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A Case of Severe Acute Pancreatitis

Kristin Welch, DVM, DACVECC

“Marcus” is a 5.5 yr CM Mixed Breed dog that was presented to his primary veterinarian for a 2 day history of lethargy and anorexia after known dietary indiscretion.  Initial diagnostics included comprehensive bloodwork, radiographs and abdominal ultrasound.   Baseline bloodwork revealed markedly elevated amylase and lipase and elevated liver values (ALP 228 U/dL, Total Bilirubin 2.4 mg/dL) and a neutrophilic leukocytosis (20,000 WBC/uL).  Abdominal radiographs revealed decreased serosal detail and moderate gas distension of the stomach and small intestinal loops.  Preliminary abdominal ultrasound confirmed peritoneal effusion and demonstrated a potentially edematous pancreas.  Marcus was treated for a presumptive diagnosis of pancreatitis with IV fluids, antibiotics, antiemetics, and a lidocaine CRI for analgesia.  He was referred to Charleston Veterinary Referral Center for continued in-patient care.

On presentation to CVRC, Marcus had severe abdominal pain and frequent regurgitation.  Marcus was started on intravenous symptomatic and supportive care including a continuous infusion of metoclopramide, IV fluids, famotidine, maropitant, and buprenorphine.  Abdominal ultrasound was completed to evaluate the pancreas and rule out concurrent intra-abdominal disease.   Abdominal ultrasound revealed an edematous right limb of the pancreas consistent with pancreatitis.  The left limb of the pancreas was replaced with an echogenic fluid filled structure surrounded by a hyperechoic capsule and bright intraabdominal fat.  The remainder of the abdomen including the billiary tract was unremarkable.

Differentials for the fluid filled structure in the region of the left limb of the pancreas included a pancreatic abscess, pancreatic neoplasia with abscessation or severe acute necrotizing pancreatitis.  In this patient, I had a high index of suspicion for pancreatic abscessation based on the classic ultrasonographic appearance of the lesion.  An ultrasound guided fine needle aspiration of the fluid filled structure was completed and 1 ml of thick mucoid pink-tan fluid was removed.    A fluid to peripheral glucose and lactate differential were completed which were consistent with septic effusion (fluid glucose <20 mg/dL, fluid lactate 12.9 mmol/L).  Cytologically, the fluid consisted of degenerate and nondegenerate neutrophils and rod shaped bacteria confirming the diagnosis of septic pancreatic abscess[K.F.1] .

Marcus was taken immediately into surgery for abdominal lavage and pancreatic omentalization.  Broad spectrum antibiotics (ampicillin/sulbactam, enrofloxacin, metronidazole) were instituted and an aerobic and anaerobic culture of the pancreatic abscess was obtained.  On examination, the left limb of the pancreas was dark red to black, markedly edematous and friable.  A biopsy of the pancreatic abscess was obtained and the region was omentalized.  The right limb of the pancreas was mildly edematous but otherwise appeared to be within normal limits.  A Jackson-Pratt abdominal drain was placed to continually evacuate inflammatory and infected fluid from the abdomen in the initial postoperative period.

Nutrition was a primary concern in this patient because of the severity of pancreatitis.   While in anesthetic induction, an esophagostomy tube was placed.  In the OR, a jejunostomy tube was fed through the esophagostomy tube and into the jejunum to allow for nutrition to be instituted immediately post-op.  The benefits of an esophagostomy to jejunostomy tube (E to J tube) is that the jejunostomy tube can be used as soon as the patient recovers from anesthesia and since the tube ends in the jejunum, nutrition can be continued in spite of regurgitation or vomiting.  Additionally, food delivered into the jejunum does not trigger pancreatic enzyme secretion.  A triple lumen jugular catheter was also placed to allow for frequent blood sampling and administration of intravenous nutrition via a dedicated central catheter port.

Postoperatively, Marcus was started on a continuous rate infusion of Clinicare at 25% of his resting energy requirements via the jejunostomy tube.  He was continued on broad spectrum antibiotics and was treated with a fentanyl CRI for postoperative analgesia.  He was continued on crystalloids but Hetastarch was started in anticipation of large protein losses via abdominal 3rd spacing.

Marcus remained hospitalized for the following 10 days.  Via the jejunostomy tube, he received incrementally increasing amounts of Clinicare reaching 100% of his resting energy requirement.  However, Marcus developed refractory regurgitation and on the 3rd day post-op, his jejunostomy tube was removed by pulling it through the E tube.  We were concerned that maintaining patency of the lower esophageal sphincter (LES) may be contributing to esophagitis and regurgitation because with an E to J tube, the jejunostomy tube passes though the lower LES and the pyloric sphincter before reaching the jejunum.   On day 4, he was fed a blenderized diet of Royal Canin Low Fat instituted at 25% of his resting energy requirement as small bolus feedings every 4 hours via the esophageal feeding tube.  The bolus feedings were well tolerated and during this time, he also received partial parenteral nutrition which supplied an additional 25% of his resting energy requirement intravenously.   Unfortunately, Marcus developed severe regurgitation refractory to medical management on the 5th day post-op necessitating a 48 hour period where nothing was administered by mouth.  During this period he continued to receive 25% RER via intravenous nutrition.   Lower esophagitis and gastritis are the probable causes of the severe regurgitation and both were treated aggressively throughout hospitalization with a combination of antacids (pantoprazole, a proton pump inhibitor), sucralfate, and prokinetics (ranitidine, metoclopramine, erythromycin) to ensure rapid gastric emptying.   Refeeding was instituted on day 8 with small amounts of a low fat commercial diet by mouth and was well tolerated without regurgitation or nausea.

At the time of writing, Marcus is preparing to be discharged from the hospital.  He will continue on antacid therapy with omeprazole, sucralfate, erythromycin as a prokinetic, and amikacin as directed by bacterial culture.  The culture of the pancreatic abscess grew a resistant Pseudomonas sensitive only to aminoglycoside antibiotics.

The histopathology of the pancreas was consistent with a septic pancreatic phlegmon, a rare complication of severe acute necrotizingpancreatitis.  A phlegmon is a solid mass of swollen inflamed pancreas and pancreatic fat containing large areas of necrosis.  Pancreatic phlegmon, as in this case, can be early, unorganized, and liquifactive, or chronically over months can become an organized mass.

Current veterinary literature provides supportive evidence for early surgical treatment of certain complications of pancreatitis in dogs including extrahepatic bile duct obstruction (EHBDO) and pancreatic necrosis.   In a recent publication of 37 dogs with acute pancreatitis treated surgically (Thompson, JVECC 2009), dogs with pancreatic necrosis treated surgically had a survival rate of 64%, while dogs with pancreatic abscessation had a survival rate of 40%.  In comparison, the survival rate of dogs with EHBDO was 80%.  The primary reason for the lower survival rate in the dogs with pancreatic necrosis or abscessation is the severity of the systemic inflammatory response or the presence of sepsis.  Many of these dogs are poor anesthetic candidates due to hemodynamic instability, coagulopathy or severe hypoalbuminemia.

While the majority of cases of acute pancreatitis are able to be managed medically, there is a subset of cases of severe acute pancreatitis which necessitate early and aggressive surgical management and intensive care to yield a positive outcome.

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