EARLY FLUID RESUSCITATION
Aggressive management of patients with acute pancreatitis should begin early after diagnosis (eg, in the emergency department). Published data suggest that initial resuscitation can affect the outcomes of acute pancreatitis significantly. The first 24 hours have been referred to as the “golden hours” of management of acute pancreatitis23 and both under-resuscitation as well as over-resuscitation can lead to worse outcomes; accordingly, very close monitoring of these patients is needed.24-26 There is no benefit of using colloids for fluid resuscitation over crystalloids in acute pancreatitis.27 Lactated Ringer’s solution has been found to be associated with a markedly decreased incidence of SIRS compared to 0.9% sodium chloride. Though the exact mechanism for this is not known, it is hypothesized that hyperchloremic metabolic acidosis caused by normal saline can promote activation of trypsinogen in a pH dependent manner.28 Hence, lactated Ringer’s should be the initial choice for volume resuscitation in all patients with acute pancreatitis except those with hypercalcemia since it contains 3 mEq/L of calcium. Serial measurements of blood urea nitrogen and hematocrit should accompany fluid resuscitation along with close assessment of clinical condition, vital signs, and urine output. An evidence-based approach to fluid resuscitation should be utilized (see Chap. 34 on “Judging the Adequacy of Fluid Resuscitation”) and fluid resuscitation should begin early in the course of management. A large single center retrospective study showed that those patients with acute pancreatitis who received early resuscitation (receiving more than one-third of total 72-hour fluid volume within first 24 hours of presentation) had significantly lower incidence of SIRS, organ failure, admission to intensive care unit, and a reduced length of stay compared to those with late resuscitation (receiving less than one-third of total 72 hours fluid volume within first 24 hours).29
A general approach is to start with a 1000- to 2000-mL crystalloid fluid bolus followed by fluid resuscitation at a rate of 250 to 300 mL/h for 1000 to 3000 mL, to target a urine output of at least 0.5 mL/kg per hour. However, one should utilize the tools outlined in Chap. 34 to judge the adequacy of fluid resuscitation rather than following an exact recipe. Some patients with cardiopulmonary disease, particularly those with ARDS, may progress to respiratory failure and require endotracheal intubation.
NUTRITION IN ACUTE PANCREATITIS
The nutritional therapy in acute pancreatitis has significantly evolved from the concept of “pancreas rest” to efforts directed at early resumption of enteral nutrition with an aim to maintain the gut integrity and prevent bacterial translocation and associated complications. Enteral nutrition should be initiated as soon as possible. It is safe in patients with acute pancreatitis and it has been shown to be associated with lower rates of systemic infections, multiorgan failure, and mortality in comparison to parenteral nutrition.30,31 Until recently, the general practice was to avoid oral intake until resolution of abdominal pain; however, patients with mild acute pancreatitis can be fed as soon as they are hungry, without any restriction on the consistency of food. A low fat solid diet seems to be as safe as clear liquid diet.32 Nutritional support is often needed in patients with moderately severe and severe acute pancreatitis and should be started within 24 to 48 hours of initial presentation, especially when it is likely that the patient will be unable to start oral intake within the next 5 to 7 days. As noted above, enteral nutrition is preferred over parenteral nutrition. Multiple studies and meta-analyses have shown that parental nutrition is associated with vascular catheter-related complications and infections, while enteral nutrition appears to help maintain gut mucosal integrity and hence decrease bacterial translocation;30,31,33 it is associated with decreases in infections, organ failure, and length of stay.34 There has been significant debate regarding nasogastric versus nasojejunal feeding in these patients but no data are currently available to strongly favor any one approach over the other. Though traditionally nasojejunal feedings have been preferred in patients with acute pancreatitis, nasogastric tube feeding has been shown to as safe as the jejunal feeding.31,35,36 Aspiration precautions, including elevation of head end of bed, should be applied in all patients. Checking gastric residuals to guide gastric feeding has not been shown to be beneficial. In patients who cannot tolerate gastric feeding due to large fluid collections causing gastric compression or duodenal obstruction, nasojejunal tube placement is usually needed.
ROLE OF PROPHYLACTIC ANTIBIOTICS
Approximately one-fourth of patients with acute pancreatitis develop infectious complications and those with severe acute pancreatitis are at particularly high risk. Patients with infected pancreatic necrosis have a mortality of around 30%14 (Fig. 108-3). The use of prophylactic antibiotics was common in the early 2000s in patients with severe acute pancreatitis. Multiple studies and a recently published Cochrane meta-analysis have shown that the use of prophylactic antibiotics is not associated with decreased incidence of infected pancreatic necrosis, mortality, or need for surgical interventions,37-39 even though a decreased incidence of infection in pancreatic necrosis and a trend toward lower mortality were noted in patients receiving imipenem.40 However, all patients with severe acute pancreatitis requiring critical care should be monitored closely for development of any signs of sepsis or infection, since delay in starting antibiotic therapy has been shown to be associated with declining survival. Hence, recent guidelines from American College of Gastroenterology published in 2013 suggest that when an infection is suspected, it is justifiable to start empiric antibiotics covering both gram, negative and gram-positive organisms; antibiotics should be discontinued if cultures are negative and no definite source is identified.33
A 34-year-old man with a history biliary pancreatitis with epigastric abdominal pain and new onset of fever and chills 48 hours prior to admission. CT Scan reveals walled off necrosis (WON) in the tail of the pancreas area with air (white arrow). This finding and associated symptoms are diagnostic of infected WON.
