Septic Pericarditis, Aortic Endarteritis, and Osteomyelitis in a Dog
A 7-year-old, female spayed rottweiler was referred with a history of an acute onset of collapse attributable to cardiac tamponade. Thoracic radiographs revealed an enlarged cardiac silhouette compatible with pericardial effusion, sternal osteomyelitis, and an unusual mineralized lesion determined later to be within the aortic wall. The pericardial effusion was a septic exudate secondary to infection with Staphylococcus species and hemorrhage into the pericardium through a mineralized aortic lesion. The case demonstrates the importance of complete evaluation of thoracic radiographs in a patient with cardiac disease and the potential value of cytopathologicalevaluation of pericardial fluid.
Case Report
A 7-year-old, female spayed rottweiler was referred with a history of an acute onset of collapse following a 1-day history of lethargy. The dog had been previously normal except for a 1-month history of mild, bilateral, mucopurulent ocular discharge that was responsive to topical antibiotic therapy. The dog was well vaccinated, on heartworm prophylaxis, and had no history of trauma, surgery, or signs of systemic illness.
On physical examination, the dog was in good body condition but was recumbent and depressed. Temperature (38.5°C [101.3°F]) was within reference ranges, but heart rate (160 beats per minute) and respiratory rate (48 breaths per minute) were increased. Femoral pulse quality was poor, jugular vein distention was present, and the mucous membranes were pale with slow capillary refill time. Systolic arterial blood pressure by Doppler was 70 to 80 mm Hg. Thoracic auscultation revealed muffled heart sounds with normal breath sounds. The eyes were dull and sunken with no apparent discharge. Physical examination was suggestive of pericardial disease and associated cardiogenic shock.
Blood was collected for a minimum database prior to administration of a bolus of lactated Ringer’s solution [50 mL/kg body weight, intravenously (IV)]. A complete blood count (CBC) revealed neutrophilic leukocytosis with a left shift and marked toxicity (leukocytes, 42.9 × 103/μL; reference range, 6.0 to 17.0 × 103/μL; mature neutrophils, 22.0 × 103/μL; reference range, 3.0 to 11.5 × 103/μL; band neutrophils, 14.7 × 103/μL; reference range, 0.0 to 0.3 × 103/μL). Mild nonregenerative anemia (packed cell volume, 35%; reference range, 37% to 55%; red blood cell count, 5.2 × 106/μL; reference range, 5.5 to 8.5 × 106/μL; hemoglobin, 11.4 g/dL; reference range, 12.0 to 18.0 g/dL; mean corpuscular volume, 67 fL; reference range, 60 to 77 fL; mean corpuscular hemoglobin concentration, 32.8 g/dL; reference range, 30.0 to 36.9 g/dL) and thrombocytopenia (platelets, 177 × 103/μL; reference range, 200 to 500 × 103/μL) were also noted. Serum biochemical profile revealed an elevated blood urea nitrogen (32 mg/dL; reference range, 8 to 29 mg/dL), cholesterol (365 mg/dL; reference range, 120 to 247 mg/dL), globulin (5.0 g/dL; reference range, 1.7 to 3.8 g/dL), and alkaline phosphatase (ALP, 1608 IU/L; reference range, 24 to 147 IU/L). Urinalysis obtained after IV fluids revealed marked pyuria, hematuria, and proteinuria with a urine specific gravity of 1.025. Unfortunately, results of the urinalysis were not available until after the dog had been euthanized, and a sterile sample of urine was not available for culture.
Thoracic radiographs showed generalized cardiomegaly compatible with the suspected pericardial effusion [Figures 1A, 1B]. There were several irregular linear mineralized opacities in the plane of the cranial lung lobes and cranial waist of the heart of uncertain etiology. Additional thoracic radiographic changes included osteolytic changes in the fourth and fifth sternebrae and osteolysis of the vertebral end plates at the seventh to eighth thoracic (T7–T8) vertebrae and at T8 to the ninth thoracic (T9) vertebra with adjacent bony sclerosis.
Echocardiography revealed moderate pericardial effusion with flocculent debris. The right and left ventricles were compressed and underfilled, compatible with severe cardiac tamponade. Electrocardiography revealed sinus tachycardia with normal amplitude QRS complexes without electrical alternans.
