Abstract

Résumé

Case description

An 11-year-old 30-kg intact male mixed-breed dog was presented to the emergency service at Ospedale Veterinario Gregorio VII because of laborious breathing. Recent history included 3 d of decreased appetite and hyperthermia (39.2°C to 39.5°C).

On presentation, the dog was bright and alert but tachypneic (> 80 breaths/min) and with abdominal splinting; the mucous membranes were pink but tacky. The dog was slightly tachy-cardic (140 beats/min) with strong and normal femoral pulses, normal sinus rhythm, and normal heart sounds on auscultation. Rectal temperature was 39.2°C. A succussion splash and metallic tinkling sounds were audible and palpable over the left dorsal thoracic wall; severe pain was evoked on palpation of the cranial abdomen. Blood pressure was normal (140/90 mmHg).

An 18-G intravenous catheter was placed in the cephalic vein and a baseline venous measurement was evaluated while the dog was started on 75 mL/h of normosol-R solution (Baxter Viaflo; AIC Baxter, Rome, Italy) and methadone hydrochloride (Molteni & C.F.lli Alitti, Scandicci, Florence, Italy), 0.1 mg/kg body weight (BW), IM. Venous blood gas showed mild respiratory alkalosis, pH 7.48 [reference interval (RI): 7.35 to 7.46], pCO₂ 21.2 mmHg (RI: 30.8 to 42.8 mmHg), normal PCV of 40% and normal total protein (TP), 68 g/L (RI: 58 to 80 g/L). An arterial blood gas showed pCO₂ 27.3 mmHg (RI: 30.8 to 42.8 mmHg), pO₂ 47.9 mmHg (RI: 80.0 to 110.0 mmHg), sO2 82.3% and pO₂/FiO₂ ratio of 2.28.

Chest radiographs were consistent with pneumopericardium, pneumothorax, pleural effusion, and alveolar interstitial disease of the right caudal and accessory lung lobes (Figure 1). Abdominal radiographs showed loss of serosal detail.

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Figure 1

A — Right lateral view of the chest showing an elevated cardiac silhouette and pneumothorax (white arrowhead). Note the pleural fissures (white arrows), the alveolar interstitial pattern in the caudal and accessory lung lobes (white asterisks), the lack of peripheral vasculature; the pericardium is highlighted by free air within the pericardial sac (black arrows); B — Left lateral view of the chest showing abnormal density of the ventral thoracic area (black empty arrowhead), the elevated cardiac silhouette, pleural fissures (white arrows), the alveolar interstitial pattern in the caudal and accessory lung lobes (white asterisks), the pneumothorax (white empty arrowhead), and the lack of peripheral vasculature; the pericardium is highlighted by free air within the pericardial sac (black arrows). C — Ventrodorsal view of the chest showing the pneumopericardium (black arrows), the pneumothorax (white arrows), and consolidation of the caudal lung lobe (white asterisk).

Thoracentesis allowed us to retrieve 800 mL of air and 600 mL of hemorrhagic fluid; chest radiographs were repeated afterwards and showed persistence of the alveolar interstitial pattern in both the caudal and accessory lung lobe and persistence of pneumopericardium (Figure 2). Pericardiocentesis was not performed because the dog was not showing signs of cardiac tamponade. The dyspnea improved after thoracentesis.

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Figure 2

Right lateral view of the thorax after thoracentesis. Note the persistence of pleural effusion and pleural thickening, consolidation of the accessory and caudal lung lobes (white asterisks) and persistence of the pneumopericardium (black arrows).

Abdominal ultrasound showed marked enlargement and increased hyperechogenicity of the liver, hyperechogenicity of the cranial abdomen, and presence of peritoneal fluid. Abdominocentesis was performed and 200 mL of sero-hemorrhagic fluid were removed. The pleural and peritoneal fluids were submitted for cytological evaluation and preserved in transport media for bacterial culture.

Results of a complete blood (cell) count (CBC) showed mild anemia (Hct 36%; RI: 37% to 55%), marked leucocytosis, 33 600 cells/μL (RI: 6.0 to 17.0 × 10³ cells/μL) with mature neutrophilia, 26 208 cells/μL; (RI: 3.0 to 10.5 × 10³ cells/μL) and monocytosis, 6048 cells/μL (RI: 0.1 to 1.4 × 10³ cells/μL). Biochemistry panel showed increased alkaline phosphatase (ALP), 161 U/L (0 to 110 U/L), gamma-glutamyl transpeptidase (GGT), 9.6 U/L (RI: 0 to 6.5 U/L) and C-reactive protein, 35.1 mg/L (RI: 0.1 to 2.5 mg/L) and reduction of albumin, 24 g/L (RI: 25 to 40 g/L). Coagulation panel showed an increased prothrombin time, 9.4 s (RI: 5.8 to 8.8 s), activated partial thromboplastin time, 16.4 s (RI: 8.6 to 12.8 s) and D-dimers 1.67 μg/mL (RI: 0.01 to 0.33 μg/mL), decreased antithrombin III, 79% (RI: 90% to 165%) and fibrinogen, 4.3 μmol/L (RI: 4.4 to 8.5 μmol/L).

