To characterize clinical features, comorbidities, frequency of bacterial isolation, and survival time in cats with suppurative cholangitis-cholangiohepatitis syndrome (S-CCHS).
168 client-owned cats with S-CCHS.
Data were prospectively (1980 to 2019) collected regarding clinical features, comorbidities, bacterial infection, illness duration, and treatments. Variables were evaluated for associations with survival time.
Median age of cats was 10.0 years, with no breed or sex predilection observed. Common clinical features included hyporexia (82%), hyperbilirubinemia (80%), lethargy (80%), vomiting (80%), jaundice (67%), weight loss (54%), and hypoalbuminemia (50%). Comorbidities included extrahepatic bile duct obstruction (53%), cholelithiasis (42%), cholecystitis (40%), and ductal plate malformation (44%) as well as biopsy-confirmed inflammatory bowel disease (60/68 [88%]) and pancreatitis (41/44 [93%]). Bacterial cultures were commonly positive (69%) despite prebiopsy antimicrobial administration in most cats. Of surgically confirmed choleliths, diagnostic imaging identified only 58%. Among 55 cats with “idiopathic pancreatitis,” 28 (51%) were documented to have transiting choleliths, and 20 had pancreatic biopsies confirming pancreatitis. Cholelithiasis (with or without bile duct obstruction) and cholecystectomy were associated with survival advantages. Survival disadvantages were found for leukocytosis, ≥ 2-fold increased alkaline phosphatase, and hyperbilirubinemia. Cholecystoenterostomy had no survival impact. Cats with ductal plate malformations were significantly younger at diagnosis and death than other cats. Chronic treatments with antimicrobials, S-adenosylmethionine, and ursodeoxycholic acid were common postbiopsy.
S-CCHS in cats was associated with bacterial infection and various comorbidities and may be confused with pancreatitis. Surgically correctable morbidities (ie, cholecystitis, cholecystocholelithiasis) and cholecystectomy provided a significant survival advantage.
PROCEDURES Dogs were randomly assigned to receive either oxygen (Fio2 > 0.9 [100% oxygen]; n = 11; control group) or a mixture of nitrogen and oxygen (Fio2 = 0.4; 11; 40% oxygen group) as the carrier gas for isoflurane while anesthetized. All dogs were allowed to breathe spontaneously while anesthetized. For each dog, the Pao2, Paco2, other indices of oxygenation, and extent of sedation were monitored at predetermined times during and for 1 hour after anesthesia. Measured variables were compared between the 2 treatment groups and over time within each treatment group.
RESULTS None of the measured variables differed significantly between the control and 40% oxygen groups at any time during the postanesthesia period. Within each treatment group, the Paco2 and extent of sedation decreased over time during the postanesthesia period.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that indices of oxygenation did not differ significantly between healthy dogs in which the Fio2 was maintained at > 0.9 and those in which the Fio2 was maintained at 0.4 while anesthetized for ovariohysterectomy. Thus, the addition of nitrogen to the carrier gas for an inhalant anesthetic conferred neither an advantage nor disadvantage in regard to oxygenation during the first hour of anesthesia recovery.
To characterize the association between peritoneopericardial diaphragmatic hernia (PPDH) or congenital central diaphragmatic hernia (CCDH) and ductal plate malformations (DPMs) in dogs and cats.
18 dogs and 18 cats with PPDH or CCDH and 19 dogs and 18 cats without PPDH or CCDH.
Evaluation of clinical details verified PPDH or CCDH and survival times. Histologic features of nonherniated liver samples were used to categorize DPM. Immunohistochemical staining for cytokeratin-19 distinguished bile duct profiles per portal tract and for Ki-67–assessed cholangiocyte proliferation. Histologic features of herniated liver samples from PPDH or CCDH were compared with those of pathological controls (traumatic diaphragmatic hernia, n = 6; liver lobe torsion, 6; ischemic hepatopathy, 2).
DPM occurred in 13 of 18 dogs with the proliferative-like phenotype predominating and in 15 of 18 cats with evenly distributed proliferative-like and Caroli phenotypes. Congenital hepatic fibrosis DPM was noted in 3 dogs and 2 cats and renal DPM in 3 dogs and 3 cats. No signalment, clinical signs, or clinicopathologic features discriminated DPM. Kaplan Meier survival curves were similar in dogs and cats. Bile duct profiles per portal tract in dogs (median, 5.0; range, 1.4 to 100.8) and cats (6.6; 1.9 to 11.0) with congenital diaphragmatic hernias significantly exceeded those in healthy dogs (1.4; 1.2 to 1.6) and cats (2.3; 1.7 to 2.6). Animals with DPM lacked active cholangiocyte proliferation. Histologic features characterizing malformative bile duct profiles yet without biliary proliferation were preserved in herniated liver lobes in animals with DPM.
CONCLUSIONS AND CLINICAL RELEVANCE
DPM was strongly associated with PPDH and CCDH. Because DPM can impact health, awareness of its coexistence with PPDH or CCDH should prompt biopsy of nonherniated liver tissue during surgical correction of PPDH and CCDH.
Objective—To determine risk, clinical features, and treatment responses for gallbladder disorders in Shetland Sheepdogs.
Design—Retrospective case-control study.
Animals—38 Shetland Sheepdogs with gallbladder disease.
Procedures—Medical records were reviewed for signalment, history, physical findings, laboratory results, imaging features, coexistent illnesses, histologic findings, treatments, and survival rates.
Results—Mature dogs with gastrointestinal signs were predisposed (odds ratio, 7.2) to gallbladder disorders. Gallbladder mucocele was confirmed in 25 dogs. Concurrent problems included pancreatitis, hyperlipidemia, corticosteroid excess, hypothyroidism, protein-losing nephropathy, diabetes mellitus, cholelithiasis, and gallbladder dysmotility. Mortality rate was 68% with and 32% without bile peritonitis. Nonsurvivors had high WBC and neutrophil count and low potassium concentration. Although preprandial hypercholesterolemia, hypertriglyceridemia, and high serum liver enzyme activities were common, gallbladder disease was serendipitously discovered in 11 of 38 dogs. Histologic examination (n = 20 dogs) revealed gallbladder cystic mucosal hyperplasia in 20 dogs, cholecystitis in 16, periportal hepatitis in 9, and vacuolar hepatopathy in 7. Surgery included cholecystectomy (n = 17) and cholecystoenterostomy (4). In 1 hyperlipidemic dog without clinical signs, gallbladder mucocele resolved 6 months after beginning use of a fat-restricted diet and ursodeoxycholic acid.
Conclusions and Clinical Relevance—Shetland Sheepdogs are predisposed to gallbladder disorders, with mucoceles and concurrent dyslipidemia or dysmotility in many affected dogs. Most dogs were without clinical signs during mucocele development. Low survival rate after cholecystectomy in clinically affected dogs suggested that preemptive surgical interventions may be a more appropriate treatment strategy.