Marisa Cevasco
Stanley W. Ashley
Amy L. Rezak
Presentation
A 39-year-old male with a history of alcohol abuse presents to the emergency department complaining of epigastric abdominal pain for the past 36 hours. He describes the pain as constant and radiating to his back. He also complains of nausea and has vomited several times. He had a normal bowel movement one day prior to presentation and denies melena. The patient is currently unemployed and recently divorced from his wife. He admits to drinking a case of beer each day for the past week. He denies smoking and illicit drug use. His family history is significant for hypertriglyceridemia.
Physical exam reveals abdominal distension and diffuse tenderness to palpation, worse over the epigastrium, but no guarding or rigidity. He is not jaundiced and has no Grey-Turner or Cullen signs. His vital signs are notable for a temperature of 101°F, sinus tachycardia, and hypotension with a blood pressure of 90/60 mm Hg. He has palpable distal pulses and no pretibial edema.
Differential Diagnosis
Epigastric abdominal pain radiating to the back, in a patient with a history of heavy alcohol consumption and a family history of hypertriglyceridemia, suggests acute pancreatitis. However, in a patient who is tachycardic, hypotensive, and vomiting, the differential diagnosis would also include perforated gastroduodenal ulcer disease and esophageal rupture (Boerhaave’s syndrome). Cholecystitis and cholangitis are other important considerations, as these patients may present with fever, tachycardia, hypotension, and abdominal pain.
Presentation Continued
The patient has been hospitalized in the past for acute pancreatitis. He has no history of gallstone disease. Laboratory tests were notable for lipase of 18,200 U/L, amylase of 7,800 U/L, and mildly elevated transaminases (AST of 124 IU/L and ALT of 79 IU/L). Alkaline phosphatase, total bilirubin, and creatinine were within normal limits. Serum glucose was elevated at 230 mg/dL and lactate dehydrogenase (LDH) was 411 IU/L. He had a hematocrit of 48% and an elevated white blood cell (WBC) count of 16,400 cells/cm3. Triglycerides were 1,100 mg/dL. His respiratory rate was 16 and an arterial blood gas was notable for a pH of 7.31 and a PaO2 of 72 mm Hg. A Ranson score of 3 was calculated upon admission (Table 1).
A contrast-enhanced computerized tomographic (CT) scan of the abdomen and pelvis reveals stranding, inflammation, and edema within the peripancreatic area and extending inferiorly along the paracolic gutters to the pelvis (Figure 1). The low attenuation area in the tail of the pancreas is consistent with necrosis and represents approximately 30% of the pancreatic parenchyma (Figure 2). Bowel wall thickening was also seen at the hepatic flexure of the transverse colon. There was no free air or evidence of biliary disease, and no occlusion or thrombosis of the peripancreatic vasculature.
TABLE 1. Ranson Criteria
FIGURE 1 • CT scan of the abdomen with IV and oral contrast reveals stranding, inflammation, and edema within the peripancreatic area.
FIGURE 2 • CT scan of the abdomen with IV and oral contrast reveals low attenuation of the tail of the pancreas. This is consistent with necrosis and represents approximately 30% of the pancreatic parenchyma.
Workup
This patient presents with severe acute necrotizing pancreatitis. The most common etiology of acute pancreatitis is obstructive biliary tract disease, responsible for up to 40% of cases. Excessive alcohol use is the second most common cause of pancreatitis, responsible for approximately 35% of cases. Other causes include hypertriglyceridemia, endoscopic retrograde pancreatography (ERCP), anatomic abnormalities (e.g., pancreatic divisum), and abdominal trauma.
Nearly 20% to 30% of patients with acute pancreatitis have pancreatic necrosis; therefore, it is vital to determine the severity of pancreatitis. The Ranson score, based on the presence of 11 clinical signs (five measured at the time of admission and six measured 48 hours after admission), indicates the risk of systemic complications and the likelihood of pancreatic necrosis (Table 1). The presence of three or more Ranson criteria (or if the patient is in shock, renal insufficiency, or pulmonary insufficiency) indicates severe pancreatitis and a greater likelihood of necrosis. Severe pancreatitis is associated with multiple organ dysfunction syndrome (MODS) and mortality rates that typically exceed 15%. In contrast, patients with mild disease generally recover completely with conservative management.
