The CT appearance of the lungs of people with various lung diseases correlate to histopathologic findings1–14 and prognosis.5,14 However, the correlation between the CT appearance of disease-affected lungs of dogs and cats and histopathologic findings have only been described for a few parasitic15–18 and inflammatory diseases,19–21 pulmonary fibrosis,22 and primary lung tumors.23,24 This knowledge gap is predominantly because of the infrequency of combined CT examination and antemortem collection and histologic examination of lung specimens. One method to overcome this gap is to characterize and correlate CT, gross, and histopathologic findings in cadaveric animals.
Postmortem CT is a relatively new diagnostic tool for animals.25–29 In a study30 of Bernese Mountain Dogs with confirmed histiocytic sarcoma, PMCT and subsequent histologic examination of a CT-guided needle biopsy specimen was as accurate as necropsy and subsequent histologic examination of harvested tissue specimens to detect pulmonary histiocytic sarcoma. Postmortem CT may be a useful adjunct to necropsy; by providing diagnostic information in advance of necropsy, PMCT findings may help guide pathologists to harvest tissues from diseased organs such that the probability of obtaining a diagnosis is greater than with necropsy alone. Additionally, PMCT images can be stored and retrospectively reevaluated, if necessary. However, the problem with PMCT of the lungs is atelectasis and subsequent difficulty to clearly see any lung lesions. Atelectasis develops because of time-dependent hypostasis after death.
Ventilated PMCT was developed to improve the identification of lung lesions in people; it has been shown to adequately overcome postmortem atelectasis, thereby improving visualization of lesions.31–36 Atelectasis may lead to a misdiagnosis of pulmonary edema or aspiration or other pneumonias.31 For live animals, CT assessment of the lungs is optimized when an inspiratory breath-hold technique is used.37 Atelectasis can occur because of poor ventilation when animals are anesthetized for CT, and an inspiratory breath-hold technique can counter atelectasis. Ventilated PMCT involves aeration of the lungs by applying positive ventilation pressure to the lungs through an orotracheal tube during CT of the lungs. Ventilated PMCT of animals has not been previously described. Because VPMCT improves the visualization of lung lesions in people, it may similarly improve visualization in animals.
The objectives of the study reported here were to identify the optimal ventilation pressure for VPMCT assessment of the lungs in cadaveric dogs and compare the optimal ventilation pressures between dogs with and without focal lung lesions. We hypothesized that dogs with focal lung lesions would require a higher ventilation pressure than dogs without focal lung lesions.
Materials and Methods
Animals
Eligible dogs were those that were euthanized or had died at the Veterinary Teaching Hospital at the University of Sydney between February 2018 and August 2019 and subsequently necropsied with owner consent. Dogs with pleural disease (eg, pleural effusion, thickening of pleura), determined antemortem with radiography or ultrasonography or postmortem with VPMCT, were excluded. For analysis, dogs were divided into 2 groups on the basis of the CT presence (group A) or absence (group B) of focal lung lesions.
Procedure
Postmortem thoracic CT images were acquired with a 16-slice multidetector helical CT scannera between 30 and 180 minutes after euthanasia. Dogs were positioned in sternal recumbency with the forelimbs extended cranially. Scanner settings were 120 kVp, 150 mAs, collimation of 16 × 1.5 mm, gantry rotation speed of 0.5 seconds, field of view of 180 mm, matrix of 512 × 512 pixels, slice thickness of 2 mm (at 1-mm increments), and collimator pitch of 1.438.
Each dog was orotracheally intubated, and an initial PMCT was performed to serve as baseline (ventilation pressure, 0 cm H2O). Then, each dog's lungs were aerated with oxygen (flow rate, 2 L/min) to ventilation pressures of 10, 15, 20, 25, 30, and 35 cm H2O, and, while VPMCT was performed, pressures were maintained by closure of the pop-off valve of the anesthesia machine and manual compression of the rebreathing bag. Pressure was released between each scan. Order of ventilation pressures was not randomized; rather, for each dog, the first VPMCT scan was at a ventilation pressure of 10 cm H2O and pressures were increased by 5 cm H2O, with the last scan at 35 cm H2O.