The neutrophilia, hyperglobulinemia, bony lesions, and flocculent debris within the pericardial fluid were suggestive of a systemic inflammatory or infectious cause of pericarditis. Although percutaneous pericardiocentesis with cytopathological analysis of the fluid was offered as a therapeutic option, pericardectomy was considered preferable following patient stabilization with fluid therapy. Pericardectomy provides relief of the cardiac tamponade and permits collection of samples of the fluid and tissues for definitive diagnosis, with minimal contamination of the pleural space with any potential infectious agents. The owners were not interested in medical or surgical therapy and elected to euthanize the dog, but they authorized necropsy.
A sample of the pericardial fluid was collected aseptically following euthanasia. A direct smear of the fluid revealed high cellularity with many nucleated cells randomly arranged in a background of granular protein, lysed cells, and few erythrocytes. The nucleated cells consisted of 99% slightly to markedly degenerate neutrophils, with the remainder being markedly reactive mesothelial cells. Rarely seen within the cytoplasm of the neutrophils was a small population of bacterial cocci. The bacteria were generally seen as pairs and rarely as singlets. Aerobic culture of the pericardial fluid yielded moderate growth of a coagulase-positive Staphylococcus species. Anaerobic culture yielded no growth.
Necropsy Findings
In addition to moderate pericardial effusion, approximately 30 mL of clotted blood was found in the pericardial sac. A curvilinear mineralized lesion was present in the ascending and descending aorta and proximal brachycephalic trunk [Figure 2]. A 5-mm, linear perforation extended from the aortic lumen in the mineralized portion of the ascending aorta through the aortic wall and pericardial fat into the pericardium, and it was identified as the likely source of the intrapericardial hemorrhage [Figures 3A, 3B].
Multiple lytic lesions were identified in the intersternebral cartilage of the fourth and fifth sternebrae [Figure 4]. Collapse of the fifth thoracic (T5) to T8 intervertebral disk spaces was noted, but the radiographically apparent osteolytic spinal lesions could not be identified. Extensive infarction of both kidneys was present [Figure 5]. Culture of the kidney and liver revealed growth of coagulase-positive Staphylococcus; the sternal lesion was inadvertently placed in formalin prior to collection of material for culture.
Microscopic examination of the aortic lesion revealed chronic, focal, septic, necrotizing endarteritis, with medial degeneration and calcification with multifocal colonies of Gram-positive cocci [Figure 6]. Subacute, diffuse, marked, fibrinous, suppurative pericarditis and epicarditis were also present. Examination of the intersternebral cartilage of the fourth and fifth sternebrae revealed chronic, severe, suppurative, septic osteomyelitis with marked to severe chondroid degeneration and multifocal colonies of Gram-positive cocci. Chronic interstitial nephritis with moderate fibrosis and locally extensive triangular areas of fibrosis with associated cortical depression confirmed the presence of renal infarctions. Mild, subacute, passive hepatic congestion was present. The spinal column was histopathologically examined in the T5 to T8 region and revealed no evidence of suppurative inflammation or positive Gram staining. The spinal lesions were characterized by chondroid dysplasia, degeneration and fibrosis with collapse of the disk space, and dorsal protrusion of the dorsal annulus fibrosis. Mild fibrosis and granulation tissue changes were noted to cross the vertebral end plate.
