lumen and subsequentrisk for aspiration pneumonia, in theory.

    Diagnosis

    A presumptive diagnosis of aspiration pneumonia is based on the history, physical examination findings, and radiographic findings consistent with aspiration pneumonia. Often, the history includes a predisposing condition, but the actual aspiration eventis usually not witnessed.25 The owner may report regurgitation, coughing, panting, or labored breathing.25 However, patients may present with nonspecific signs such as lethargy and poor appetite.25,26 Dogs that aspirate while hospitalized may have an acute onset of labored breathing.26

    Physical examination findings often include fever, tachypnea, and/or dyspnea.25,26 Thoracic auscultation may reveal increased lung sounds, wheezes, crackles, or dull lung sounds. However, retrospective studies have demonstrated that 31% to 57% of dogs with aspiration pneumonia had a normal rectal temperature, 58% had a normal respiratory rate, and 28% to 31% had normal lung sounds at the time of diagnosis.25,26

    Thoracic radiography is the gold standard for preliminary diagnosis of aspiration pneumonia (FIGURE 1A and FIGURE 1B). Three-view radiographs are advised because multiple lung lobes may be involved.25,26 Interstitial, alveolar, and mixed pulmonary patterns may be evident.25,26 Diagnostic differentials for radiographic lung lobe consolidation are listed in BOX 2. The lung lobe(s) involved depend on the position of the patient during the aspiration event; however, the right middle, right cranial, and left cranial lung lobes are most frequently affected.25,26 In most patients, more than one lung lobe is affected, with an average of 1.7 to 1.9 lung lobes involved in the disease process.25,26

    Box 2. Common Differentials for Lung Lobe Consolidation

    • Aspiration or bacterial pneumonia
    • Pulmonary hemorrhage
    • Lung lobe torsion
    • Neoplasia
    • Granulomatous disease

    Cytology/Culture and Antimicrobial Sensitivity

    Definitive diagnosis of aspiration pneumonia is made based on microbiologic cultures of exudate from the pulmonary airways. Tracheal wash (transtracheal or endotracheal), bronchoalveolar lavage (BAL), and bronchial brushing or biopsy are all means of sampling the pulmonary tract and airway secretions for cytology and culture.27,28

    A tracheal wash is easily performed, minimally invasive, inexpensive, and does not require specialized equipment.29 A transtracheal wash (TTW) can be performed in an awake or lightly sedated patient. Because the use of minimal or no sedation preserves the cough reflex, the patient is more likely to expectorate during the procedure, enhancing sample yield. An endotracheal wash (ETW) requires brief general anesthesia and hence may preclude coughing; however, coupage helps to mobilize secretions (FIGURE 2A,  FIGURE 2B ,  FIGURE 2C ,  FIGURE 2D ,  FIGURE 2E , and FIGURE 2F).29 ETW is more appropriate for patients that have coagulopathies or a conformation that makes the trachea difficult to isolate; are vomiting or regurgitating as the airway is secured during the procedure; or are aggressive.29 It also allows for gastric emptying before extubation in patients with compromised esophageal or laryngeal function or that are vomiting or regurgitating frequently.

    Clinical Pearls

    • Patients may present with no signs referable to the respiratory tract.
    • A history of a predisposing condition should alert the physician to the possibility of aspiration pneumonia.
    • Tracheal washes are easy and inexpensive to perform.

    Cell morphology is not well preserved in TTW/BAL samples, and the cells are fragile; therefore, fresh smears should be prepared within 30 minutes of collection. Direct smears of turbid fluid, cytocentrifuged samples, or mucus may provide the most information.30 These smears can be made by the blood smear or line smear technique; the latter may concentrate nucleated cells for analysis.31 To preserve cellular morphology, additional fluid samples should be placed in EDTA tubes and refrigerated before submission to a referral laboratory for analysis.31 A portion of the sample should also be placed in an appropriate culture medium and/or a sterile tube. The sensitivity of transtracheal wash cultures has been reported at 50% to 90%,27 77%,32 and 44%33. Specificity has not generally been found to be as high, often due to contamination from the oral cavity.27 To our knowledge, a comparison of diagnostic yield between ETW and TTW samples has not been performed. Even for patients in which antimicrobials have been initiated, culture and sensitivity testing of samples has been shown to be useful.4

    In the human field, sputum cultures and cultures of deep oral swabs are often used.34 Recently, a study of use of deep oral swabs to obtain samples for culture and antimicrobial sensitivity testing was performed in puppies and adult dogs.35 Swab samples were collected from the epiglottis after tracheal palpation and coupage, and results were compared with those obtained from samples collected by transoral tracheal wash. The cultures of the swab and tracheal wash were found to be similar in most of the adult dogs, but not the younger dogs. The results of this study suggest that deep oral swabs may be a useful diagnostic tool in dogs with hospital-acquired pneumonia, but further studies to investigate this diagnostic modality are needed.

