Aspiration Pneumonitis and Pneumonia

Chapter 23 Aspiration Pneumonitis and Pneumonia



Robert Goggs, BVSc, MRCVS, Amanda K. Boag, VetMB, DACVIM, DACVECC, MRCVS



KEY POINTS



• Aspiration pneumonitis has a biphasic pathogenesis. Initial events are caused by direct chemical injury. This is followed by localized inflammatory mediator cascades producing neutrophil chemotaxis, sequestration, and subsequent increased permeability edema.

• Aspiration pneumonia is an infectious process caused by either aspiration of contaminated material or by bacterial colonization of damaged lungs subsequent to a sterile aspiration episode. Acid-induced lung injury enhances bacterial adherence to and reduces bacterial clearance from the lungs.

• Diagnosis is typically based on history, physical examination, and radiography. The severity of respiratory compromise is best monitored by arterial blood gas analysis.

• Management is principally supportive, consisting of airway management, cardiovascular support, oxygen therapy, and respiratory physiotherapy.

• Antimicrobial drug therapy should be directed by cytologic testing, Gram stain, and bacterial culture and sensitivity on samples collected by tracheal wash (TW) or bronchoalveolar lavage (BAL).

• The incidence of aspiration pneumonia can be reduced by recognizing the risk factors and attempting to control or minimize them.


INTRODUCTION


Aspiration pneumonitis and pneumonia frequently coexist in veterinary patients and may cause significant morbidity and mortality. The pathophysiology of both conditions shares some common features, namely the initiation of a localized inflammatory cascade with resultant impairment of respiratory function. Both conditions may incite development of acute respiratory distress syndrome (ARDS) or the systemic inflammatory response syndrome (SIRS).1 A number of risk factors exist for aspiration of gastric contents (Box 23-1). Emergency clinicians should be aware of these risk factors and have an understanding of the subsequent pathogenesis of pulmonary damage to aid in prevention and early recognition in order to enable optimal patient monitoring and treatment.



Box 23-1 Disorders and Conditions Predisposing to Aspiration of Gastric Contents



Large Volumes of Intragastric Food or Fluid


Delayed gastric emptying


Gastric outflow obstruction


Pain medication or opioid administration


Gastrointestinal motility disorders


Ileus


Pregnancy


Obesity


Recent meal


Overfeeding by the enteral route



Esophageal Disorders


Esophageal obstruction


Esophageal dysmotility


Megaesophagus


Myasthenia gravis


Esophageal reflux


Lower esophageal sphincter impairment


Drug administration


Nasogastric tube placement



Impaired Consciousness


Sedation, general anesthesia


Head trauma


Seizures


Encephalopathy


Coma



Impaired Airway Function


Laryngeal or pharyngeal dysfunction or surgery


Airway trauma



Other


Tracheostomy


Gastric intubation


Cleft palate


Weakness, paresis, paralysis



ASPIRATION PNEUMONITIS



Etiology


Aspiration pneumonitis is defined as acute lung injury due to inhalation of chemical irritants such as acidic stomach contents, hydrocarbons, or water (saltwater or fresh water near-drowning). The most common cause of aspiration pneumonitis is inhalation of gastric contents, and this will be the focus of the ensuing discussion.


Inhalation of small quantities of oropharyngeal material contaminated by bacteria likely occurs in normal animals, but bacterial colonization of the airway mucosa is prevented by rapid removal of this material by mucociliary clearance. In human patients with decreased levels of consciousness secondary to head trauma, seizures, sedation, or anesthesia the incidence of aspiration is greatly increased.2 A landmark study in 1946 reported acute respiratory failure in 66 women due to aspiration of stomach contents during anesthesia for obstetric procedures and suggested causal mechanisms for the associated pulmonary injury.3 The study also investigated the effects of a variety of solutions on the lungs of rabbits and concluded that aspirate acidity was the key factor in determining the severity of injury.


Factors affecting severity have since been further described. The magnitude of lung injury depends on the pH, volume, osmolality, and presence of nonsterile particulate matter in the aspirate.4,5 Severe histologic damage is caused by aspirates more acidic than pH 1.5, but little or no damage is caused by those with pH greater than 2.4.6 Particulate matter causes pulmonary injury by airway obstruction, prolongation of the inflammatory response, and by acting as a source of and nidus for bacterial infection.6,7 Aspiration of gastric contents containing particulate matter may cause severe pulmonary injury even if the pH is above 2.5.8,9



ASPIRATION PNEUMONIA



Etiology


Aspiration pneumonia refers to a pulmonary bacterial infection that develops following aspiration, but the distinction between pneumonitis and pneumonia is poorly defined in veterinary species. Aspiration pneumonia can result from bacterial colonization of lungs injured by acid aspiration or from aspiration of contaminated material. Because oropharyngeal colonization with pathogenic bacteria such as Pasteurella spp is extremely common in dogs and cats, both mechanisms likely occur. Aspiration of saltwater, oils, and liquid hydrocarbons may be included in the definition of aspiration pneumonia even though concurrent bacterial infection may not be present.