Discussion
Pericardial effusion is most commonly due to neoplasia or idiopathic pericarditis. Infectious pericarditis of the dog is relatively rare.12 Reported cases have been associated with a predisposing underlying condition, such as foreign-body or bite-wound penetration, or as a local manifestation of a systemic inflammatory/infectious disease.3–6 Etiological agents associated with infectious pericarditis include fungal (Coccidioides), bacterial (Actinomyces, Bacteriodes, Pasteurella, Pseudomonas, Staphylococcus, Streptococcus spp.), and parasitic (aberrant dirofilariasis, leishmaniasis) infections.7–13 Purulent pericarditis is widely recognized in humans and cattle and is inducible as a sequelae to septicemia in birds.14
Although the multifocal isolation of coagulase-positive Staphylococcal organisms suggests septicemia was present, a definitive source of bacterial contamination was not identified. The owner denied any history of trauma, but unrecognized penetrating trauma to the sternum or foreign body migration through this site could not be ruled out. The sternal osteomyelitis lesion may have represented a source or a consequence of septicemia, and the cause of this lesion remains undetermined. The increased ALP and cholesterol were potentially suggestive of hyperadrenocorticism, which could also cause dystrophic calcification and immunosuppression, predisposing the dog to septicemia, but the history and necropsy findings were not compatible with this disease. Elevation of ALP is a common, nonspecific finding in sepsis and may be associated with the negative effects of bacterial toxins on the hepatic parenchyma, with resultant partial intrahepatic cholestasis.15 However, hepatic histopathology in this dog revealed marked, diffuse, sinusoidal and venous congestion that was likely secondary to cardiac tamponade. Hypothyroidism could also cause hypercholesterolemia and appears to be associated with increased risk of atherosclerosis that could have contributed to aortic disruption; but this was not histopathologically evident. The aortic calcification in the dog of this study was most likely dystrophic calcification secondary to endarteritis. No apparent aortic valvular or subvalvular lesions were identified as a cause of turbulence in the aorta.
The pericardial effusion was likely present for several days or weeks prior to presentation, as was evidenced by the hypertrophied pericardium. The aortic perforation and associated hemorrhage likely caused the dog’s acute deterioration secondary to cardiac tamponade. The outcome with surgical treatment and drainage of infectious pericardial effusion can be favorable.4 However, in this case, the presence of the erosive aortic mineralized lesion would have likely complicated recovery and could have caused sudden death. Sternal osteomyelitis is also difficult to eradicate medically, and the dog may have later required partial sternectomy.16
The necropsy and histopathological findings did not support the antemortem suspicion of diskospondylitis. The T5 to T8 spinal segments were examined histologically and Gram stained, and no evidence of diskospondylitis was apparent. Degeneration and fibrosis with collapse of the disk spaces and dorsal protrusion of the dorsal annulus fibrosis were noted in these segments, and Schmorl’s nodules (i.e., herniations of intervertebral disk material into the vertebral bodies) may have been the cause of the observed radiographic lesions.17
Conclusion
Although uncommon, infectious pericarditis can be readily diagnosed by cytopathological evaluation of pericardial fluid, and limited cases have been reported to be associated with a favorable outcome following appropriate surgical and medical intervention. A favorable outcome would not have been expected in this case, given the severity of concurrent disease. Osteolytic lesions and dystrophic mineralization may be identified on routine thoracic radiographs, emphasizing the importance of complete systematic evaluation of radiographs. Routine laboratory evaluation and diagnostic investigation of any abnormalities noted may also provide valuable insight into the systemic condition of a dog with pericardial disease prior to implementation of a definitive therapeutic plan.
Citation: Journal of the American Animal Hospital Association 39, 6; 10.5326/0390528
Citation: Journal of the American Animal Hospital Association 39, 6; 10.5326/0390528
Citation: Journal of the American Animal Hospital Association 39, 6; 10.5326/0390528
Citation: Journal of the American Animal Hospital Association 39, 6; 10.5326/0390528
Citation: Journal of the American Animal Hospital Association 39, 6; 10.5326/0390528
Citation: Journal of the American Animal Hospital Association 39, 6; 10.5326/0390528
(1A) Lateral and (1B) ventrodorsal thoracic radiographs of a rottweiler with evidence of cardiogenic shock. Note the generalized cardiomegaly, osteolytic lesions in the sternum and spine (thin white arrows), and a mineralized opacity overlying the cranial cardiac silhouette (wide white arrow).
Necropsy photographs of the heart from the dog in Figures 1 and 2, after reflection of the pericardial sac. (A) Hemorrhage was noted within the pericardial sac, with clotted blood overlying the aorta at the site of aortic penetration (arrowheads). RA=right atrium; RVOT=right ventricular outflow tract. (B) View from within the aortic lumen reveals an irregular, mineralized lesion penetrating the aortic wall (arrow) with direct communication to the pericardial sac. AAo=ascending aorta; BT=brachiocephalic trunk; DAo=descending aorta.
Photomicrograph of the lesion in the aortic wall, showing numerous cocci admixed with necrotic cellular debris, crystals of hematoidin, and scattered erythrocytes (Hematoxylin and eosin stain, 1000×; bar=20 μm).
Contributor Notes
