Pathology in Practice.

In collaboration with the American College of Veterinary Pathologists.

Ultrasonographic features and prevalence of presumed gastric wall edema in dogs with hypoalbuminemia.

BACKGROUND: Ultrasonographic features of gastric wall edema have not been reported in dogs with hypoalbuminemia. OBJECTIVES: To describe the prevalence and ultrasonographic features of gastric wall thickening in dogs with hypoalbuminemia and analyze correlation with serum albumin concentrations. ANIMALS: Forty-two dogs with abdominal ultrasound and diagnosis of hypoalbuminemia (<2.3 g/dL). METHODS: Retrospective search in the medical records from 2018 to 2019 was performed. Ultrasound studies were reviewed and >5 mm were considered gastric wall thickening. The gastric wall changes such as thickness, layering appearance, echogenicity, echotexture, distribution of lesions, and presence of peritoneal effusion were recorded. Serial ultrasonographic examination and histopathological findings were recorded if available. Mean serum albumin concentration of dogs with and without gastric wall thickening was compared. RESULTS: Prevalence of gastric wall thickening in dogs with hypoalbuminemia was 21.4% (95% confidence intervals 7.4-35.4%). Mean gastric wall thickness was 10.0 ± 2.0 mm. Preserved mucosal layer and thickening of submucosal layer were observed in all 9 dogs. Five dogs had 3-layer appearance in thickened submucosal layer. Diffuse wall thickening was observed in 6 dogs. All 9 dogs had peritoneal effusion. Subsequent changes of gastric wall thickening were observed in 3 dogs (range 4-70 days). Gastric wall edema was confirmed histopathologically in 2 dogs via necropsy. There was no correlation between serum albumin concentration of the dogs and gastric wall thickness. CONCLUSIONS AND CLINICAL IMPORTANCE: Findings indicated that gastric wall edema is a common finding in dogs with hypoalbuminemia. However, serum albumin concentrations did not correlate with the gastric wall thickness.

Benign Duodenal Stricture Treated with Surgical Correction and Dietary Therapy in a Golden Retriever.

A benign duodenal stricture is a well-documented condition of humans that has not been characterized in dogs. In this case report, the clinical, radiographic, ultrasonographic, endoscopic, surgical, and histopathologic findings of a single benign duodenal stricture in a Golden Retriever are reported. Definitive diagnosis was made possible with the utilization of esophagogastroduodenoscopy (EGD). Surgical correction of the stricture, paired with dietary therapy that utilized a highly digestible diet, resolved the clinical signs in the case reported. Several inciting causes were identified as possible drivers of stricture formation, including nonsteroidal anti-inflammatory drug (NSAID) administration, mucosal ulceration, traumatic injury, or inflammatory intestinal disease. A benign duodenal stricture should be considered an infrequent cause of intermittent, chronic gastrointestinal signs that may have a favorable outcome via surgical correction and dietary management.

Ultrasonographic features of presumed gastric wall edema in 14 dogs with pancreatitis.

BACKGROUND: Gastric wall edema has not been reported as a complication of acute pancreatitis in dogs. OBJECTIVE: To describe the ultrasonographic features of gastric wall thickening in dogs with acute pancreatitis. ANIMALS: Fourteen dogs with ultrasonographic evidence and clinical diagnosis of acute pancreatitis, with ultrasonographic evidence of increased gastric wall thickness (>5 mm). METHODS: A retrospective search in the medical records from 2014 to 2016 was performed to identify dogs that had ultrasonographic evidence of acute pancreatitis, that had increased thickness of the gastric wall and that were diagnosed with acute pancreatitis clinically. The gastric wall changes such as thickness, layering appearance, echogenicity, distribution of lesions, and perigastric changes were recorded. Serial ultrasonographic examination and histopathological findings were recorded if available. RESULTS: Mean gastric wall thickness was 9.9 ± 4.0 mm (SD). A complete loss of wall layering was observed in 2 dogs. Thickening of the submucosal layer was observed in 12 dogs, and 5 of them had concurrent muscularis layer thickening. The echogenicity of thickened submucosal layer was intermediate hyperechoic. Lacy appearances were present within the thickened submucosal layer in 7 dogs and in the muscularis layer of 1 dog. Thickening was focal in 12 dogs and adjacent to the diseased pancreas. Subsequent resolution of gastric wall thickening was observed in 3 dogs (range 3-28 days) via follow-up ultrasound. One dog underwent necropsy, and gastric wall edema was confirmed histopathologically. CONCLUSIONS AND CLINICAL IMPORTANCE: Findings indicated that gastric wall thickening presumably because of edema could be a complication of acute pancreatitis.