Image analysis
Image segmentation, measurements, and interpretation were performed by 1 investigator (MPYL) with an image-analysis workstationb and software.c For each CT examination, 5 ROIs were selected for review on the basis of the following anatomical landmarks: the terminal bifurcation of the bronchus of the right cranial lung lobe, tracheal bifurcation, origin of the bronchus of the right middle lung lobe, origin of the bronchus of the accessory lung lobe, and terminal bifurcation of the bronchus of the left caudal lung lobe. For these ROIs, the lungs in transverse plane were manually segmented and separated from the rest of the thorax as an ROI. The boundaries for each ROI were defined by the parietal and mediastinal margins of the lungs, with exclusion of the trachea, mainstem bronchi, and hilar blood vessels.
Images were initially evaluated for pneumothorax and pneumomediastinum, then for postmortem changes and focal lesions. Focal lesions were defined as abnormalities, such as nodules, that were localized to a portion of the lung.
Images of lung ROIs were exported into a multi-image analysis graphic user interface toold (ie, viewer for medical images with analysis tools) and analyzed pixel by pixel for determining lung attenuation. Lung attenuation data were exported into a spreadsheet,e and histograms of the data were created. The lungs of each ROI were categorized on the basis of lung attenuation values26 as follows: hyperaerated (−1000 to −901 HU), normo-aerated (−900 to −501 HU), poorly aerated (−500 to −101 HU), and nonaerated (−100 to 100 HU). Additionally, the percentage of lung in each ROI that was hyperaerated, normo-aerated, poorly aerated, and nonaerated were reported. For each dog, CT images obtained at each ventilation pressure were compared to determine the optimal ventilation pressure. The optimal ventilation pressure was defined as the pressure that yielded CT images with the greatest percentage of normo-aerated lung and lowest percentage of abnormally aerated lung (ie, hyperaerated, poorly aerated, or nonaerated lung).
Statistical analysis
Continuous variables, including age and time between euthanasia and VPMCT, were evaluated for normality with the Shapiro-Wilk test. If the data were normally distributed, a t test was used to determine whether the time between euthanasia and VPMCT significantly differed between the dogs of group A and group B. A Mann-Whitney U test was used to determine whether optimal ventilation pressures significantly differed between groups. Values of P < 0.05 were considered significant.
Results
Thirteen deceased dogs were available for inclusion in the study. However, 1 dog was excluded because of VPMCT-confirmed pleural effusion. Six dogs each were assigned to groups A and B on the basis of the presence (A) and absence (B) of VPMCT-confirmed lung lesions. Each group had 2 spayed female and 4 neutered male dogs. Group A included 1 each of American Staffordshire Terrier, Australian Bulldog, Border Collie, Cavalier King Charles Spaniel, Cocker Spaniel–Poodle mixed breed, and Shih Tzu. Group B included 1 each of British Bulldog, French Bulldog, Italian Greyhound, Koolie, Labrador Retriever, and Schnauzer-Poodle mixed breed. Age of dogs in group A ranged from 6 to 14 years (mean ± SD, 11 ± 3.0 years) and group B, 6 to 15 years (11 ± 3.7 years). Ages were normally distributed, and no outliers were noted on the basis of visual inspection of a box-and-whisker plot (not shown). Age did not significantly (P = 0.868) differ between groups. Five of 6 dogs in group A and 6/6 dogs in group B were euthanized with IV pentobarbitone administration. One dog in group A had died of cardiac arrest, likely secondary to septic shock.
Recorded times between euthanasia and VPMCT were normally distributed, and no outliers were noted on the basis of visual inspection of a box-and-whisker plot (not shown). Dogs in group A and group B had VPMCT performed 30 to 60 minutes (mean ± SD, 43.3 ± 10.8 minutes) and 30 to 120 minutes (60.0 ± 33.0 minutes), respectively, after euthanasia. Time between euthanasia and VPMCT did not significantly (P = 0.267) differ between groups.
For all dogs, VPMCT revealed a reduction in lung attenuation in all 5 ROIs, and lung aeration for VPMCT did not create pneumothorax or pneumomediastinum. Aeration permitted clear detection of structured lung lesions (group A; Figures 1 and 2). Four dogs had nodules that affected multiple lung lobes, 1 dog had consolidation of the ventral portions of the right and left cranial and right middle lung lobes, and 1 dog had nodules in the right cranial lung lobe and a focal, irregular soft tissue–attenuated area in the dorsomedial portion of the cranial segment of the left cranial lung lobe. Additionally, aeration permitted detection of a mild mosaic pattern (ground-glass appearance) affecting the lung lobes of all dogs (Figure 3).