Contrast-enhanced abdominal CT is the gold standard for noninvasive diagnosis of pancreatic necrosis. CT is >90% accurate in diagnosing necrosis if more than 30% of the gland is affected. There are several CT-based classification schemes that predict disease severity and mortality. However, several recent studies revealed that the associated radiation exposure was significant and that, after CT imaging, changes in clinical management were infrequent. Subsequently, it is recommended that the use of CT be restricted to patients with severe pancreatitis.
Diagnosis and Treatment
Initial treatment of the patient with severe pancreatitis includes monitoring, fluid resuscitation, and pain control with patient-administered or epidural analgesia (PCA). A Foley catheter to measure urine output should be considered. Oxygenation should be monitored closely and early intubation should be considered in the patient whose respiratory function is deteriorating. Caloric support should be initiated early in the hospital course, and enteral feeding via a nasojejunal tube is preferred if the patient’s ileus is not too severe.
In patients who are appropriately resuscitated, infectious complications are considered to be the main cause of mortality in severe pancreatitis. Multiple trials have examined the value of prophylactic antibiotics and this remains controversial; selection for resistant organisms and Candida species may be associated with even worse outcomes.
For patients with MODS and signs of sepsis, CT-guided (FNA) of the necrotic areas should be performed to determine the presence of bacterial contamination. Although these developments may be the result of infection, MODS and the systemic inflammatory response syndrome can result from pancreatic necrosis alone. Infected pancreatic necrosis is an indication for intervention with either surgical or radiologic drainage. In extremely ill patients, a percutaneous drain placed at the time of the FNA can help stabilize the patient prior to surgery, and may be used to temporize or even definitively treat infected necrosis. If possible, waiting at least 4 weeks prior to necrosectomy will allow demarcation of necrosis, thereby minimizing resection of viable pancreas and the accompanying morbidity. Sterile necrotizing pancreatitis, on the other hand, has not been shown to benefit from drainage or debridement and may be managed nonoperatively. In patients who develop abdominal compartment syndrome, surgical decompression may improve respiratory, cardiovascular, and renal parameters, but it is unclear if this is associated with an improvement in mortality.
Presentation Continued
The patient was admitted to the intensive care unit. His pain was controlled with a PCA, and his electrolytes were closely monitored. A postpyloric feeding tube was placed under endoscopic guidance. Although he initially stabilized, on the eighth hospital day, the patient became tachycardic and hypotensive. His WBC count continued to rise, and his creatinine became elevated. An intra-abdominal pressure was measured at 15 mm Hg. He became increasingly dyspneic and required intubation. CT-guided FNA revealed gram-negative rods, and a percutaneous drain was placed. Despite this, the patient continued to deteriorate and the decision was made to proceed with surgical debridement.
Surgical Approach
The approach to pancreatic debridement is determined by the interval to operation. Over time, the pancreatic necrosis becomes increasingly organized, permitting a more focused and even minimally invasive approach. In patients undergoing operation prior to a month after onset, open pancreatic necrosectomy is often required.
Open pancreatic necrosectomy (Table 2). Preoperative imaging should be used to guide placement of the incision. A vertical midline or Chevron incision may be employed. The greater omentum is usually separated from the middle of the transverse colon for a distance sufficient to expose the pancreas. When the collection extends into the mesocolon and the small bowel mesentery, a direct approach from below the transverse colon may be more appropriate. Once the pancreas is exposed, the capsule is opened and all purulent material and necrotic tissue is removed from the pancreatic bed, being careful to preserve viable pancreatic tissue. Sharp dissection is usually avoided; it is typically sufficient to remove tissue that comes easily with a ring forceps or irrigation. The transverse colon should be inspected for viability; if the colon is compromised, an extended right hemicolectomy should be performed. Care should be taken to minimize intra-operative hemorrhage. Depending on the organization of the necrosis, the anticipated need for further debridement, and the degree of hemorrhage, it may be appropriate to pack the pancreatic bed and plan reoperation. In cases where the laparotomy incision will be closed, Jackson-Pratt (JP) drains should be placed to maximize postoperative drainage of debris. Closed continuous lavage of the retroperitoneum may be appropriate in patients where ongoing necrosis is anticipated.