    Ancillary Diagnostics

    Findings on routine blood work are neither sensitive nor specific for aspiration pneumonia; however, certain abnormalities are considered consistent with this condition. Leukocytosis or leukopenia, often with toxic changes present in the neutrophils, may be seen on a complete blood count (CBC), but a normal leukogram does not rule out pneumonia. A serum chemistry profile may be normal or may reflect comorbid disease. A 2008 study demonstrated elevations of liver enzymes and decreased albumin levels in more than half of 58 dogs with aspiration pneumonia.26 A platelet count and coagulation profile are indicated before performing a TTW to rule out a coagulopathy.

    Pulse oximetry evaluates patient oxygenation status. Arterial blood gas analysis not only allows a more precise evaluation of patient oxygenation but also evaluates ventilation and acid/base status. These diagnostic tests help direct oxygen therapy and determine the potential need for positive-pressure ventilation.

    Causative Agents

    Bacterial agents of aspiration pneumonia are often commensals of the oropharyngeal cavity.1 Dogs with aspiration pneumonia show a preponderance of Escherichia coli, Pasteurella, Staphylococcus, Streptococcus, Klebsiella, Enterococcus, and Mycoplasma infections as diagnosed by tracheal wash.4,25,33 In most cases, infections are mixed, although single-agent infections can occur.33 Anaerobic bacteria are rare unless pulmonary abscessation or a nidus of infection (e.g., food material) within the pulmonary tree exists.

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    References

    1. Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med 2001;344(9):665-671.

    2. Marik PE. Pulmonary aspiration syndromes. Curr Opin Pulm Med 2011;17(3):148-154.

    3. Goggs R, Boag AK. Aspiration pneumonitis and pneumonia. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine. St. Louis, MO: Saunders-Elsevier; 2009:97-101.

    4. Barton L. Aspiration pneumonia. In: King LG, ed. Textbook of Respiratory Disease in Dogs and Cats. St. Louis, MO: Elsevier; 2004:422-429.

    5. Mendelson C. The aspiration of stomach contents into the lungs during obstetric anesthesia. Am J Obstet Gynecol 1946;52:191-205.

    6. Kogan DA, Johnson LR, Sturges BK, et al. Etiology and clinical outcome in dogs with aspiration pneumonia: 88 cases (2004-2006). J Am Vet Med Assoc 2008;233(11):1748-1755.

    7. Alwood AJ, Brainard BM, LaFond E, et al. Postoperative pulmonary complications in dogs undergoing laparotomy: frequency, characterization and disease-related risk factors. J Vet Emerg Crit Care 2006;16(3):176-183.

    8. Brainard BM, Alwood AJ, Kushner LI, et al. Postoperative pulmonary complications in dogs undergoing laparotomy: anesthetic and perioperative factors. J Vet Emerg Crit Care 2006;16(3):184-191.

    9. Wilson DV, Boruta DT, Evans AT. Influence of halothane, isoflurane, and sevoflurane on gastroesophageal reflux during anesthesia in dogs. Am J Vet Res 2006;67(11):1821-1825.

    10. Wilson DV, Evans AT, Miller RA. Effects of preanesthetic administration of morphine on gastroesophageal reflux and regurgitation during anesthesia in dogs. Am J Vet Res 2005;66(3):386-390.

    11. McBrearty AR, Ramsey IK, Courcier EA, et al. Clinical factors associated with death before discharge and overall survival time in dogs with generalized megaesophagus. J Am Vet Med Assoc 2011;238(12):1622-1628.

    12. Stanley BJ, Hauptman JG, Fritz MC, et al. Esophageal dysfunction in dogs with idiopathic laryngeal paralysis: a controlled cohort study. Vet Surg 2010;39(2):139-149.

    13. Hammel SP, Hottinger HA, Novo RE. Postoperative results of unilateral arytenoids lateralization for treatment of idiopathic laryngeal paralysis in dogs: 39 cases (1996-2002). J Am Vet Med Assoc 2006;228(8):1215-1220.

    14. MacPhail CM, Monnet E. Outcome of and postoperative complications in dogs undergoing surgical treatment of laryngeal paralysis: 140 cases (1985-1998). J Am Vet Med Assoc 2001;218(12):1949-1956.

    15. Java MA, Drobatz KJ, Gilley RS, et al. Incidence of and risk factors for postoperative pneumonia in dogs anesthetized for diagnosis or treatment of intervertebral disk disease. J Am Vet Med Assoc 2009;235(3):281-287.

    16. Herzig SJ, Howell MD, Long HN, et al. Acid-suppressive medication use and the risk for hospital-acquired pneumonia. JAMA 2009;301(20):2120-2128.