Transverse CT images from 1 of 6 dogs with lung lesions (group A) in 1 of 5 ROIs (origin of the bronchus of the accessory lung lobe) without (PMCT; A) and with lung aeration (VPMCT; B and C). A—Lung attenuation, particularly in the gravity-dependent regions. B—Lung aeration at ventilation pressure of 25 cm H2O. C—Lung aeration at ventilation pressure of 35 cm H2O. Note that with increasing ventilation pressure, lung attenuation is less, such that lung nodules (asterisks) are more easily seen. The dog is positioned in sternal recumbency, and the dog's right is to the left of the images.
Citation: American Journal of Veterinary Research 81, 11; 10.2460/ajvr.81.11.879
Transverse CT images from 1 of 6 dogs with lung consolidation (group A) in 1 of 5 ROIs (origin of the bronchus of the right middle lung lobe) without (PMCT; A) and with lung aeration (VPMCT; B and C). A—Lung attenuation, particularly in the gravity-dependent regions. B—Lung aeration at ventilation pressure of 25 cm H2O. C—Lung aeration at ventilation pressure of 35 cm H2O. Note that with increasing ventilation pressure, lung attenuation is less, especially dorsally, such that lung consolidation (asterisks) is more easily seen. The dog is positioned in sternal recumbency, and the dog's right is to the left of the images.
Citation: American Journal of Veterinary Research 81, 11; 10.2460/ajvr.81.11.879
Transverse CT images from 1 of 6 dogs without lung lesions (group B) in 1 of 5 ROIs (origin of the bronchus of the accessory lung lobe) without (PMCT; A) and with lung aeration (VPMCT; B and C). A—A generalized, marked increase in lung attenuation is evident, especially in the right lung. B—Lung aeration at ventilation pressure of 25 cm H2O. C—Lung aeration at ventilation pressure of 35 cm H2O. Note that with increasing ventilation pressure, lung attenuation lessens; however, a diffuse mosaic (ground-glass) pattern is maintained. The dog is positioned in sternal recumbency, and the dog's right is to the left of the images.
Citation: American Journal of Veterinary Research 81, 11; 10.2460/ajvr.81.11.879
The optimal ventilation pressure for the dogs in group A was 25 cm H2O (1/6 dogs), 30 cm H2O (1), and 35 cm H2O (4; Figure 4) and in group B was 15 cm H2O (1/6 dogs), 20 cm H2O (1), and 25 cm H2O (4; Figure 5). Distribution of the optimal ventilation pressures was similar between the 2 groups. Median optimal ventilation pressure was significantly (P = 0.009) higher in group A (35 cm H2O) than group B (25 cm H2O). The percentage of normo-aerated lung for all evaluated ventilation pressures for group-B dogs was optimal at lower pressures than for group-A dogs, and pressures > 25 cm H2O caused the percentage of normo-aerated lung to decrease.
Mean percentage of normo-aerated lungs in 5 ROIs evaluated with VPMCT at ventilation pressures of 0, 10, 15, 20, 25, 30, and 35 cm H2O for the 6 dogs with VPMCT-confirmed lung lesions (group A). Optimal pressure (highest percentage of normo-aerated lungs) was 25 cm H2O for 1 dog, 30 cm H2O for 1 dog, and 35 cm H2O for 4 dogs.
Citation: American Journal of Veterinary Research 81, 11; 10.2460/ajvr.81.11.879
Mean percentage of normo-aerated lungs in 5 ROIs evaluated with VPMCT at ventilation pressures of 0, 10, 15, 20, 25, 30, and 35 cm H2O for the 6 dogs without VPMCT-confirmed lung lesions (group B). Optimal pressure (highest percentage of normo-aerated lungs) was 15 cm H2O for 1 dog, 20 cm H2O for 1 dog, and 25 cm H2O for 4 dogs.
