The pancreas consists of 98% exocrine and 2% endocrine tissue. The acinar cells of the exocrine pancreas secrete amylase, proteases, and lipases. These enzymes are responsible for the digestion of carbohydrate, protein, and fat. Besides enzymes, pancreatic juice contains bicarbonate for neutralization of gastric acid, factors that facilitate absorption of cobalamin, zinc and colipase C, and antibacterial ­factors.

The most common disease of the exocrine pancreas is pancreatitis. The pathogenesis, underlying causes, and risk factors for pancreatitis are not well known, and most cases are considered idiopathic in origin.⁴ Regardless of the underlying cause, after initiation of pancreatitis, autodigestion of the gland starts to occur. The most common clinical signs of pancreatitis in dogs are anorexia, vomiting, weakness, abdominal pain, and diarrhea.⁵ In cats, anorexia and lethargy are most common; vomiting only occurs in a minority of cases, and diarrhea is usually not observed.⁶

Pancreatic abscesses are mucopurulent necrotic exudates within the pancreatic parenchyma that can also extend into adjacent tissues.⁷ Because pancreatic abscesses are usually a sequela to pancreatitis, their clinical signs parallel those of pancreatitis.

Pancreatic pseudocysts are collections of pancreatic secretions, debris, and blood in a nonepithelialized fibrous tissue sac.⁸ Pseudocysts most likely form after premature activation of digestive enzymes, resulting in autodigestion of pancreatic parenchyma, leading to inflammation and necrosis. Pancreatic pseudocysts may be asymptomatic, or animals may be presented with clinical signs of pancreatitis. If parts of the pancreas are devoid of a pancreatic duct, for example, as a result of leaving a distal part of the pancreas intact during partial resection, this can also cause pancreatic cyst or abscess formation.

Pancreatic (adeno)carcinomas are highly malignant tumors that originate from acinar or ductal epithelial cells. These tumors most commonly occur in older animals that present with weight loss, anorexia, abdominal pain, ascites, vomiting, and icterus. Benign pancreatic adenomas are extremely rare and are often incidental findings.⁹

Scattered through the exocrine pancreas are the islets of Langerhans that form the endocrine part of the pancreas. Islets are composed of five distinct cell types : α cells that secrete glucagon, β cells that create insulin, δ cells that secrete somatostatin, and ε cells that secrete ghrelin, and PP cells that secrete pancreatic polypeptide. The main function of the endocrine pancreas is to regulate glucose metabolism through insulin and glucagon secretion.

The most common disease of the endocrine pancreas is insulinoma, an insulin-secreting β cell tumor.^10,11 These tumors hypersecrete insulin, leading to hyperinsulinemia. The resulting hypoglycemia causes clinical signs such as seizures, generalized weakness, posterior paresis, lethargy, ataxia, and muscle tremors. Insulinomas and other endocrine tumors of the pancreas are extremely rare in cats.

Other tumors of the endocrine pancreas are very rare and include gastrinomas and glucagonomas.^12,13 Gastrinomas are malignant islet tumors of dogs and cats. The secretion of excessive amounts of gastrin results in gastric acid hypersecretion and is associated with gastric and intestinal ulceration and associated clinical signs. Glucagonomas are glucagon-secreting carcinomas of α cells in dogs. Serum glucagon increases and causes a decrease in plasma amino acids, albumin and albumin-bound zinc, and essential fatty acids. These changes probably contribute to the cutaneous manifestation of glucagonoma syndrome: erosions, ulceration and hyperkeratosis of footpads, and crusting and alopecia around mucocutaneous junctions.