Association of fecal calprotectin concentrations with disease severity, response to treatment, and other biomarkers in dogs with chronic inflammatory enteropathies.

BACKGROUND: Calprotectin is a marker of inflammation, but its clinical utility in dogs with chronic inflammatory enteropathies (CIE) is unknown. OBJECTIVE: Evaluation of fecal calprotectin in dogs with biopsy-confirmed CIE. ANIMALS: 127 dogs. METHODS: Prospective case-control study. Dogs were assigned a canine chronic enteropathy clinical activity index (CCECAI) score, and histologic lesions severity was assessed. Fecal calprotectin, fecal S100A12, and serum C-reactive protein (CRP) were measured. Food- or antibiotic-responsive cases (FRE/ARE, n = 13) were distinguished from steroid-/immunosuppressant-responsive or -refractory cases (SRE/IRE, n = 20). Clinical response to treatment in SRE/IRE dogs was classified as complete remission (CR), partial response (PR), or no response (NR). RESULTS: Fecal calprotectin correlated with CCECAI (ρ = 0.27, P = .0065) and fecal S100A12 (ρ = 0.90, P < .0001), some inflammatory criteria, and cumulative inflammation scores, but not serum CRP (ρ = 0.16, P = .12). Dogs with SRE/IRE had higher fecal calprotectin concentrations (median: 2.0 µg/g) than FRE/ARE dogs (median: 1.4 µg/g), and within the SRE/IRE group, dogs with PR/NR had higher fecal calprotectin (median: 37.0 µg/g) than dogs with CR (median: 1.6 µg/g). However, both differences did not reach statistical significance (both P = .10). A fecal calprotectin ≥15.2 µg/g separated both groups with 80% sensitivity (95% confidence interval [95%CI]: 28%-100%) and 75% specificity (95%CI: 43%-95%). CONCLUSIONS AND CLINICAL IMPORTANCE: Fecal calprotectin could be a useful surrogate marker of disease severity in dogs with CIE, but larger longitudinal studies are needed to evaluate its utility in predicting the response to treatment.

Effect of gastric acid-suppressive therapy and biological variation of serum gastrin concentrations in dogs with chronic enteropathies.

BACKGROUND: Serum gastrin concentration can help diagnose gastrinomas in dogs if >3-10× the upper reference limit (URL), but antisecretory therapy and other conditions can also cause hypergastrinemia. Effects of antisecretory therapy (famotidine or ranitidine, omeprazole) on serum gastrin concentration in dogs with chronic enteropathy (CE) and its biological variation (BV) are unknown. Aim of the study was to evaluate serum gastrin in acid-suppressant-treated or -naïve CE dogs; test the association between serum gastrin and histopathologic findings in acid-suppressant-naïve CE dogs; and evaluate the BV of serum gastrin in dogs not receiving any gastric acid suppressive therapy. Samples from 231 dogs were used and serum gastrin was measured by chemiluminescence assay. Gastric and duodenal histologic lesions were evaluated and graded. BV of serum gastrin was evaluated in serial samples. RESULTS: Serum gastrin concentrations were significantly higher in acid-suppressant-treated than acid-suppressant-naïve dogs (P = 0.0245), with significantly higher concentrations in proton pump inhibitor (PPI)- than H2-antihistamine-treated patients (P = 0.0053). More PPI- than H2-antihistamine-treated dogs had gastrin concentrations above URL (P = 0.0205), but not >3× nor >10× the URL. Serum gastrin concentrations correlated with the severity of gastric antral epithelial injury (P = 0.0069) but not with any other lesions or the presence/numbers of spiral bacteria in gastric biopsies. Intra- and inter-individual BV were 43.4 and 21.6%, respectively, in acid-suppressant-naïve dogs, with a reciprocal individuality index of 0.49 and a critical difference of ≥29.5 ng/L. CONCLUSIONS: Antisecretory (particularly PPI) treatment leads to hypergastrinemia in CE dogs, but the concentrations seen in this study are unlikely to compromise a diagnosis of gastrinoma. Use of a population-based URL for canine serum gastrin and a URL of ≤27.8 ng/L are appropriate.

Retrospective evaluation of the impact of early enteral nutrition on clinical outcomes in dogs with pancreatitis: 34 cases (2010-2013).