Citation: American Journal of Veterinary Research 81, 11; 10.2460/ajvr.81.11.879
Discussion
Results of the present study indicated that VPMCT reduces lung attenuation in dogs, and these results were similar to those reported in people.31–34,36,38 Furthermore, results of the present study indicated that the amount of ventilation pressure to aerate the lungs was important. We identified that increasing ventilation pressure increased the percentage of normo-aerated lungs in all dogs, but group-A dogs required a significantly greater optimal ventilation pressure than group-B dogs. The disparity in pressures may be because lung disease (in group A) decreased lung compliance39; compliance may be decreased because of increased interstitial fluid and alveolar surface tension and pulmonary fibrosis.40
Another possible contributing cause for the disparity is the time of onset of rigor mortis. Individual variation in the degree of rigor mortis at the time of VPMCT was possible, and rigor mortis affects chest wall compliance.41 After death and subsequent exhaustion of ATP, muscles become increasingly fixed in a contracted state.41 Consequently, chest wall compliance decreases as time elapses from the time of death. Because total respiratory compliance is a function of lung and chest wall compliance,40 a decrease in chest wall compliance will decrease total respiratory compliance. This suggests that with increasing rigor mortis, high ventilation pressures are required to overcome postmortem atelectasis. Rigor mortis typically begins 2 to 6 hours after death and lasts 36 hours. However, multiple factors can affect rigor mortis timing, including body temperature at time of death, antemortem activity, and cause of death.41 These factors were not controlled in the present study because of the small number of eligible dogs and dog owner preferences (eg, after euthanasia, some owners spent more time than others with their dogs). Studies that include determination of the degree of rigor mortis (ie, thoracic area as an indirect measure of chest wall compliance) in deceased dogs and its impact on optimal ventilation pressure for VPMCT could be considered.
Results of the present study suggested that a ventilation pressure of 35 cm H2O may be optimal for VPMCT visualization of focal lung lesions in cadaveric dogs. However, for cadaveric dogs without focal lung lesions noted on VPMCT, a ventilation pressure > 25 cm H2O resulted in a greater percentage of alveolar hyperinflation and a subsequent reduced percentage of normo-aerated lung. In live animals, lung hyperinflation at high ventilation pressures (ie, > 15 cm H2O) secondary to an inspiratory breath-hold technique is not considered ideal for CT studies of the lungs because lung hyperinflation may be misinterpreted as an abnormality (eg, air trapping), and hyperinflation may result in lung damage.37 In cadaveric dogs, however, hyperinflating the lungs for differentiating focal lung disease from postmortem atelectasis is less concerning, and hyperinflation may instead help to illuminate the presence of any focal lung lesions. Yet, postmortem lung damage secondary to lung aeration may impede histologic identification of lesions; therefore, this phenomenon should be considered when performing VPMCT.
In the present study, unfortunately, histologic evaluation of the lungs of the dogs was not available. In live dogs, an alveolar recruiting maneuver, inflating the lungs to and sustaining at 40 cm H2O for 20 seconds, was performed without clinical complications.42,43 In a study of rats,44 researchers reported that ultrastructure of the lungs was preserved in rats without acute lung injury after the lungs were subjected to an alveolar recruiting maneuver of 40 cm H2O for 40 seconds; however, the same alveolar recruiting maneuver resulted in detachment of alveolar epithelium in rats with moderate to severe acute lung injury. Thus, a ventilation pressure of 35 cm H2O for VPMCT, despite some lung hyperinflation, may not significantly affect the microscopic architecture of the lungs of cadaveric dogs without lung lesions and can be considered in situations when the presence of lung disease is unknown. Investigating the microscopic (histologic) effects of postmortem lung aeration is required.
This study also characterized the PMCT appearance of dog lungs. In all dogs, a mild mosaic pattern (ground-glass appearance), consistent with increased lung attenuation, was noted in all lung lobes. Because this change was noted in all dogs, it possibly was a postmortem change. A similar PMCT finding is reported in people and is likely attributed to regional differences in the distribution of blood and air in the lungs, relaxation of the respiratory muscles, and displacement of the diaphragm toward the thoracic cavity secondary to abdominal gas formation.36,45 However, unstructured interstitial lung disease, such as interstitial fibrosis and infiltrative neoplasia, that accounted for this mosaic pattern cannot be excluded for the dogs of the present study because lung specimens were not collected for histologic examination.