    17. Shiun XW, Lo XJ, Lin O. Preoperative fasting in dogs. Rev Electronica Clin Vet 2006;1(1):5b. http://www.veterinaria.org/revistas/recvet.

    18. Savvas I, Rallis T, Raptopoulos D. The effect of pre-anaesthetic fasting time and type of food on gastric content volume and acidity in dogs. Vet Anaesth Analg 2009;36:539-546.

    19. Wilson DV, Evans AT, Maurer WA. Influence of metoclopramide on gastroesophageal reflux in anesthetized dogs. Am J Vet Res 2006;67(1):26-31.

    20. Favarato ES, Souza MV, Costa PRS, et al. Evaluation of metoclopramide and ranitidine on the prevention of gastroesophageal reflux episodes in anesthetized dogs. Res Vet Sci 2011;91(3):e25-e27. doi:10.1016/j.rvsc.2011.01.027.

    21. Panti A, Bennett RC, Corletto F, et al. The effect of omeprazole on oesophageal pH in dogs during anesthesia. J Small Anim Pract 2009;50:540-544.

    22. Zacuto AC, Marks SL, Osborn KL, et al. The influence of esomeprazole and cisapride on gastroesophageal reflux during anesthesia in dogs. J Vet Intern Med 2012;26(3):518-525. doi: 10.1111/j.1939-1676.2012.00929.x. Accessed April 23, 2012.

    23. Clark K, Lam LT, Gibson S, et al. The effect of ranitidine versus proton pump inhibitors on gastric secretions: a meta-analysis of randomized control trials. Anaesthesia 2009;64:652-657.

    24. Bersenas AME, Mathews KA, Allen DG, Conlon PD. Effects of ranitidine, famotidine, pantoprazole, and omeprazole on intragastric pH in dogs. Am J Vet Res 2005;66(3):425-431.

    25. Tart KM, Babski DM, Lee JA. Potential risks, prognostic indicators, and diagnostic and treatment modalities affecting survival in dogs with presumptive aspiration pneumonia: 125 cases (2005-2008). J Vet Emerg Crit Care 2010;20(3):319-329.

    26. Kogan DA, Johnson LR, Jandrey KE, Pollard RE. Clinical, clinicopathologic, and radiographic findings in dogs with aspiration pneumonia: 88 cases (2004-2006). J Am Vet Med Assoc 2008;233(11):1742-1747.

    27. Moser KM, Maurer J, Jassy L, et al. Sensitivity, specificity and risk of diagnostic procedures in a canine model of Streptococcus pneumoniae pneumonia. Am Rev Respir Dis 1982;125(4):436-442.

    28. Creevy KE. Airway evaluation and flexible endoscopic procedures in dogs and cats: laryngoscopy, transtracheal wash, tracheobronchoscopy, and bronchoalveolar lavage. Vet Clin North Am Small Anim Pract 2009;39:869-880.

    29. Syring RS. Tracheal washes. In: King LG, ed. Textbook of Respiratory Disease in Dogs and Cats. St. Louis, MO: Elsevier; 2004:128-134.

    30. English K, Cowell RL, Tyler RD, et al. Transtracheal and bronchoalveolar washes. In: Cowell RL, Tyler RD, Meinkoth JH, et al, eds. Diagnostic Cytology and Hematology of the Dog and Cat. 3rd ed. St. Louis, MO: Mosby-Elsevier; 2008:256-275.

    31. Meinkoth JH, Cowell RL, Tyler RD, et al. Sample collection and preparation. In: Cowell RL, Tyler RD, Meinkoth JH, et al, eds. Diagnostic Cytology and Hematology of the Dog and Cat. 3rd ed. St. Louis, MO: Mosby-Elsevier; 2008:1-18.

    32. Sanchez-Mejorada G, Calva JJ, Ponce de Leon SR, et al. Usefulness and risks of transtracheal aspiration in the diagnosis of pulmonary infections [abstract]. Rev Invest Clin 1991;43:285-292.

    33. Angus JC, Jang SS, Hirsh DC. Microbiological study of transtracheal aspirates from dogs with suspected lower respiratory tract disease: 264 cases (1989-1995). J Am Vet Med Assoc 1997;210(1):55-58.

    34. Kabra SK, Alok A, Kapil A, et al. Can throat swab after physiotherapy replace sputum for identification of microbial pathogens in children with cystic fibrosis? Indian J Pediatr 2004;71:21-23.

    35. Sumner CM, Rozanski EA, Sharp CR, Shaw SP. The use of deep oral swabs as a surrogate for transoral tracheal wash to obtain bacterial cultures in dogs with pneumonia. J Vet Emerg Crit Care 2011;21(5):515-520.

    References »

    NEXT: Aspiration Pneumonia in Dogs: Treatment, Monitoring, and Prognosis

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