ASPIRATION PNEUMONITIS AND PNEUMONIA



Pathophysiology


The accepted biphasic model for acute lung injury following acid aspiration was developed following murine experiments in which lung permeability changes following direct tracheal instillation of hydrochloric acid were evaluated and the chronology of the histologic changes described.10


The first phase of lung injury, which begins immediately following aspiration, results from direct effects of the acidic aspirate. This is initially a chemical burn that damages the bronchial and alveolar epithelium and the pulmonary capillary endothelium.11 Pulmonary capillary permeability increases following acid stimulation of sensory neurons in the tracheobronchial smooth muscle. These sensory (substance P–immunoreactive) nerves are involved in the control of bronchial smooth muscle tone and vascular permeability. Stimulation of these nerves induces release of multiple tachykinin neuropeptides such as substance P and neurokinin A.12 Neurogenic inflammation, bronchoconstriction, bronchial mucus secretion, cough, vasodilation, and increased vascular permeability result. Permeability changes are maximal 1 to 2 hours after aspiration. Histologically, first phase damage consists of epithelial and endothelial degeneration, necrosis of type I alveolar cells, and intraalveolar hemorrhage.


The second phase of acid-induced lung injury starts 4 to 6 hours after aspiration and may continue for up to 2 days. It is characterized by additional, larger increases in pulmonary capillary permeability and protein extravasation than during the first phase, leading to extensive pulmonary edema formation, further compromising gas exchange and depleting intravascular volume.10 Neutrophils initially are attracted to the lungs by chemotactic mediators such as interleukin-8, tumor necrosis factor-α, and macrophage inflammatory protein-2 released by alveolar macrophages following the initial aspiration episode.13-15 The second phase involves the generation of a localized proinflammatory state by activation of sequestered neutrophils. Interleukin-8 is the main stimulus for neutrophil chemotaxis and also upregulates neutrophil β2-integrin endothelium receptors, mediates transendothelial neutrophil migration, and primes neutrophils for activation.13 Combination acid-particulate aspirates induce larger and longer lasting tumor necrosis factor-α expression than aspiration of acid alone.16 Neutrophils damage tissue by production and release of oxygen free radicals and proteolytic enzymes. High levels of serine proteases released by the sequestered, activated neutrophils seem to play a more important role in causing tissue damage than leukocyte-derived reactive oxygen species.17


The contralateral lung may be affected even if aspiration is unilateral. Complement activation resulting from mast cell degranulation stimulated by tachykinins mediates this response.18,19 In guinea pig models, tachykinin release in the lungs occurs following esophageal stimulation by gastric acid due to the presence of nonadrenergic, noncholinergic neural networks between the esophagus and the trachea.20


Aspiration pneumonia may develop concomitantly with pneumonitis if the aspirated contents are contaminated with oropharyngeal bacteria. Alternatively, aspiration pneumonia may develop from pneumonitis by subsequent bacterial colonization of the respiratory tract. Likely bacteria include commensals such as Staphylococcus spp, coliforms such as E. coli and Klebsiella spp, oropharyngeal Mycoplasma spp, and primary respiratory pathogens including Pasteurella spp, Pseudomonas spp, Bordetella spp, and Streptococcus spp.21-24 Gastric acid aspiration enhances bacterial adherence to the respiratory epithelium and reduces pulmonary clearance of bacteria. Acid injury may also facilitate bacterial adherence by upregulating expression of certain receptors providing de novo binding sites or by damaging epithelial cells, allowing respiratory pathogens to bind preferentially.25 Bacterial adherence may be mediated by pili, which access the cell surface following acid injury.26,27


Ultimately, the vascular permeability changes lead to pulmonary edema formation, focal atelectasis, and collapse of alveoli, resulting in hypoventilation and shunting. The inflammatory response to bacterial infection exacerbates this and hypoxia may develop as a consequence of ventilation-perfusion (V/Q) mismatch and reduced lung compliance.

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Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Aspiration Pneumonitis and Pneumonia

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