Three 21-week-old sexually intact female domestic shorthair cats were brought to the after-hours emergency service of the Veterinary Medical Center, Western College of Veterinary Medicine, because of sudden respiratory distress. The cats were littermates and had no prior history of disease. They had been adopted at 8 weeks of age and were up-to-date on all vaccinations. All 3 cats had been left confined in a room for the day (approx 10 hours), with food and water. When the owner returned home in the evening, the cats appeared lethargic, with difficulty standing up, and were visibly tachypneic. The room in which the cats had been confined was approximately 50 square feet in area. An ozone-generating air purifiera was present and operating as set for an 1,800- to 3,500-square-foot room. The 3 cats had never been left confined in this room prior to this event.
One cat (cat 1) appeared more severely affected than the others and was brought in first to the emergency center. Two hours later, the respiratory signs worsened in the other 2 cats (cats 2 and 3), so they were brought for evaluation as well.
On initial evaluation, cat 1 (body weight, 2.5 kg [5.5 lb]; body condition score, 3/5) was minimally responsive. Heart rate (150 beats/min; reference interval, 150 to 220 beats/min) and rectal temperature (38.4°C [101.1°F]; reference interval, 37.8° to 39.5°C [100.0° to 103.1°F]) were unremarkable, but respiratory rate was markedly high (80 breaths/min; reference interval, 16 to 40 breaths/min). Mucous membranes were pale, pink, and slightly tacky, and capillary refill time was < 2 seconds. No heart murmur, gallop sounds, or arrhythmias were detected on cardiac auscultation, and peripheral pulses were strong and synchronous. However, crackles were auscultated over both lung fields. Abdominal palpation revealed no abnormalities, and no lymphadenomegaly was evident.
Cats 2 and 3 were similar to cat 1 (respective body weights, 2.2 and 2.5 kg [4.8 and 5.5 lb]), with respective respiratory rates of 72 and 80 breaths/min and an unremarkable heart rate and rectal temperature. Mucous membranes were tacky, and pulmonary crackles were audible over both hemithoraxes.
No burn marks consistent with electrocution from chewing on an electric cable were visible on oral examination of any cat, and the owner reported finding no evidence of any damaged electrical cords in the room where the cats were confined. According to the owner, there were no other possible toxicants or hazards in that room, such as chemicals, medications, cosmetics, or other electric devices, that the cats could have been exposed to.
Following physical examination of cat 1, an IV catheter was placed, and a blood sample was collected for emergency assessment tests that included PCV, blood total protein concentration as measured via refractometer, blood glucose concentration as measured via glucometer, and BUN concentration as estimated via a test strip.b Results for these tests were within reference intervals, except for BUN concentration, which was mildly high (16 to 25 mmol/L; reference interval, 5 to 15 mmol/L). Three-view (ventrodorsal and left and right lateral) thoracic radiographs were obtained and interpreted by a board-certified veterinary radiologist (GSS), revealing a marked, diffuse increase in pulmonary soft tissue opacity, characterized by a marked, peribronchial, unstructured interstitial pulmonary pattern that coalesced to a patchy alveolar pattern (Figure 1). Findings were deemed most suggestive of airway inflammation (eg, bronchitis or pneumonitis) with concurrent pulmonary edema of noncardiogenic origin. Because of the concern for CPE, the cat was treated with furosemidec (2 mg/kg [0.9 mg/lb], IV) and placed in an oxygen cage providing 80% oxygen. Similarly, because of the concern for asthma crisis, terbutaline sulfated was also administered (0.01 mg/kg [0.005 mg/lb], IM).
The same procedures were performed for cats 2 and 3, and of the emergency assessment tests performed, only results for BUN concentration were abnormal (16 to 25 mmol/L). Three-view thoracic radiography revealed a moderate to marked unstructured interstitial pattern coalescing to a marked alveolar pulmonary pattern in the peripheral lung lobes, causing effacement of portions of the border of the cardiac silhouette, vascular margins (including the caudal vena cava), and diaphragm. Compared with findings for cat 1, the pulmonary pattern for cats 2 and 3 had a patchier appearance, with the more prominent changes located within the periphery of the caudal lung lobes. A milder bronchial pulmonary pattern was noted. Inflammatory airway disease with concurrent NCPE was considered the primary differential diagnosis. Cats 2 and 3 were provided the same treatments as cat 1 and were placed in the same oxygen cage with their littermate.
Over the next 8 hours in the oxygen cage, cats 2 and 3 had a return of respiratory rate to within the reference interval, whereas cat 1 had a decrease to 50 breaths/min. All 3 cats at this point had signs of considerable improvement in the respiratory effort. Pulmonary crackles were no longer audible in cats 2 and 3 and had substantially improved in cat 1. Radiography was repeated for cat 1, revealing no noticeable improvement (Figure 2).
After the cats had spent 24 hours in the oxygen cage at 80% oxygen saturation, respiratory rates and thoracic auscultation findings were unremarkable for all 3 cats. The oxygen concentration was then progressively decreased by increments of 10% every 2 hours until the cats were breathing room air. With room air, respiratory rates remained unremarkable, and all 3 cats appeared able to breathe normally. Pulse oximetry measurement was attempted multiple times, but none of the cats allowed this. Because of concerns for worsening of the respiratory distress during blood sample collection, no arterial blood gas analysis was attempted for any cat. No echocardiography was performed because of the unavailability of the veterinary cardiologist at the time, and no cardiac biomarker measurement was performed owing to financial concerns of the owner.
