In the last 20 years, the diagnosis of pancreatitis has become more frequent as a result of improved diagnostic modalities such as abdominal ultrasound examination, advanced imaging, and immunoassays for the measurement of pancreatic lipase. Our aim is to provide a state-of-the-art overview of the clinical diagnosis of acute pancreatitis (AP) in dogs with a particular focus on pancreatic lipase assay validation and clinical performance, in addition to advanced imaging modalities. We also discuss the potential indications for cytology and histopathology in dogs with suspected AP.

Background: The sensitivity, specificity, and agreement of 4 diagnostic assays (SNAP canine pancreatic lipase (cPL), specific cPL (Spec cPL), VetScan cPL Rapid Test, and Precision PSL) for pancreatitis in dogs have not been directly compared. Hypothesis/Objectives: To determine the level of agreement among each of the 4 assays and a clinical suspicion score, level of agreement among the assays, and sensitivity and specificity of each assay in a clinically relevant patient group. Animals: Fifty client-owned dogs with clinical signs of gastrointestinal disease. Methods: Prospective study. History, physical examination, complete blood count, serum biochemistry, abdominal ultrasound examination, and the 4 diagnostic assays for pancreatitis were performed. Intraclass correlation coefficients (ICC) were used to determine the level of agreement between each assay and a clinical suspicion score determined by a panel of 5 board-certified veterinary internists. Results: The ICC between the clinical suspicion score and the 4 assays were SNAP cPL, 0.61; Spec cPL, 0.68; VetScan cPL Rapid Test, 0.68; and Precision PSL, 0.60. The sensitivities of the assays ranged from 73.9 to 100.0%, whereas the specificities were SNAP cPL, 71.1–77.8%; Spec cPL, 74.1–81.1%; VetScan cPL Rapid Test, 76.9–83.8%; and Precision PSL, 64.0–74.3%. Conclusions and Clinical Importance: A good to excellent level of agreement was demonstrated among the 4 assays. The previously unreported sensitivity and specificity of the VetScan cPL Rapid Test were 73.9–83.3% and 76.9–83.8%, respectively. Results of any of the 4 diagnostic assays alone, in the absence of supporting clinical findings, are insufficient to establish a diagnosis of clinical pancreatitis in dogs.

Lipases are water-soluble enzymes that hydrolyze water-insoluble lipid molecules, such as triglycerides, phospholipids, and galactolipids. They are ubiquitous in nature and are present in humans, animals, insects, plants, fungi, and microorganisms. While we commonly consider pancreatic lipase, this review provides an overview of several lipases that are important for the digestion and metabolism of lipids in veterinary species. All of these enzymes have specific functions but share a common α/β-hydrolase fold and a catalytic triad where substrate hydrolysis occurs. The pancreatic lipase gene family is one of the best characterized lipase gene families and consists of 7 mammalian subfamilies: pancreatic lipase, pancreatic lipase related proteins 1 and 2, hepatic lipase, lipoprotein lipase, endothelial lipase, and phosphatidylserine phospholipase A1. Other mammalian lipases that play integral roles in lipid digestion include carboxyl ester lipase and gastric lipase. Although most enzymes have preferred substrate specificity, much overlap occurs across the plethora of lipases because of the similarities in their structures. This has major implications for the development and clinical utilization of diagnostic assays. These implications are further explored in our companion Currents in One Health article by Lim et al in the August 2022 issue of the Journal of American Veterinary Medical Association, which focuses on pancreatic lipase assays for the diagnosis of pancreatitis.

Background A clinical diagnosis (CDx) of pancreatitis includes evaluation of clinical signs, abdominal ultrasound (AUS), and pancreatic lipase. However, practitioners are using AUS to diagnose pancreatitis and are using AUS severity to guide decisions. The validity of this is unknown. Objectives To determine whether (1) there is a correlation between AUS, specific canine pancreatic lipase (Spec cPL) assay, and CDx; (2) individual AUS abnormalities correlate more closely with CDx than others; (3) AUS severity mirrors clinical severity indices; (4) changes in AUS can be used as a marker for changes in Spec cPL or CDx; and (5) the sensitivity and specificity of AUS for pancreatitis. Animals One hundred fifty‐seven dogs. Methods In this retrospective case study, inclusion criteria were signs of gastrointestinal, pancreatic disease, or both, in addition to having a Spec cPL and AUS performed within 30 hours. Information extracted from the records included bloodwork, Spec cPL, AUS images/clips, and severity of ultrasonographic findings. Results AUS was weakly correlated with Spec cPL (r_s = .0178, P = .03) and moderately correlated with CDx (r_s = .379, P = <.001). Pancreatic size (r_s = .285, P = <.001), echogenicity (r_s = .365, P = <.001), and mesenteric echogenicity (r_s = .343, P = <.001) were correlated with CDx. Change in AUS was not correlated with Spec cPL or CDx changes. When pancreatic enlargement, echogenicity, or altered mesenteric echogenicity were required for a diagnosis, the sensitivity and specificity were 89% (95% confidence interval [CI] 71.8, 97.7) and 43% (95% CI 34.0, 51.6). When all 3 criteria were required, the sensitivity and specificity were 43% (95% CI 24.5, 62.8) and 92% (95% CI 85.3, 95.7). Conclusions AUS should not be used in isolation to diagnose pancreatitis and is a poor indicator of severity.

While most cases of pancreatitis in dogs are thought to be idiopathic, potential risk factors are identified. In this article we provide a state-of-the-art overview of suspected risk factors for pancreatitis in dogs, allowing for improved awareness and detection of potential dog-specific risk factors, which might guide the development of disease prevention strategies. Additionally, we review important advances in our understanding of the pathophysiology of pancreatitis and potential areas for therapeutic manipulation based thereof. The outcome of pathophysiologic mechanisms and the development of clinical disease is dependent on the balance between stressors and protective mechanisms, which can be evaluated using the critical threshold theory.

Background: Limited recent data exists regarding discospondylitis in dogs. Hypothesis/Objectives: (i) Describe the signalment, clinical and imaging findings, etiologic agents, treatment, and outcome of dogs with discospondylitis, (ii) determine diagnostic agreement between radiographs, CT, and MRI with regard to the presence of discospondylitis and its location, and (iii) determine risk factors for relapse and progressive neurological deterioration. Animals: Three hundred eighty-six dogs. Methods: Multi-institutional retrospective study. Data extracted from medical records were: signalment, clinical and examination findings, diagnostic results, treatments, complications, and outcome. Potential risk factors were recorded. Breed distribution was compared to a control group. Agreement between imaging modalities was assessed via Cohen's kappa statistic. Other analyses were performed on categorical data, using cross tabulations with chi-squared and Fisher's exact tests. Results: Male dogs were overrepresented (236/386 dogs). L7-S1 (97/386 dogs) was the most common site. Staphylococcus species (23/38 positive blood cultures) were prevalent. There was a fair agreement (κ = 0.22) between radiographs and CT, but a poor agreement (κ = 0.05) between radiographs and MRI with regard to evidence of discospondylitis. There was good agreement between imaging modalities regarding location of disease. Trauma was associated with an increased risk of relapse (P = .01, OR: 9.0, 95% CI: 2.2-37.0). Prior steroid therapy was associated with an increased risk of progressive neurological dysfunction (P = .04, OR: 4.7, 95% CI: 1.2-18.6). Conclusions and Clinical Importance: Radiograph and MRI results could be discrepant in dogs with discospondylitis. Prior trauma and corticosteroids could be associated with relapse and progressive neurological dysfunction, respectively.