History

An 8-year-old 527-kg (1,161-lb) healthy Quarter Horse gelding was properly anesthetized and intubated and underwent sham ventral median celiotomy, with minimal intestinal manipulation, as part of the control group of an intestinal ischemia and reperfusion study. Food, but not water, was withheld from the horse overnight before the induction of anesthesia.

After 2 hours of an uneventful anesthetic episode, the celiotomy site was closed routinely. The horse was placed in left lateral recumbency in a recovery box, and 9 minutes after discontinuing inhalation anesthesia (when a swallowing reflex was present), the horse was extubated. The nasopharyngeal tubes were also removed at this time, and nasal breathing was ascertained. The horse had a prolonged recovery from anesthesia (1 hour and 40 minutes' duration) and required considerable encouragement to stand. Gastric contents were observed exiting from the nostrils during the early part of the recovery period.

Clinical, Clinicopathologic, and Gross Findings

Within 6 hours following recovery to a standing position, the horse became febrile (rectal temperature, 38.9°C [102.1°F]), tachycardic (60 beats/min), and tachypneic (28 breaths/min). The horse's mucous membranes became injected, and it developed marked signs of depression. At 12 hours after surgery, the lung sounds became harsh on auscultation of the cranioventral portion of the thorax; by 18 hours after surgery, harsh lung sounds were ausculted throughout the entire thorax. A CBC revealed mild leukocytosis, mild neutrophilia with a left shift and toxic change, mild lymphopenia, and mild monocytosis.

The horse was euthanized by means of an overdose of pentobarbital sodium for the purpose of research, and a necropsy was performed. On gross examination, the cranial lobe and the craniodorsal and caudodorsal parts of the caudal lobes of the right and left lungs failed to collapse and were firm, discolored yellow, and covered by an adherent layer of friable material (fibrin). There was marked congestion of the caudodorsal surface of both lungs (Figure 1). On cut sections, feed material could be grossly observed within the large bronchi, and marked separation of the interlobular septa (pulmonary edema) was present. The lesions in the left lung were more severe than those in the right lung. No abnormalities were observed in other organs.

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Photograph of the dorsal surface of the fresh right lung (A) and fixed left lung (B) of an 8-year-old Quarter Horse gelding anesthetized for a celiotomy with minimal intestinal manipulation and subsequently euthanized 18 hours after recovery from anesthesia as part of a research project. There is discoloration along the cranioventral aspect of the caudal lobe of the right lung (*). Congestion of the caudodorsal aspect of the right lung is present (†). A large amount of fibrin, particularly on the cranial ventral portion of the left lung (‡), is evident.

Citation: Journal of the American Veterinary Medical Association 251, 4; 10.2460/javma.251.4.409

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Histopathologic Findings

Tissue samples from the right lung were fixed with 4% paraformaldehyde for 24 hours at 4°C and embedded in paraffin. The entire left lung was instilled with fixative (4% paraformaldehyde and 0.1% glutaraldehyde in HEPES) in situ, removed, fixed for 24 hours at 4°C, and sectioned for paraffin embedding. Paraffin blocks were sectioned a 5 μm and stained with H&E stain. Throughout the examined tissue sections, lesions were multifocal; those in sections from the left lung were considered more severe than those in sections from the right lung.

Alveoli within affected areas were filled with large numbers of viable and degenerate neutrophils, fine fibrillar eosinophilic material (fibrin), protein-rich edema fluid, and small amounts of hemorrhage. Occasionally, alveoli were filled with cellular and nuclear debris (necrosis). Alveolar septa were moderately congested and frequently necrotic. Interlobular septa were markedly expanded and filled with fibrin, edema, and an inflammatory cell population similar to that observed in the alveoli (Figure 2). Similar changes were present on the pleural surface of affected sections. Large airways (bronchi and bronchioles) were clear of material, and the epithelium was intact.

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Photomicrographs of a section of the cranial lobe of the left lung from the horse in Figure 1. A—Notice the marked expansion of the interlobular septa and pleura with fibrin and edema (*), marked infiltration of inflammatory cells (‡), and pulmonary edema (†). H&E stain; bar = 2.0 mm. B—Higher-magnification view of the section in panel A. Although aspirated feed material was grossly visible in the airways, it was not evident histologically. H&E stain; bar = 100 μm.

Citation: Journal of the American Veterinary Medical Association 251, 4; 10.2460/javma.251.4.409

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Morphologic Diagnosis and Case Summary

Morphologic diagnosis: severe acute multifocal to coalescing fibrinonecrotizing, suppurative pneumonia with marked pulmonary edema and fibrinous pleuritis.