Cytology of the abdominal fluid was consistent with an aseptic exudate characterized by a total nucleated cell count of 8200 cells/μL, TP of 42 g/L; microscopy showed a hemorrhagic background with prevalence of non-degenerate neutrophils, rare small lymphocytes, and rare macrophages with foamy cytoplasm. Cytology of the pleural fluid was consistent with a septic exudate characterized by total nucleated cell count of 368 000/μL, TP of 42 g/L; microscopy showed a hemorrhagic background, prevalence of degenerate neutrophils, intracellular and extracellular bacteria (cocci, rods, and filamentous organisms), rare small lymphocytes, eosinophils, reactive mesothelial cells and macrophages with phagocytosis of erythrocytes and nucleated cells.

The dog was hospitalized but drainage chest tube placement was declined by the owner. The dog received 80 mL/h of normosol^®-R solution, methadone hydrochloride, 0.1 mg/kg BW, IM, q6h, ceftriaxone (Rocefin Fidia Farmaceutici, Abano Terme, Padua, Italy), 20 mg/kg BW, IV, q12h and low molecular weight heparin (Fragmin; Pfizer Italia, Rome, Italy), 100 U/kg BW, SQ, q24h. The dog remained stable and subsequent arterial blood gases showed normal saturation sO₂ 96.2% and 97%, normalization of the pO₂ 82.3 and 92.3 mmHg and improvement of the pO₂/FiO₂ ratio 3.92 and 4.40.

The day after, computed tomography (CT) was performed with slice width between 3 and 5 mm, and additional images of 1 to 3 mm thickness were acquired through the areas of interest. Computed tomograpy showed the presence of marked pneumopericardium, moderate pneumothorax, and pleural effusion with hypoventilated lung lobes on pilot scans (Figures 3A, B). A thoracentesis was performed and the dog hyperventilated to allow for increased pulmonary inflation and enhanced parenchymal visualization. Five minutes later, pericardiocentesis was also performed because of sudden decrease of systemic blood pressure and weak femoral pulses suggestive of cardiac tamponade. All parameters returned to normal after pericardiocentesis.

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Figure 3

Computed tomography findings. A — Transverse scan at T6 level shows severe pneumopericardium (black arrows), moderate pneumothorax (white arrow), and mild pleural effusion on the right side (black arrowhead). Peripheral air bronchograms are detectable in each lung lobe. B — Dorsal multi-planar reconstruction shows the pneumopericardium (black arrows). C — Transverse scan at the level of T7 after thoracentesis and inflation. Note the residual pneumopericardium (full white arrowhead) and right pneumothorax (empty white arrowhead), consolidation of the accessory and caudal lung lobes (white asterisks), and a peripheral lesion characterized by air content and thickened margins on the right side (white arrows) and a mineralized focus. D — Dorsal reconstruction. Note the air-filled structure (white arrow) and consolidation of the caudal apex of the right caudal lung lobe, the residual pneumothorax on the right side (empty white arrowhead), the minimal residual pneumopericardium (full white arrowhead) and consolidation of the accessory lung lobe (black asterisk).

After pericardiocentesis, subsequent CT scans of the thorax showed minimal residual pneumopericardium, mild residual pneumothorax and pleural effusion, enlarged size of the cranial mediastinal lymph nodes (1.8 cm), persistent consolidation of the accessory and right caudal lung lobes. On the lateral margin of the right caudal lung lobe, there was an air-filled structure (0.8 cm) surrounded by a thickened parenchymal wall with local pleural thickening (Figures 3C, 3D) and marginal air bronchograms at the basal periphery of each lung lobe. A CT of the abdomen showed moderate liver enlargement, increased size of the portal lymph nodes (1.7 cm), thickening and irregularity of the endoabdominal fat and mild abdominal effusion. After intravenous administration of non-ionic iodinate contrast [Omnipaque 350 (Iohexol); GE Healthcare, Milan, Italy], 400 mg I/kg BW no significant changes were detected.

One hour after recovery from anesthesia, the dog had an acute episode of loss of consciousness associated with horizontal nystagmus, bradycardia (60 beats/min) and bradypnea (10 breaths/min), weak femoral pulses and low blood pressure (70 mmHg). The dog regained consciousness after a few seconds and vital parameters returned to normal after a bolus of crystalloids (normosol-R 500 mL) and colloids (voluven; Fresenus Kabi Italia, Isola Della Scala, Italy, 300 mL); a convulsive crisis or a thromboembolic event was the most likely cause.

