History
A 3-year-old 19.0-kg (41.8-lb) sexually intact male English Bulldog with a history of congenital renal disease was referred for evaluation because of acute respiratory distress and a 1-week history of vomiting and lethargy. On physical examination, the dog was tachypneic (60 breaths/min; reference range, 18 to 35 breaths/min) and tachycardic (140 beats/min; reference range, 70 to 120 beats/min) and had weak femoral pulses, consistent with hypovolemic shock. Supplemental oxygen was administered by nasal insufflation, and after approximately 10 minutes, results of pulse oximetry indicated that the dog's oxygen saturation of hemoglobin was 94% (reference range, 96% to 98%). Results of hematologic and serum biochemical analyses indicated mild anemia (Hct, 30%; reference range, 37% to 55%), severe azotemia (high concentrations of serum creatinine [5.82 mg/dL; reference range, 0.5 to 1.5 mg/dL] and urea [576.3 mg/dL; reference range, 21.4 to 59.9 mg/dL]), and moderate hypoalbuminemia (serum albumin concentration, 1.76 g/dL; reference range, 2.6 to 3.33 g/dL). Left lateral and dorsoventral radiographs of the dog's thorax were obtained (Figure 1).
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Diagnostic Imaging Findings and Interpretation
Thoracic radiography revealed a soft tissue opacity in the region of the right cranial and middle lung lobes that lacked evidence of vascular structures but had air bronchograms, consistent with an alveolar pattern (Figure 2). In addition, the right middle lung lobe had multiple small rounded areas of gas opacity reflective of a vesicular gas pattern combined with a diffuse bronchial pattern and likely bronchiectasis. In both thoracic radiographic views, evidence of mild bilateral retraction of the lungs from the costal wall with a fluid opacity in the pleural space was noted, consistent with pleural effusion. Differential diagnoses included severe aspiration pneumonia, bronchopneumonia, or lung lobe torsion, the latter of which was least likely because the dog's bronchi appeared radiographically to have been positioned correctly. The dog also had abnormalities (bronchial pattern and likely bronchiectasis) that were consistent with chronic pneumonia or chronic bronchitis, alone or in combination.
During stabilization efforts, the dog had cardiopulmonary arrest with no response to resuscitation. With owner consent, postmortem CT was performed with a 16-slice CT scanner for scientific interest. Findings included multiple small gas-attenuating cavities and an alveolar pattern with air bronchograms in the right middle and right cranial lung lobes, a mild generalized interstitial infiltrate with ground-glass appearance in the ventral region of all lung lobes, and multifocal pleural thickening combined with moderate pleural effusion (Figure 3). Findings also allowed bronchi to be traced sufficiently to rule out lung lobe torsion. Differential diagnoses, therefore, included chronic bronchitis or bronchopneumonia, necrotizing pneumonia (NP), and aspiration pneumonia. Because of the dog's young age, pulmonary neoplasia with necrotic centers and pleural involvement was considered unlikely.
Treatment and Outcome
Necropsy revealed extensive areas of necrosis in the pulmonary parenchyma and extending into the pleura. Results of histologic examination indicated extensive fibrin deposits and neutrophils, scattered macrophages, and multifocal bacterial colonies in the affected tissues, consistent with fibrinonecrotic pleuropneumonia secondary to aspiration pneumonia. Bacterial culture yielded abundant colonies of an Enterococcus sp.
Comments
The pathogenesis of NP is unclear but suspected to involve venous thrombosis following either an inflammatory response to toxins produced by invasive microorganisms or an infection-associated vasculitis.1 In dogs, NP is rare and has involved infection with Pseudomona aeruginosa, Escherichia coli, or canine adenovirus (alone or in combination), or Streptococcus equi subsp zooepidemicus.1,2
Contrast-enhanced CT is the gold standard diagnostic imaging modality used in the diagnosis of NP in humans and is helpful in evaluating the pulmonary parenchymal abnormalities (eg, pulmonary consolidation with areas of low signal attenuation indicating areas of necrosis1) that cannot be appreciated with thoracic radiography.3 For instance, pulmonary cavitary lesions created by liquefactive necrosis and filled with fluid have a similar radiographic opacity as the adjacent consolidated lung tissue; however, the pulmonary lesions become more visible with radiography later in the course of NP, when the necrotic lesion fluid drains into the communicating bronchi and is replaced in the lesion by gas.4 In the dog of the present report, small gas cavities were radiographically evident, which indicated that the dog had advanced NP.
To our knowledge, there are only 2 reports1,5 describing CT findings in dogs with NP. However, CT findings in people with NP are more extensively described.4,6 Diagnostic features of NP on CT images include poor or absent vascularity, loss of pulmonary architecture, and cavitated lesions in the pulmonary parenchyma. Initially, multiple small thin-walled cavities that are filled with gas or fluid are usually seen and often in just a single lung lobe. These lesions lack contrast medium enhancement, indicating poor perfusion. In addition, loculated fluid or gas in the pleural space is generally present during this early stage; however, differentiating between the parenchyma and the pleural space can be difficult when a parapneumonic effusion is present.4 As the disease progresses and the pulmonary tissue undergoes further liquefactive necrosis, the multiple small cavities may coalesce and form larger cavities, including gas-filled pneumatoceles. Lung abscesses evolving from NP, however, are thick walled and contrast enhancing and often have a gas-fluid level. Therefore, on the basis of CT revealing pulmonary cavities with thin, well-defined walls in the dog of the present report, a lung abscess in this dog was less likely.
In human medicine, focal NP is more commonly observed in nondependent pulmonary regions and not frequently related to aspiration pneumonia.6 In contrast, the cranioventral region was most affected in the dog of the present report, hence we suspected that NP was caused by aspiration following vomition, which was secondary to uremia caused by the dog's congenital nephropathy.
Findings in the dog of the present report strengthened our belief that veterinarians should consider NP as a differential diagnosis in patients with a vesicular gas pattern evident in the lung field on thoracic radiography and multiple gas cavities in the pulmonary parenchyma on CT.
References
1. Garber JB, Saile K, Rademacher N, et al. Pneumothorax in a dog caused by necrotizing pneumonia secondary to heatstroke. J Vet Emerg Crit Care (San Antonio) 2015;25:759–764.
2. Almes KM, Janardhan KS, Anderson J, et al. Fatal canine adenoviral pneumonia in two litters of Bulldogs. J Vet Diagn Invest 2010;22:780–784.
3. Tsai YF, Ku Yh. Necrotizing pneumonia: a rare complication of pneumonia requiring special consideration. Curr Opin Pulm Med 2012;18:246–252.
4. Masters IB, Isles AF, Grimwood K. Necrotizing pneumonia: an emerging problem in children? Pneumonia (Nathan) 2017;9:11–19.
5. Lee SK, Cho KO, Alfajaro MM, et al. Use of computed tomography and minimum intensity projection in the detection of lobar pneumonia mimicking lung lobe torsion in a dog [published online ahead of print Oct 16, 2017]. Vet Radiol Ultrasound doi: 10.1111/vru.12565.
6. Seo H, Cha S, Shin K, et al. Focal necrotizing pneumonia is a distinct entity from lung abscess. Respirology 2013;18:1095–1100.