Case summary: aspiration pneumonia resulting from aspiration of gastric contents during recovery from anesthesia and systemic inflammatory response syndrome (SIRS) in a horse.

Comments

Unlike in carnivores, regurgitation leading to aspiration of stomach contents during anesthesia is exceedingly rare in horses owing to the unique muscular distribution within their esophagus and strong cardiac sphincter, which prevent regurgitation of stomach contents.^1,2 However, it is common practice to induce anesthesia with an indwelling nasogastric tube in a horse prior to colic surgery to reduce the risk of aspiration from spontaneous gastric reflux that may occur as a result of an overly distended stomach.^1,2 The horse of the present report underwent celiotomy with minimal intestinal manipulation because it was part of a control group for an intestinal ischemia and reperfusion study. The risk of regurgitation of gastric contents for this horse in the perianesthetic period was considered insignificant because the horse was apparently healthy, had food withheld overnight prior to surgery, had minimal intestinal manipulation with normal intestinal motility observed during surgery, and had no complications with tracheal intubation following induction of anesthesia.

For the horse of the present report, the airway was assumed to be protected and sealed during anesthesia because there were no problems associated with a deflated cuff or the ability to effectively use the ventilator. Therefore, aspiration most likely occurred while the horse was in left lateral recumbency following extubation, which was supported by the greater severity of lesions located in the left (dependent) lung, compared with those in the right lung, identified during gross and histologic examinations. The anesthetic protocol used in this horse was considered to be routine at our hospital. Many drugs used for the anesthetic protocol are known to lower esophageal sphincter tone in dogs, including α₂-adrenergic receptor agonists, propofol, and volatile anesthetics^3–5; however, the action of these drugs on the equine lower esophageal sphincter is unknown.

The reason for the apparent regurgitation and aspiration during recovery from anesthesia in the horse of the present report was not evident on the basis of the gross necropsy findings. It is possible that the horse had abnormal gastroesophageal function that led to regurgitation during recovery or that it had some type of pharyngeal or laryngeal dysfunction that prevented protection of the larynx during swallowing. Idiopathic gastroesophageal reflux in an adult horse has previously been reported.⁶ In that horse, despite it having severe distal esophageal ulceration, no physical or mechanical reason for the gastro-esophageal reflux could be determined, and it was proposed that the horse's gastroesophageal sphincter was incompetent. No evidence of distal esophageal ulceration was present in the horse of the present report.

In addition to signs of pneumonia (harsh lung sounds and tachypnea), the horse in the present report also had signs of SIRS, including tachycardia, hyperthermia, injected mucous membranes, and leukocytosis with a left shift. In rats, it has been shown that pulmonary blood flow increases immediately in areas damaged by gastric acid aspiration.⁷ Increased blood flow to an inflamed area would increase the amount of inflammatory mediators released into the systemic circulation, directly contributing to a systemic inflammatory response, which could explain the rapid development of SIRS in the case described in the present report. Because the horse of the present report was used for a research study investigating inflammation, it did not receive anti-inflammatory drugs or antimicrobials, which may have potentiated the development of SIRS. In clinical cases, horses would be treated with both types of drugs prophylactically and after surgery, which could delay or prevent the development of severe pneumonia and SIRS.

In humans and dogs, reflux of gastric contents during anesthetic events is not uncommon, and aspiration of gastric acid and contents may cause acute lung injury (A LI).^8–12 Acute lung injury is identified clinically in veterinary patients by sudden-onset tachypnea and labored breathing, hypoxemia, evidence of pulmonary capillary leakage without increased pulmonary capillary pressure, and a known risk factor (eg, aspiration of gastric contents) with or without evidence of diffuse pulmonary inflammation.¹³ Some of the aforementioned criteria were either not assessed or not present in the case described in the present report; thus, on the basis of the clinical signs, it is difficult to state that the horse had ALI.

In humans and laboratory animals, ALI or acute respiratory distress syndrome is characterized histomorphologically by pulmonary edema and an acute neutrophilic inflammatory response with accumulation of fibrin-rich proteinaceous exudates.^10,14 Histologic examination of sections of grossly abnormal lung tissue from the horse of the present report revealed fibrinonecrotizing, suppurative pneumonia with marked pulmonary edema and neutrophil infiltration. However, the lesions consistent with ALI were not distributed diffusely throughout the lungs, as observed in human patients and laboratory animals with ALI, but were localized to the cranioventral area of the lungs, which would be expected for a case of severe aspiration pneumonia.

In the present report, a rare occurrence of gastric contents aspiration during an anesthetic recovery period leading to the development of severe, acute aspiration pneumonia in an adult horse has been described. Aspiration of gastric contents should be considered in horses in which SIRS develops concurrently with tachypnea and increased lung sounds in the early postoperative period.