The owner declined exploratory thoracic surgery and drainage chest tube placement and bacterial cultures were not done because of financial restraints. The owner opted for medical management that consisted of supportive care, antibiotic regimen (amikacin; Lukadin S.F. Group, Roma, Italia), 5 mg/kg BW, q12h, low molecular weight heparin, 100 U/kg BW, q24h, pain medication based on clinical evaluation (methadone hydrochloride), 0.1 mg/kg BW and subsequent thoracentesis when necessary. Amikacin was chosen based on bacterial culture results of dogs treated for pyothorax at our hospital over the past 5 y. During the first 2 d of hospitalization the dog showed increase appetite, and normal arterial blood gases, normal vital parameters, but persistent abdominal pain. On day 2, chest radiographs showed the persistence of mild pleural effusion, the alveolar interstitial pattern of the accessory and both caudal lung lobes and the absence of pneumopericardium (Figure 4). The dog died suddenly on the third day but necropsy was not permitted.

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Figure 4

Right lateral view on the second day of hospitalization. Note the persistence of mild pleural effusion and thickening, consolidation of the accessory and caudal lung lobes, and the absence of pneumopericardium and pneumothorax.

Discussion

In small animals, 2 of 5 reported cases of pneumopericardium were spontaneous because they were secondary to bronchopulmonary diseases (1); however, neither of these 2 dogs had concurrent pneumothorax or pyothorax (8,10). The case reported here had imaging findings consistent with bronchopulmonary disease that was complicated by spontaneous pneumopericardium and pyopneumothorax.

Changes in CBC, biochemistry, and coagulation panel in the dog reported here were comparable to those of other studies published on pyothorax, pneumonia, and pneumopericardium such as an inflammatory leukogram, decreased albumin, and alterations in the coagulation panel resembling disseminated intravascular coagulation (1,3,10–13). Pleural effusion cytology was similar to results of other studies on pyothorax in dogs (11,13).

The cause of pneumopericardium, pneumothorax, and pyothorax herein was not determined because necropsy was not permitted. Based on clinical signs and imaging, the main differential diagnoses were a migrant foreign body or a bronchopulmonary infection of the accessory and caudal lung lobes (pneumonia versus ruptured abscess). The CT findings are similar to findings in dogs diagnosed with bronchopulmonary disease and migrant foreign body (14). Neoplasia was less likely to be a potential cause because CT features did not support this.

The dog was presented in the summer and a migrant foreign body was the first suspect; pyothorax or pneumothorax or both can be caused by a migrant foreign body. However, since necropsy was not allowed, a migrant foreign body remains a conjecture. Pain in the cranial abdomen, peritonitis, ascites, and enlarged sternal lymph nodes have also been reported in other cases of a migrant foreign body (14–18). The cause of the cranial abdominal pain and effusion herein could have been diffusion of the septic process from the thorax; an abdominal septic exudate was not completely ruled out because abdominal culture was not done. Other causes for the abdominal pain and peritonitis were not detected on abdominal ultrasound and CT.

The presence of a cavitary lesion on the right caudal lung lobe on CT and the persistence of consolidation of the accessory and caudal lung lobe on CT after inflation and on chest radiographs were consistent with bronchopulmonary disease and could have indicated pneumonia or a ruptured abscess of the accessory and/or of the right caudal lung lobe complicated by pyothorax and pneumothorax (10,11,13–15,17,19–21). As reported in humans, the most likely cause of pneumopericardium could have been migration of air through impaired air sac walls or pericardial infection by gas-forming bacteria (1–5).

To our knowledge, the concurrent presence of pyothorax and pneumothorax in small animals has been reported in only 2 retrospective studies on pyothorax and in 2 case reports. In the former studies rupture of the lung parenchyma secondary to abscess formation or pneumonia was presumed to be the cause of the pyopneumothorax, whereas in the latter pyopneumothorax was secondary to a migrant foreign body in 1 dog and to severe distemper pneumonia in the other dog (11,16,17,22). In a retrospective study on CT findings in dogs with migrant foreign bodies, it was not specified whether pyothorax and pneumothorax were coexisting (14). In small animals, pneumonia and lung abscess have been reported as a cause of pneumothorax or pyothorax (13,15). Pyothorax and pneumothorax are well-known complications of pneumonia and lung abscess especially in children; fewer cases are described in adults (23–25).

Spontaneous pneumopericardium is a rare complication in humans with pneumonia and lung abscess (1–5); only in 1 case was this associated with pyothorax (1). Spontaneous pneumopericardium was also described in 2 dogs with bronchopulmonary disease but none of these dogs had either pneumothorax or pyothorax (8,10).

In conclusion, based on clinical, imaging findings and the literature, the cause of pyopneumothorax in this dog was likely to be a migrant foreign body or a bronchopulmonary infectious disease (pneumonia or abscess). The mechanism by which spontaneous pneumopericardium developed in this dog is unknown but mechanisms proposed in humans such as direct extension of infectious processes of the lungs or by pericardial infection with gas-forming bacteria are possible. CVJ

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