For laparoscopic pancreatic surgery, no different workup is necessary compared with open surgery.¹

In most cases, the diagnosis of pancreatitis is based on the clinical signs, together with increased serum pancreatic lipase levels. On ultrasound examination, the echogenicity of the pancreas can be decreased or increased caused by pancreatic fibrosis. The echogenicity of the surrounding mesentery is often hyperechoic in acute pancreatitis as a result of inflammation.¹⁷ Pancreatic biopsy can be performed to confirm the diagnosis with histology. Ultrasonography may reveal a mass lesion within the pancreas, which is fluid filled in case of a pancreatic pseudocyst, or an abscess. Pancreatic adenocarcinomas present as mass lesions as well and histopathology of pancreatic biopsy specimens is required to distinguish between neoplasia and pancreatitis. Imaging alone may not differentiate pseudocysts from abscesses. To make a definitive diagnosis, fluid acquired by percutaneous fine-needle aspiration (FNA) should be examined. However, FNA of cavitary pancreatic masses is not without risk, and this risk must be weighed against the advantage of a preoperative diagnosis.

The presumptive diagnosis of canine insulinoma is commonly based on signalment and history combined with the fulfillment of Whipple’s triad: (1) presence of clinical signs associated with hypoglycemia, (2) fasting blood glucose concentration less than 2.2 mmol/L (<40 mg/dL), and (3) relief of clinical signs after glucose administration or feeding. Although the presence of Whipple’s triad diagnoses hypoglycemia, it is not definitive for insulinoma. The next step is to exclude differential diagnoses by determining the plasma insulin concentration. In insulinoma cases, circulating insulin concentrations are typically within the reference range or higher despite hypoglycemia. The simultaneous occurrence of blood glucose less than 3.4 mmol/L (<62.5 mg/dL) and plasma insulin greater than 70 pmol/L is diagnostic for insulinoma.¹⁸ Use of diagnostic imaging techniques, including transabdominal ultrasonography, computed tomography (CT), single-photon emission computed tomography (SPECT), and somatostatin receptor scintigraphy (SRS), have been reported in the identification and preoperative staging of insulinoma. Ultrasonography was found to have a low sensitivity in detecting canine insulinoma¹⁹ with only 5 of 14 primary insulinomas correctly identified and no lymph node metastases detected. Similar results were obtained using SPECT. CT has proved to be the most sensitive method, correctly identifying 10 of 14 primary tumors and 2 of 5 lymph node metastases. Conventional pre- and postcontrast CT was not found to be a very specific method because it also identified many false-positive lesions. More recently, dual-phase CT angiography (CTA) techniques have been developed, and the accurate use of dynamic CTA for the presurgical localization of insulinoma in four dogs has been reported.^20,21 With CTA, after an intravenous (IV) injection of contrast medium, final CT images are acquired during the arterial and venous phases. CT images of canine insulinoma are hyperattenuating at the arterial phase in 55% of cases²¹ compared with the normal pancreas. Finally, a recent case study by Choi et al. has investigated the potential of positron emission tomography CT (PET-CT) to detect an insulinoma in a dog.²² They used the radiopharmaceutical ¹⁸F-FDG, which is a glucose-derivative. PET-CT failed to detect both the primary tumor and the extent of the metastatic lesions in this case. The limited utility of FDG PET-CT in detection of canine insulinomas may be attributable to the low level of glucose turnover. Because it was used only in one case, further studies on FDG PET-CT in canine insulinomas are warranted, including time activity and dose-response studies of ¹⁸F-FDG to establish the optimal scan condition for detecting canine insulinomas.

As with insulinomas, ultrasonography frequently fails to detect gastrinomas or glucagonomas. The diagnosis of gastrinoma is usually based on clinical signs in combination with hypergastrinemia in fasted patients. Furthermore, endoscopic examination of the stomach and duodenum often reveals ulceration, and SRS has been successfully used to diagnose metastatic gastrinoma in one dog.²³ The use of CT scanning has been reported for the diagnosis of lymph node, splenic, and hepatic canine glucagonoma metastases.²⁴ Biopsies of cutaneous lesions in dogs with glucagonomas demonstrate histologic changes characteristic of metabolic epidermal necrosis. In 90% of canine cases with metabolic epidermal necrosis, however, the skin condition is associated with severe liver dysfunction rather than the presence of a glucagonoma. Furthermore, plasma glucagon levels can also be increased in hepatocutaneous syndrome without the presence of a glucagonoma. Therefore, liver disease and other dermatological differential diagnoses need to be ruled out before the diagnosis of glucagonoma can be made.