Limitations of the present study included the small number of dogs and breeds, such that determining whether habitus affects the required pressure to achieve optimal aeration of the lungs was not possible. Obese people have reduced chest wall compliance because of increased mechanical loading on the respiratory muscles.46,47 Therefore, obese people are prone to spontaneous atelectasis in the perioperative period, compared with people of ideal weight, and positive-end–expiratory pressure and alveolar recruiting maneuvers are recommended for induction and maintenance of anesthesia to reduce the risk of spontaneous atelectasis.46 Because of the effect of obesity on chest wall compliance in people, obesity may similarly affect dogs, such that higher ventilation pressures than those reported for the dogs of the present study may be required to achieve optimal postmortem lung aeration.
Additionally, lungs of all dogs were aerated to every ventilation pressure (10, 15, 20, 25, 30, and 35 cm H2O) sequentially from the lowest to the highest. Although pressure was released between each VPMCT scan, air may have remained in the lungs after each scan, such that the optimal ventilation pressure may have actually been higher than those reported. For 4 of the group-A dogs, optimal ventilation pressure was 35 cm H2O, the highest investigated ventilation pressure. However, we cannot exclude whether pressures > 35 cm H2O would have instead been optimal.
Another limitation was the lack of histologic examination of VPMCT-identified lung lesions. Dogs were divided into 2 groups on the basis of the presence (group A) and absence (B) of focal, VPMCT-identified lung lesions. However, postmortem atelectasis may have been mischaracterized as focal lung lesions in the group-A dogs. Yet, mischaracterization is unlikely because visualized lung lesions (nodules) were in gravity-nondependent ROIs in the majority (5/6) of dogs at their respective optimal ventilation pressures, and atelectasis favors gravity-dependent regions.31,37 One dog had consolidation in the ventral portions of the right and left cranial and right middle lung lobes at a ventilation pressure of 35 cm H2O. Although histologic examination of those lobes was lacking, the likelihood that the described consolidation represented postmortem atelectasis was low because the percentage of nonaerated and poorly aerated lung was minimal at 35 cm H2O in all group-B dogs. Lack of histologic examination of lung specimens may have also mischaracterized group-B dogs as free of lung disease; those dogs may have still had diffuse lung disease (eg, pulmonary fibrosis or infiltrative neoplasia).
Further investigation with a larger number of dogs with and without lung lesions and lung aeration to only 1 ventilation pressure is required to confirm the results of the present study. Randomization of ventilation pressures was not performed in the present study and could also be considered for future studies; however, as discussed previously, air may remain in the lungs after each scan and, therefore, randomization may not mitigate any effect of air accumulation. Additional future studies could include the investigation of a wider range of ventilation pressures, a fixed death-to-necropsy time interval, and the histologic examination of lung tissue specimens to confirm the presence or absence of lung lesions.
In conclusion, optimal ventilation pressures for VPMCT were noted for all dogs, and subsequently, lung lesions were identified in a subset of those dogs. Results demonstrated that cadaveric dogs with focal lung lesions required higher ventilation pressures than cadaveric dogs without focal lung lesions. A ventilation pressure of 35 cm H2O may be optimal for VPMCT.
ABBREVIATIONS
| PMCT | Postmortem CT |
| ROI | Region of interest |
| VPMCT | Ventilated postmortem CT |
Footnotes
Philips, 16-slice Brilliance CT V2.3, Philips Medical Systems Netherlands, Eindohoven, Netherlands.
Macbook Pro macOS High Sierra, version 10.13.5, Cupertino, Calif.
OsiriX, version 9.5 64-bit, Pixmeo SARL, Bernex, Switzerland.
Mango version 4.0.1, Research Imaging Institute, University of Texas Health Science Center, San Antonio, Tex.
Microsoft Excel for Mac, version 16.14.1, Microsoft Corp, Redmond, Wash.
References
1. Verschakelen JA. Computed tomography of the lung: a pattern approach. Heidelberg, Germany: Springer Berlin Heidelberg, 2007.
2. Arcadu A, Byrne SC, Pirina P, et al. Correlation of pulmonary function and usual interstitial pneumonia computed tomography patterns in idiopathic pulmonary fibrosis. Respir Med 2017;129:152–157.
3. Guimarães MD, Marchiori E, de Souza Portes Meirelles G, et al. Fungal infection mimicking pulmonary malignancy: clinical and radiological characteristics. Lung 2013;191:655–662.
4. Gupta N, Meraj R, Tanase D, et al. Accuracy of chest high-resolution computed tomography in diagnosing diffuse cystic lung diseases. Eur Respir J 2015;46:1196–1199.
