Asparaginase-associated pancreatitis in a dog

A dog with lymphosarcoma was evaluated for vomiting, lethargy, and abdominal pain 48 h after treatment with L-asparaginase. Based on drug administration, clinical signs, bloodwork, and elevated canine pancreatic lipase immunoreactivity, L-asparaginase-associated pancreatitis was diagnosed. This is an acknowledged toxicity; however, its pathophysiology and incidence rate in veterinary patients are unknown and sparsely documented.     

Zinc-associated acute pancreatitis in a dog

Zinc-induced haemolytic anaemia is a common phenomenon in dogs in the USA following the ingestion of pennies minted after 1982. A case of acute pancreatitis secondary to zinc toxicosis in a dog is described. Acute pancreatitis has been reported in humans, following the ingestion of liquid zinc chloride, but zinc-associated pancreatitis has not been reported previously in the dog. The mechanism of toxicity is unknown, although the pathophysiology may relate to the role of the pancreas in zinc excretion. Acute pancreatitis as a sequela to zinc toxicosis in the dog represents a complication that may prolong hospitalisation and worsen the prognosis.     

Common bile duct obstruction secondary to chronic fibrosing pancreatitis: treatment by use of cholecystoduodenostomy in the dog

Six small to medium-sized, middle-aged, female dogs with histories of acute pancreatitis developed clinical signs of extrahepatic biliary obstruction. Clinical findings were similar in the 6 dogs and included icterus. Serum biochemical analyses indicated high concentrations of total bilirubin and cholesterol and high alkaline phosphatase and alanine transaminase activities. Exploratory abdominal surgery was performed in each dog. Each dog had a firm mass involving the body of the pancreas, with obstruction of the distal portion of the common bile duct, marked peripancreatic inflammation, and omental adhesions. Cholecystoduodenostomy, using an open mucosal appositional technique for biliary redirection, was performed in each dog. Clinically, results of surgery were good to excellent (ie, lack of postoperative icterus, anorexia, lethargy, or weight loss and absence or infrequency of vomiting). The mean postoperative evaluation period for the 6 dogs was 35 months (range, 20 to 48 months); 5 dogs were alive and healthy at the end of the study. Histologic examination of tissue specimens of the pancreatic mass indicated chronic active fibrosing pancreatitis in the 6 dogs.     

犬急性胰腺炎的诊疗

胰腺炎是多发生在成年犬的一种消化系统疾病,该病发病率不高,占门诊或临床发病率的0.5%,但是该病死亡率高,特别是幼犬的发病率和死亡率偏高.从接触的病例来看,只有极少数的病例属于原发病,大多数病例是继发于肠胃炎、犬细小病毒、犬瘟热和肝炎等疾病.     

Progression of chronic renal disease in the dog

Progressive loss of nephron function may be caused by persistence of factors that initiated renal disease. However, newer studies suggest that nephron damage is self-perpetuating once renal mass is reduced to some critical level. Original theories on mechanisms of self-perpetuated nephron injury focused on intraglomerular hypertension and glomerular hypertrophy, but several other factors have now been incriminated, including tubulointerstitial responses, proteinuria, and oxidative stress. Studies of dogs with surgically reduced renal mass (remnant kidney model of chronic renal disease) have allowed investigation of the self-progression theory in this species. Use of this model eliminates pre-existing renal disease as a confounding factor. Data from these studies indicate that self-perpetuated renal injury is initiated when mild azotemia is induced (plasma creatinine concentration = 2 to 4 mg/dL). Thus, with naturally occurring renal disease(s), it is likely that self-perpetuated nephron damage is occurring before or at the time when most cases of chronic renal disease are diagnosed. In dogs with remnant kidneys, loss of renal function often occurs at a linear rate over time, but non-linear patterns are common as well. The reciprocal of plasma creatinine concentration, which has been used to monitor rate of progression, is only a fair marker of renal function when compared to GFR. Thus, clinical results from creatinine measurements on cases of naturally occurring disease should not be interpreted too stringently. In remnant kidney dogs, the magnitude of proteinuria (UPC ratio) was not predictive of the rate in decline of GFR, casting doubt on importance of proteinuria in causing progression of renal disease. However, progressive increases in UPC may be a marker of an accelerated rate of renal injury. Self-perpetuation of renal injury in dogs could be the sole mechanism by which naturally occurring renal diseases progress. When more information is available on the rate of progression of naturally occurring diseases, it may become apparent whether factors initially inciting renal damage have an additive effect on rate of progression.     