OBJECTIVE: To evaluate the effect of early enteral nutritional therapy on time to return to voluntary intake, maximum food consumption, incidence of gastrointestinal intolerance (GI), and total hospitalization time for dogs with acute pancreatitis. DESIGN AND SETTING: Retrospective analysis of dogs with pancreatitis at a veterinary teaching hospital between 2010 and 2013. ANIMALS: Thirty-four client-owned dogs diagnosed with acute or acute-on-chronic pancreatitis. PROCEDURES AND INTERVENTIONS: Medical records of dogs evaluated for inappetence, anorexia, and GI for which a diagnosis of pancreatitis was recorded were reviewed. The time to initiation of food offerings since hospitalization were recorded in addition to signalment, historical medical conditions, chief complaint, physical examination findings, diagnostic results, treatments provided, timing of food offering (within 48 h of hospitalization, early feeding group (EFG) versus delayed feeding group (DFG), diet therapy (low fat versus high fat), caloric intake (% resting energy requirement), incidence of GI (%), and length of hospitalization (LOH) (days). A Clinical Severity Index Score (CSIS) was determined for each patient. MEASUREMENTS AND MAIN RESULTS: Dogs in the EFG demonstrated a decreased time to return of voluntary intake (2.1 days, EFG versus 2.7 days, DFG; P = 0.05) and time (days) to maximum intake (3, EFG versus 3.4 DFG) as compared to the DFG dogs. The DFG exhibited more GI versus EFG irrespective of CSIS grouping (60% versus 26%, P = 0.04). A CSIS ≥ 7 was associated with prolonged LOH (P = 0.004); however, time to initiation of feeding and diet selection did not impact LOH (P = 0.8). CONCLUSIONS AND CLINICAL RELEVANCE: Results of the study suggested that feeding within 48 hours of hospitalization for canine pancreatitis has a positive impact on return to voluntary intake and decreases the frequency of GI in these patients, independent of CSIS. The traditional protocol of withholding food during hospitalization may not be necessary nor yield the most benefit for patient recovery; subsequently early enteral refeeding should be considered.

Serum and fecal canine α1-proteinase inhibitor concentrations reflect the severity of intestinal crypt abscesses and/or lacteal dilation in dogs.

Gastrointestinal (GI) protein loss, due to lymphangiectasia or chronic inflammation, can be challenging to diagnose. This study evaluated the diagnostic accuracy of serum and fecal canine α1-proteinase inhibitor (cα1PI) concentrations to detect crypt abscesses and/or lacteal dilation in dogs. Serum and fecal cα1PI concentrations were measured in 120 dogs undergoing GI tissue biopsies, and were compared between dogs with and without crypt abscesses/lacteal dilation. Sensitivity and specificity were calculated for dichotomous outcomes. Serial serum cα1PI concentrations were also evaluated in 12 healthy corticosteroid-treated dogs. Serum cα1PI and albumin concentrations were significantly lower in dogs with crypt abscesses and/or lacteal dilation than in those without (both P <0.001), and more severe lesions were associated with lower serum cα1PI concentrations, higher 3 days-mean fecal cα1PI concentrations, and lower serum/fecal cα1PI ratios. Serum and fecal cα1PI, and their ratios, distinguished dogs with moderate or severe GI crypt abscesses/lacteal dilation from dogs with only mild or none such lesions with moderate sensitivity (56-92%) and specificity (67-81%). Serum cα1PI concentrations increased during corticosteroid administration. We conclude that serum and fecal α1PI concentrations reflect the severity of intestinal crypt abscesses/lacteal dilation in dogs. Due to its specificity for the GI tract, measurement of fecal cα1PI appears to be superior to serum cα1PI for diagnosing GI protein loss in dogs. In addition, the serum/fecal cα1PI ratio has an improved accuracy in hypoalbuminemic dogs, but serum cα1PI concentrations should be carefully interpreted in corticosteroid-treated dogs.

Fecal and urinary N-methylhistamine concentrations in dogs with chronic gastrointestinal disease.