Three days after initial evaluation, the 3 cats continued to have unremarkable respiratory rates and no audible crackles or wheezes on thoracic auscultation. Three-view thoracic radiography was repeated for all 3 cats, revealing almost complete resolution of the previously noted abnormalities, with only a residual minimal ventral interstitial pattern persisting on the right lateral view (Figure 3). The cardiac silhouette and associated peripheral pulmonary vessels appeared unremarkable, as did the pleural space and mediastinum. All 3 cats were discharged from the hospital at this time. The high BUN concentrations at initial evaluation were believed to be likely attributable to dehydration, and because the 3 cats were in good clinical condition with noteworthy improvement of the radiographic lesions, this analyte was not reevaluated prior to discharge.
The owner stated that the 3 cats began to behave normally as soon as they returned home. On recheck examination 3 months after the episode, findings for all 3 cats were unremarkable. Follow-up thoracic radiography was performed, and findings were unremarkable as well.
Cardiogenic pulmonary edema
Noncardiogenic pulmonary edema
Reactive oxygen species
Fresh Air LA-3500 v2.0 Living Lightning Alpine air purifier, Alpine Air Technologies, Santa Ana, Calif.
Azostick reagent strips, Siemens Health Care Diagnostics Inc, Tarrytown, NY.
Salix 5%, Merck Animal Health, Kirkland, QC, Canada.
Chiron, Guelph, ON, Canada.
Alpine Air XL-12/LA Lightning Air RA 2500, Alpine Air Technologies, Santa Ana, Calif.
5. Dennis R, Kirberger RM, Barr F, et al. Techniques and differential diagnoses. In: Handbook of small animal radiology and ultrasound. 2nd ed. New York: Elsevier, 2010;156–164.
7. Bouyssou S, Specchi S, Desquilbet L, et al. Radiographic appearance of presumed noncardiogenic pulmonary edema and correlation with the underlying cause in dogs and cats. Vet Radiol Ultrasound 2017;58:259–265.
8. Drobatz KJ, Saunders HM, Pugh CR, et al. Noncardiogenic pulmonary edema in dogs and cats: 26 cases (1987–1993). J Am Vet Med Assoc 1995;206:1732–1736.
9. Ciencewicki J, Trivedi S, Kleeberger SR. Oxidants and the pathogenesis of lung diseases. J Allergy Clin Immunol 2008;122:456–468.
10. Grimsrud PA, Xie H, Griffin TJ, et al. Oxidative stress and covalent modification of protein with bioactive aldehydes. J Biol Chem 2008;283:21837–21841.
11. Bao A, Liang L, Li F, et al. Effects of acute ozone exposure on lung peak allergic inflammation of mice. Front Biosci (Landmark Ed) 2013;18:838–851.
12. Fabbri LM, Aizawa H, Alpert SE, et al. Airway hyperresponsiveness and changes in cell counts in bronchoalveolar lavage after ozone exposure in dogs. Am Rev Respir Dis 1984;129:288–291.
13. Larsen ST, Matsubara S, McConville G, et al. Ozone increases airway hyperreactivity and mucus hyperproduction in mice previously exposed to allergen. J Toxicol Environ Health A 2010;73:738–747.
14. McBride DE, Koenig JQ, Luchtel DL, et al. Inflammatory effects of ozone in the upper airways of subjects with asthma. Am J Respir Crit Care Med 1994;149:1192–1197.
15. Driscoll KE, Vollmuth TA, Schlesinger RB. Acute and subchronic ozone inhalation in the rabbit: response of alveolar macrophages. J Toxicol Environ Health 1987;21:27–43.
16. Bhalla DK, Daniels DS, Luu NT. Attenuation of ozone-induced airway permeability in rats by pretreatment with cyclophosphamide, FPL 55712, and indomethacin. Am J Respir Cell Mol Biol 1992;7:73–80.
17. Kleeberger SR, Kolbe J, Adkinson NF, et al. The role of mediators in the response of the canine peripheral lung to 1 ppm ozone. Am Rev Respir Dis 1988;137:321–325.
18. Phillips T, Jakober C. Evaluation of ozone emissions from portable indoor “air cleaners” that intentionally generate ozone. Sacramento, Calif: California Environmental Protection Agency, 2006.
19. Bhalla DK. Ozone-induced lung inflammation and mucosal barrier disruption: toxicology, mechanisms, and implications. J Toxicol Environ Health B Crit Rev 1999;2:31–86.
20. Snow SJ, Gordon CJ, Bass VL, et al. Age-related differences in pulmonary effects of acute and subchronic episodic ozone exposures in brown Norway rats. Inhal Toxicol 2016;28:313–323.
21. Bhalla DK, Mannix RC, Lavan SM, et al. Tracheal and bronchoalveolar permeability changes in rats inhaling oxidant atmospheres during rest or exercise. J Toxicol Environ Health 1987;22:417–437.
22. Devlin RB, McDonnell WF, Mann R, et al. Exposure of humans to ambient levels of ozone for 6.6 hours causes cellular and biochemical changes in the lung. Am J Respir Cell Mol Biol 1991;4:72–81.
23. Phalen RF, Crocker TT, McClure TR, et al. Effect of ozone on mean linear intercept in the lung of young Beagles. J Toxicol Environ Health 1986;17:285–296.
24. Young BC, Strom AM, Prittie JE, et al. Toxic pneumonitis caused by inhalation of hydrocarbon waterproofing spray in two dogs. J Am Vet Med Assoc 2007;231:74–78.
25. Neall M. Severe respiratory signs in two cats following the inhalation of a footwear proofing aerosol. J Feline Med Surg 2010;12:183–184.
26. Mader DR, Yike I, Distler AM, et al. Acute pulmonary hemorrhage during isoflurane anesthesia in two cats exposed to toxic black mold (Stachybotrys chartarum). J Am Vet Med Assoc 2007;231:731–735.