Pancreatic biopsies for the identification of pancreatitis are preferably taken laparoscopically. Laparoscopic partial pancreatectomy is indicated in cases with isolated pancreatic masses, pseudocysts, or abscesses located in the distal two thirds of either the right or left pancreatic lobe. If complete excision of a pancreatic abscess is not possible, it should be surgically drained and omentalized using either an open or laparoscopic technique. If focal lesions are located close to the pancreatic body, local enucleation can be attempted. In case of lesions located in the pancreatic body, laparotomy is still preferred over laparoscopic surgery in most cases, but novel positioning techniques of the patient may allow successful laparoscopic approaches. Open surgery is the preferred technique in cases in which pancreatic tumors have extensive metastases to abdominal lymph nodes or the liver, requiring extensive exploration and palpation of organs. However, selected abdominal lymph nodes are accessible using a laparoscopic technique.

No data are available in small animal medicine that compare minimally invasive versus open pancreatic surgery; therefore, it is presumed that prognostic factors will not differ between the two approaches when they are performed correctly.

An overall survival rate of 63% of dogs with acute pancreatitis treated surgically has been reported.²³ The severity of symptoms at initial diagnosis was not correlated with clinical outcome. The prognosis for dogs with pancreatic abscesses is guarded with postoperative survival rates of 14% to 55%. The prognosis for dogs that had surgery (including repeated percutaneous aspiration) of pancreatic pseudocysts is better and resulted in a survival rate of 75%.

At the authors’ institution, dogs with insulinomas have a mean postoperative survival time of 25 months (3–41 months). Dogs with a negative insulinoma Ki67 index or with their insulinoma confined to the pancreas and with primary tumors smaller than 2 cm survive significantly longer postoperatively than dogs with a positive Ki67 index or with insulinomas that have spread to lymph nodes and distant sites or larger tumors.¹¹ Furthermore, dogs that are hyperglycemic or normoglycemic immediately postoperatively survive significantly longer than dogs with hypoglycemia postoperatively. The prognosis for other pancreatic neoplasms is poor. In cases where surgery is feasible in pancreatic adenocarcinoma cases, most dogs only survive 3 months postoperatively. Regarding canine glucagonoma and gastrinoma, only a limited number of cases have been reported with varying outcomes after surgery.^24,25

Dry food should be withheld 12 hours before surgery. Canned food can be fed until 6 hours before surgery. In case of insulinomas and if dogs are clinically hypoglycemic, liquid, easily digestible food preparations should be given until 1 to 2 hours before surgery. If clinical signs of hypoglycemia occur in the immediate preoperative period, the dog should be administered a glucose solution intravenously (1–5 mL of 50% dextrose administered over 10 minutes based on clinical effect) to stabilize blood glucose concentration before surgery. In cases of pancreatitis, it is important to pay attention to factors that could increase the complication rate, including hypoproteinemia, disseminated intravascular coagulation, and diabetes mellitus. Any abnormalities in fluid and electrolyte balance, coagulation, oncotic pressure, or plasma glucose levels should be corrected preoperatively.

For a ventral midline laparoscopic approach, the abdomen should be clipped from the xiphoid process to the pubis. Laterally, the patient should be clipped to approximately the mid-abdomen level as for open pancreatic surgery. It is important to perform wide clipping and aseptic preparation because it might be necessary intraoperatively to convert to an open procedure or change the position of the dog. The authors prefer a 360-degree clip to allow an approach from all sides for complicated laparoscopic pancreatic surgery. For a flank approach only, the left or right caudal hemithorax and the lateral abdomen should be clipped and prepared for aseptic surgery.

There are no indications in laparoscopic pancreatic surgery for the use of prophylactic antibiotics. Only in febrile patients with septic complications of pancreatitis, prophylactic antibiotics should be used. However, septic complications are rare in cases of pancreatitis, and these cases should preferably be approached using open instead of minimally invasive surgery.