Due to their ability to release inflammatory mediators, such as histamine, mast cells are potentially important in gastrointestinal disease. The purpose of this study was to measure N-methylhistamine (NMH), a histamine metabolite, in fecal and urine samples from dogs with chronic gastrointestinal disease. Fecal and urinary NMH concentrations were compared between dogs with chronic gastrointestinal disease and control dogs, and/or to control ranges. Correlation between fecal and urinary NMH concentrations, serum C-reactive protein (CRP) concentration, the clinical disease activity index (CCECAI), and gastrointestinal mucosal mast cell numbers (where available) in dogs with gastrointestinal disease was evaluated. Seven of 16 dogs with gastrointestinal disease had increased urinary or fecal NMH concentrations, but there was no correlation between NMH concentrations and the CCECAI or mucosal mast cells numbers. Urinary NMH concentrations were positively associated with histological grading and serum CRP concentrations. The lack of correlation between NMH concentrations and the CCECAI suggests that NMH may not be a good marker for clinical disease activity in dogs as determined by the CCECAI. Based on their association with severity of intestinal mucosal inflammation, urinary NMH concentrations may potentially have clinical utility as a marker of intestinal inflammation in certain groups of dogs with chronic gastrointestinal disease, but future studies in a larger number of dogs are necessary to further characterize the role of mast cell-mediated inflammation in dogs with chronic gastrointestinal disease.

In vitro effects of lipid emulsion on platelet function and thromboelastography in canine blood samples.

OBJECTIVE: To determine whether soybean oil emulsion has an in vitro effect on platelet aggregation and thromboelastography in blood samples obtained from healthy dogs. ANIMALS: 12 healthy adult dogs. PROCEDURES: Blood samples were collected from each dog into tubes containing EDTA, hirudin, or sodium citrate for a CBC, collagen- and ADP-induced impedance aggregometry, or thromboelastography, respectively. Whole blood platelet aggregation, determined with ADP or collagen agonists, was measured in blood samples containing hirudin and final lipid concentrations of 0, 1, 10, and 30 mg/mL. The thromboelastographic variables R (reaction time), K (clotting time), α angle, and maximum amplitude were evaluated in blood samples containing sodium citrate and final lipid concentrations equivalent to those used for assessment of platelet aggregation. RESULTS: Median maximum ADP- and collagen-induced platelet aggregation in blood samples containing 1, 10, or 30 mg of lipid/mL did not differ significantly from the value for the respective lipid-free blood sample. Maximum amplitude determined via thromboelastography was significantly reduced in blood samples containing 10 and 30 mg of lipid/mL, compared with findings for lipid-free blood samples. Values of other thromboelastographic variables did not differ, regardless of lipid concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: Maximum amplitude determined via thromboelastography in canine blood samples was significantly affected by the addition of lipid to final concentrations that are several orders of magnitude higher than clinically relevant lipid concentrations in dogs. Lipid treatment appears to have no significant effect on hemostatic variables in dogs, although clinical studies should be performed to confirm these in vitro findings.

Serum cobalamin and methylmalonic acid concentrations in dogs with chronic gastrointestinal disease.

OBJECTIVE: To determine the prevalence of hypocobalaminemia or methylmalonic acidemia (or both) in dogs with chronic gastrointestinal disease. SAMPLE: Serum samples from 56 dogs with chronic gastrointestinal disease and 43 control dogs. PROCEDURES: Serum cobalamin and methylmalonic acid (MMA) concentrations were measured in all samples and compared between groups. A correlation between serum cobalamin and MMA concentrations and the canine chronic enteropathy clinical activity index was evaluated via the Spearman rank correlation. RESULTS: 20 of 56 (36%) dogs with gastrointestinal disease had hypocobalaminemia. Serum cobalamin concentrations were significantly lower in dogs with gastrointestinal disease than in control dogs. Five of 56 (9%) dogs with chronic gastrointestinal disease and 5 of 20 (25%) hypocobalaminemic dogs had increased MMA concentrations. There was a significant negative correlation (Spearman r = -0.450) between serum cobalamin and MMA concentrations in dogs with gastrointestinal disease. No correlation was found between the canine chronic enteropathy clinical activity index and serum cobalamin or MMA concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: These data indicated the prevalence of hypocobalaminemia in dogs with chronic gastrointestinal disease was 20 of 56 (36%). Five of 20 (25%) hypocobalaminemic dogs had increased serum MMA concentrations, which indicated that although hypocobalaminemia was common in these dogs, it did not always appear to be associated with a deficiency of cobalamin on a cellular level. Hypocobalaminemia is a risk factor for negative outcome in dogs with chronic gastrointestinal disease and should be considered in every patient with corresponding clinical signs.

Imaging diagnosis--spontaneous intramural canine duodenal hematoma.