Dacryocystomaxillorhinostomy for chronic dacryocystitis in a dog

A 10-year-old female spayed Vizsla had intermittent mucoid ocular discharge from the right eye for 7 years. History, clinical findings, imaging studies, and culture and histopathology results confirmed chronic dacryocystitis with granuloma. A dacryocystomaxillorhinostomy was performed to preserve the functional portions of the nasolacrimal system remaining in this patient, as well as to promote healing of the lacrimal sac granuloma and secondary infection. Complete resolution of the clinical abnormalities was achieved, and the dog remains healthy 3 years postoperatively.     

Characterization of chronic pancreatitis in English Cocker Spaniels

Background: Chronic pancreatitis (CP) is common in dogs. The cause is unknown. In humans, different causes of pancreatitis have histologically distinct appearances. The histopathologic lesions in English Cocker Spaniels (ECS) with CP were noted to be histologically different than those of other breeds with CP. Hypothesis: CP in ECS is distinct from CP in other breeds and is characterized by a duct destruction similar to what is observed in autoimmune CP of humans. Animals: Eight ECS and 9 other breeds with histologically confirmed CP recruited over an 8‐year period and 50 postmortem control dogs with CP. Methods: Clinical, clinicopathological, and ultrasonographic findings were recorded. Histological sections were compared with a normal dog and 59 dogs of other breeds with CP. Immunohistochemistry using anti‐CD3, anti‐CD79a, and anti‐cytokeratin antibodies was used to evaluate distribution and type of lymphocytic inflammation and appearance of pancreatic ducts. Results: Four male and 4 female ECS presented at a mean age of 7.2 years. Clinical signs were similar in ECS and other breeds. The pancreas was enlarged and hypoechoic in 4 ECS and 2 controls. Histopathology was characterized by interlobular and periductular fibrosis and inflammation in ECS compared with intralobular disease in most other breeds. Immunohistochemistry identified prominent anti‐CD3⁺ lymphocytic infiltrates around venules and ducts and a marked absence of interlobular ducts in ECS compared with mixed T‐cell infiltration and ductular hyperplasia in most other breeds with CP. Conclusions and Clinical Importance: CP in ECS is distinct from CP in other breeds and is notably duct destructive.     

Pulmonary edema in a dog with acute pancreatitis and cardiac disease

Acute pancreatitis and cardiac disease were diagnosed in a dog with pulmonary edema. The early clinical course and initial thoracic radiographs suggested that the pulmonary edema was noncardiogenic. The late clinical course was complicated by heart failure. The dog died, and a necropsy was performed. Histologically, an acute, severe capillary-alveolar membrane lesion was found in the lungs. Review of the human medical literature indicated that respiratory complications, including pulmonary edema, are commonly recognized in people with acute pancreatitis. Furthermore, in acute pancreatitis of human beings, the existence of specific mechanisms of pulmonary injury is suspected. Retrospective consideration of this case suggested that the initial pulmonary edema was induced by acute pancreatitis.     

Essential features of the treatment of chronic renal failure in the dog

The consequences of chronic renal failure are enumerated and the recommended measures for mitigating them are described. Treatments vary according to whether the disease is in the compensated or terminal phase. Résumé. On énumère les conséquences des maladies rénales chroniques et on décrit les mesure recommandées pour les atténuer. La traitements varient selon que la maladie se trouve au stade compensé ou terminal. Zusammenfassung. Die Folgen chronischen Nierenversagens werden aufgezählt und die empfohlenen Massnahmen zu ihrer Linderung beschrieben. Die Behandlung richtet sich danach, ob die Krankheit sich in der Kompensationsoder terminalen Phase befindet.