TABLE 2. Key Technical Steps and Potential Pitfalls in Open Pancreatic Necrosectomy
Laparoscopic pancreatic necrosectomy. For critically ill, hemodynamically unstable patients or if the necrosis is not yet organized, laparoscopic intervention is contraindicated. However, some case series suggest that laparoscopic necrosectomy is appropriate in patients who have undergone prior percutaneous drainage and/or have limited areas of necrosis that will benefit from a single-stage procedure. Full laparoscopic procedures with carbon dioxide pneumoperitoneum and modified laparoscopic procedures aided by a hand port have been described. Postoperative drainage is recommended with both techniques. Other minimally invasive techniques, such as endoscopic transgastric or transduodenal necrosectomy or retroperitoneal percutaneous necrosectomy, may be alternatives to surgical intervention, but a full description of these techniques and their indication is beyond the scope of this text.
Special Intraoperative Considerations
Pancreatic necrosectomy may be combined with cholecystectomy if exposure is simple and mobilization is thought to be safe. However, in the patient with severe pancreatitis, even if secondary to gallstones, cholecystectomy should be deferred to a later date if the gallbladder is not easily accessible.
A subcostal incision can be performed if focal areas of necrosis are in the tail or in the head of the gland. Formal mobilization of the gastrocolic gutters is typically not performed but all areas of necrosis, identified by preoperative CT, need to be addressed. Postoperative closed irrigation with JP drains placed into the lesser sac through separate small incisions should be considered in patients with ongoing necrosis.
Postoperative Management
Postoperative complications are common and significant. They include organ failure, retroperitoneal and intra-abdominal hemorrhage, endocrine dysfunction, and secondary fungal infections. Fistulae from the pancreatic duct and gastrointestinal tract, pseudocyst formation, pancreatic abscess, and vascular complications (e.g., mesenteric or splenic venous thrombosis and arterial pseudoaneuryms) are also late complications of acute pancreatitis. Follow-up with repeat imaging is required to identify and manage these sequelae of pancreatic necrosectomy.
Case Conclusion
The patient underwent pancreatic necrosectomy via a vertical midline incision. His abdomen was left open and he returned to the operating room for two additional irrigation and debridement procedures. He tolerated these procedures well. During the second take-back, he underwent placement of a feeding jejunostomy, and his abdomen was closed. Postoperatively, he remained hemodynamically stable and was successfully weaned from the ventilator. Follow-up imaging was notable for the development of a pancreatic pseudocyst, which was managed via endoscopic cystogastrostomy. He was ultimately discharged from the hospital to a subacute care facility, on tube feeds, and starting to tolerate a small amount of oral intake.
TAKE HOME POINTS
· Postpyloric enteral feeding is the preferred method of nutritional support.
· Patients with acute necrotizing pancreatitis and a question of infection should undergo CT-guided FNA of necrotic regions of the pancreas to differentiate between sterile and infected pancreatic necrosis.
· Infected pancreatic necrosis in patients is an indication for intervention, including radiologic drainage and/or surgery.
· Surgical intervention should favor an organpreserving approach. Resection procedures such as partial or total pancreatectomy that remove vital pancreatic tissue are associated with postoperative exocrine and endocrine insufficiency and high mortality rates.
· Cholecystectomy should be performed when safe to avoid recurrence of gallstone-associated pancreatitis.
SUGGESTED READINGS
Ashley SW, Perez A, Pierce EA, et al. Necrotizing pancreatitis: a contemporary analysis of 99 consecutive cases. Ann Surg. 2001;234:572–580.
Baron TH, Morgan DE. Acute necrotizing pancreatitis. N Engl J Med. 1999;340:1412–1417.
Clancy TE, Benoit EP, Ashley SW. Current management of acute pancreatitis. J Gastrointest Surg. 2005;9:440–452.
Connor S, Alexakis N, Raraty GT, et al. Early and late complications after pancreatic necrosectomy. Surgery. 2005;137:499–505.
Dellinger EP, Tellado JM, Soto NE, et al. Early antibiotic treatment for severe acute necrotizing pancreatitis: a randomized, double blind, placebo-controlled study. Ann Surg. 2007;245:674–683.