A 9-year-old neutered female Pug with a 2-week history of pancreatitis was presented for dyspnea, icterus, and intractable vomiting. Sonographically, the gallbladder, intrahepatic bile ducts, and common bile duct were distended. The pancreas was hypoechoic with hyperechoic peripancreatic fat. A mildly heterogeneous intramural mass was present in the muscularis layer of the descending duodenum. A presumptive diagnosis of pancreatitis and smooth muscle tumor of the duodenum leading to common bile duct obstruction was made. The dog died despite supportive care. Necropsy examination confirmed the presence of pancreatitis and an intramural duodenal hematoma.

Feline exocrine pancreatic insufficiency: 16 cases (1992-2007).

Medical records of 16 cats diagnosed with exocrine pancreatic insufficiency (EPI) were reviewed. The diagnosis was confirmed with either a serum feline trypsin-like immunoreactivity (fTLI) concentration

Cranial vena caval syndrome secondary to transvenous pacemaker implantation in two dogs.

Superior vena caval syndrome is a rare, but reported complication of transvenous pacemaker implantation in humans. This syndrome can occur secondary to fibrotic and/or thrombotic obstruction of venous blood flow into the right atrium. The therapeutic approach depends on the suspicion of the presence of an active thrombus and may include antithrombotics, angioplasty and/or surgical venoplasty. We describe two dogs that developed severe pleural effusion secondary to stricture formation in the cranial vena cava 4 years after dual chamber transvenous pacemaker implantation. The stenosis was most likely due to fibrosis secondary to the transvenous pacemaker leads. Balloon angioplasty of the lesion resulted in resolution of the pleural effusion in both patients. Balloon angioplasty appears to be a viable therapeutic approach in dogs with cranial vena caval syndrome caused by focal stenotic lesions.

Pancreatic abscess in 36 dogs: a retrospective analysis of prognostic indicators.

Thirty-six dogs were diagnosed with pancreatic abscess by the presence of purulent exudate within the parenchyma of the pancreas during exploratory laparotomy. Data regarding history, physical examination findings, clinicopathological data, diagnostic imaging findings, bacteriological culture results, abdominal drainage technique, and perioperative treatment were evaluated for factors predictive of survival. Elevated blood urea nitrogen, serum alkaline phosphatase activity, and rising bicarbonate ion concentration were each found to have statistically significant (P<0.05) influences on survival to discharge. Twenty-two (71%) of 36 dogs died or were euthanized prior to discharge from the hospital.

Evaluation of clinicopathologic features, response to treatment, and risk factors associated with idiopathic neutropenia in dogs: 11 cases (1990-2002).

OBJECTIVE: To evaluate the clinicopathologic features, response to treatment, and risk factors associated with idiopathic neutropenia in dogs. DESIGN: Retrospective case series. ANIMALS: 11 dogs. PROCEDURES: Medical records of dogs with idiopathic neutropenia were reviewed. Signalment, history, clinical signs, and response to treatment were recorded and compared with that in dogs with neutropenia attributable to known causes and to dogs without neutropenia (controls). RESULTS: Compared with dogs with neutropenia attributable to known causes, dogs with idiopathic neutropenia had lower neutrophil counts and were younger. When compared with control dogs, age < 4 years was identified as a risk factor for developing idiopathic neutropenia. In all dogs with idiopathic neutropenia, remission of neutropenia occurred within 18 days after administration of prednisone (2 to 4 mg/kg [0.9 to 1.8 mg/lb], PO, daily) and no serious complications or infections developed. CONCLUSIONS AND CLINICAL RELEVANCE: An immune-mediated pathogenesis should be considered for dogs with idiopathic neutropenia in which the cause is not known. Severe neutropenia and young age were significantly associated with idiopathic neutropenia in dogs. Prognosis appeared to be excellent with prednisone treatment.

Subcutaneous emphysema, pneumomediastinum, and pulmonary emphysema in a young schipperke.

A 4-month-old, intact female schipperke was presented for evaluation and treatment of subcutaneous (SC) emphysema. Radiographs revealed pneumomediastinum and SC emphysema. Sequential radiographs confirmed a worsening of the SC emphysema. Extensive, nonsurgical evaluation failed to reveal the source of the air within the mediastinum. Exploratory thoracotomy revealed an emphysematous right middle lung lobe. Lobectomy of the right middle lung lobe resolved both the pneumomediastinum and SC emphysema. Histopathological evaluation confirmed pulmonary emphysema. A variation of congenital pulmonary emphysema was considered in this case.