5. Kang H, Lee KS, Jeong YJ, et al. Computed tomography findings of influenza A (H1N1) pneumonia in adults: pattern analysis and prognostic comparisons. J Comput Assist Tomogr 2012;36:285–290.
6. Marchiori E, Zanetti G, Hochhegger B, et al. Reversed halo sign on computed tomography: state-of-the-art review. Lung 2012;190:389–394.
7. Mehrian P, Homayounfar N, Karimi MA, et al. Features of idiopathic pulmonary alveolar proteinosis in high resolution computed tomography. Pol J Radiol 2014;79:65–69.
8. Rufino RL, Capone R, Capone D, et al. Pattern of chest computed tomography before and after treatment in patients with proven pulmonary tuberculosis. Am J Respir Crit Care Med 2015;191:A3309.
9. Sieren JC, Smith AR, Thiesse J, et al. Exploration of the volumetric composition of human lung cancer nodules in correlated histopathology and computed tomography. Lung Cancer 2011;74:61–68.
10. Tamura M, Saraya T, Fujiwara M, et al. High-resolution computed tomography findings for patients with drug-induced pulmonary toxicity, with special reference to hypersensitivity pneumonitis-like patterns in gemcitabine-induced cases. Oncologist 2013;18:454–459.
11. Torrealba JR, Fisher S, Kanne JP, et al. Pathology-radiology correlation of common and uncommon computed tomographic patterns of organizing pneumonia. Hum Pathol 2018;71:30–40.
12. Umezawa H, Naito Y, Terada J, et al. Computed tomography patterns in patients with cytotoxic drug-induced pulmonary toxicity. Eur Respir J 2016;48:PA3924.
13. Verma R, Abdoh M. Crazy paving pattern. Clin Case Rep 2017;5:533–534.
14. Walsh SLF, Sverzellati N, Devaraj A, et al. Chronic hypersensitivity pneumonitis: high resolution computed tomography patterns and pulmonary function indices as prognostic determinants. Eur Radiol 2012;22:1672–1679.
15. Dillon AR, Tillson DM, Hathcock J, et al. Lung histopathology, radiography, high-resolution computed tomography, and bronchio-alveolar lavage cytology are altered by Toxocara cati infection in cats and is independent of development of adult intestinal parasites. Vet Parasitol 2013;193:413–426.
16. Lacava G, Zini E, Marchesotti F, et al. Computed tomography, radiology and echocardiography in cats naturally infected with Aelurostrongylus abstrusus. J Feline Med Surg 2017;19:446–453.
17. Coia ME, Hammond G, Chan D, et al. Retrospective evaluation of thoracic computed tomography findings in dogs naturally infected by Angiostrongylus vasorum. Vet Radiol Ultrasound 2017;58:524–534.
18. Dennler M, Makara M, Kranjc A, et al. Thoracic computed tomography findings in dogs experimentally infected with Angiostrongylus vasorum. Vet Radiol Ultrasound 2011;52:289–294.
19. Fina C, Vignoli M, Terragni R, et al. Computed tomographic characteristics of eosinophilic pulmonary granulomatosis in five dogs. Vet Radiol Ultrasound 2014;55:16–22.
20. Mesquita L, Lam R, Lamb CR, et al. Computed tomographic findings in 15 dogs with eosinophilic bronchopneumopathy. Vet Radiol Ultrasound 2015;56:33–39.
21. Masseau I, Banuelos A, Dodam J, et al. Comparison of lung attenuation and heterogeneity between cats with experimentally induced allergic asthma, naturally occurring asthma and normal cats. Vet Radiol Ultrasound 2015;56:595–601.
22. Heikkilä HP, Lappalainen AK, Day MJ, et al. Clinical, bronchoscopic, histopathologic, diagnostic imaging, and arterial oxygenation findings in West Highland White Terriers with idiopathic pulmonary fibrosis. J Vet Intern Med 2011;25:433–439.
23. Marolf AJ, Gibbons DS, Podell BK, et al. Computed tomographic appearance of primary lung tumors in dogs. Vet Radiol Ultrasound 2011;52:168–172.
24. Aarsvold S, Reetz JA, Reichle JK, et al. Computed tomographic findings in 57 cats with primary pulmonary neoplasia. Vet Radiol Ultrasound 2015;56:272–277.
25. Franckenberg S, Kern F, Vogt M, et al. Fatal gunshot to a fox: the virtopsy approach in a forensic veterinary case. J Forensic Radiol Imaging 2015;3:72–75.
26. Hamano T, Terasawa F, Tachikawa Y, et al. Squamous cell carcinoma in a capybara (Hydrochoerus hydrochaeris). J Vet Med Sci 2014;76:1301–1304.
27. Lee K-J, Sasaki M, Miyauchi A, et al. Virtopsy in a red kangaroo with oral osteomyelitis. J Zoo Wildl Med 2011;42:128–130.
28. Brandão de Campos Fonseca Pinto AC, Rodrigues Massad MR, Massad Ribas L, et al. Complete cardiac and bronchial avulsion in a dog: post-mortem computed tomography and forensic necropsy analysis. J Forensic Radiol Imaging 2017;8:45–47.
29. Yamada K, Sato F, Horiuchi N, et al. Autopsy imaging for cardiac tamponade in a Thoroughbred foal. J Equine Sci 2016;27:115–118.
30. Hostettler FC, Wiener DJ, Welle MM, et al. Post mortem computed tomography and core needle biopsy in comparison to autopsy in eleven Bernese Mountain Dogs with histiocytic sarcoma. BMC Vet Res 2015;11:229.
31. Rutty GN, Morgan B, Germerott T, et al. Ventilated post-mortem computed tomography—historical review. J Forensic Radiol Imaging 2016;4:35–42.
32. Arthurs OJ, Guy A, Kiho L, et al. Ventilated postmortem computed tomography in children: feasibility and initial experience. Int J Legal Med 2015;129:1113–1120.
33. Germerott T, Preiss US, Ebert LC, et al. A new approach in virtopsy: postmortem ventilation in multislice computed tomography. Leg Med (Tokyo) 2010;12:276–279.
34. Robinson C, Biggs MJ, Amoroso J, et al. Post-mortem computed tomography ventilation; simulating breath holding. Int J Legal Med 2014;128:139–146.
35. Rutty GN, Biggs MJP, Brough A, et al. Ventilated post-mortem computed tomography through the use of a definitive airway. Int J Legal Med 2015;129:325–334.
36. Germerott T, Flach PM, Preiss US, et al. Postmortem ventilation: a new method for improved detection of pulmonary pathologies in forensic imaging. Leg Med (Tokyo) 2012;14:223–228.
37. Guarracino A, Lacitignola L, Auriemma E, et al. Which airway pressure should be applied during breath-hold in dogs undergoing thoracic computed tomography: breath-hold technique for thoracic CT in dogs. Vet Radiol Ultrasound 2016;57:475–481.
38. Hopper K, Haskins SC, Kass PH, et al. Indications, management, and outcome of long-term positive-pressure ventilation in dogs and cats: 148 cases (1990–2001). J Am Vet Med Assoc 2007;230:64–75.
39. Hagberg CA, Artime CA, Aziz MF. Hagberg and Benumof's airway management. 4th ed. Philadelphia: Elsevier, 2018.
40. Brooks JW. Postmortem changes in animal carcasses and estimation of the postmortem interval. Vet Pathol 2016;53:929–940.
41. Staffieri F, De Monte V, De Marzo C, et al. Alveolar recruiting maneuver in dogs under general anesthesia: effects on alveolar ventilation, gas exchange, and respiratory mechanics. Vet Res Commun 2010;34:S131–S134.
42. Di Bella C, Lacitignola L, Grasso S, et al. An alveolar recruitment maneuver followed by positive end-expiratory pressure improves lung function in healthy dogs undergoing laparoscopy. Vet Anaesth Analg 2018;45:618–629.
43. Santiago VR, Rzezinski AF, Nardelli LM, et al. Recruitment maneuver in experimental acute lung injury: the role of alveolar collapse and edema. Crit Care Med 2010;38:2207–2214.
44. Filograna L, Thali M. Post-mortem CT imaging of the lungs: pathological versus non-pathological findings. Radiol Med 2017;122:902–908.
45. Imber DA, Pirrone M, Zhang C, et al. Respiratory management of perioperative obese patients. Respir Care 2016;61:1681–1692.
46. Chanda A, Kwon JS, Wolff AJ, et al. Positive pressure for obesity hypoventilation syndrome. Pulm Med 2012;2012:568690.