ROLE OF ERCP IN ACUTE PANCREATITIS
The role of endoscopic retrograde cholangiopancreatography in ERCP in management of acute pancreatitis is limited to patients with acute gallstone pancreatitis with cholangitis and those with pancreatic duct disruption. Patients with acute pancreatitis and biliary sepsis (cholangitis) should have ERCP performed within 24 hours of admission since it has been shown to be associated with decreased morbidity and mortality.41,42 The beneficial role of ERCP in patients with gallstone pancreatitis without cholangitis is not clear. A large multicenter study and a recent meta-analysis involving 717 patients have both shown that there is no beneficial role for early ERCP in acute pancreatitis patients with severe acute biliary pancreatitis without biliary sepsis.43,44
When acute pancreatitis is mild interstitial, and biliary in origin, it is favorable to proceed with cholecystectomy prior to discharging the patient home.45 With moderate or severe biliary pancreatitis, it is favored to wait and re-image a month after the episode to assure that no fluid collections are present; if so, the gallbladder can be removed and the fluid collection treated, both during the same surgery.46 ERCP with biliary sphincterotomy should be performed to protect the pancreas against another attack of pancreatitis while waiting for the cholecystectomy or in those patients who are poor candidates for cholecystectomy.47
PANCREATIC AND PERIPANCREATIC COLLECTIONS
The recent Atlanta classification has led to a major change in the classification of the pancreatic and peripancreatic fluid collections based on the presence or absence and duration of solid material in these collections.4 The four types of fluid collections as a sequel of acute pancreatitis include acute fluid collection (AFC), pancreatic pseudocyst (PP) (Fig. 108-4), acute necrotic collection (ANC), and walled-off necrosis (WON) (Fig. 108-5). All these types of fluid collections have significantly different management strategies and hence it is very important to distinguish one from the others. AFCs develop early in acute interstitial edematous pancreatitis, are homogenous on contrast-enhanced imaging (no solid debris), do not have well-developed demarcation, and usually resolve without any intervention. If these persist beyond 4 weeks, they develop a well-demarcated wall and are known as pseudocysts, which do not contain any solid material. Acute necrotic collection (ANC), usually seen during the first 4 weeks in necrotizing pancreatitis, contains both fluid and necrotic components and is without a well-demarcated wall. These can progress to a well-defined encapsulation after 4 weeks, a condition known as walled-off necrosis. Both ANCs and WONs can become infected, which is associated with morbidity and mortality.
A 42-year-old woman with early satiety, nausea, abdominal pain, and weight loss 6 weeks after an episode of interstitial pancreatitis. Abdominal CT scan reveals a large pancreatic pseudocyst compressing the stomach. She was successfully treated with endoscopic cyst-gastrostomy with stent placement.
A 39-year-old woman with history of hypertriglyceridemia-induced necrotizing pancreatitis with early satiety, nausea, abdominal pain, and weight loss. Abdominal CT scan reveals a large pancreatic and peripancreatic collection with walled-off necrosis compressing the stomach. She was successfully treated with endoscopic transgastric cyst-necrosectomy and two percutaneous drains.
It is usually difficult to differentiate between AFC and ANC during the first week or two of acute pancreatitis since both can appear homogenous with fluid consistency on contrast imaging. Hence, delaying imaging for the first 2 weeks after admission is acceptable, unless indicated for clinical management.
Management: Majority of the AFCs resolve within a few weeks of acute pancreatitis onset and do not require any intervention; however, 6% to 7% of these can persist beyond 4 weeks as pseudocysts or walled-off pancreatic necrosis. Only symptomatic patients require treatment—asymptomatic collections do not require treatment irrespective of their size. The symptoms from pancreatic or peripancreatic collections are usually due to obstruction of adjacent viscera (gastric or duodenal outlet obstruction with early satiety, nausea and vomiting, biliary or pancreatic obstruction), infection, rupture, or bleeding. Therapy can be provided in the form of drainage or drainage along with necrosectomy in patients with walled-off necrosis. The approach depends on the local expertise and includes: endoscopic drainage (transpapillary, transgastric or transduodenal), placement of percutaneous drains by interventional radiology, or surgical intervention (video-assisted retroperitoneal debridement, laparoscopic or open surgery). While rupture requires urgent surgical exploration, bleeding into the pseudocyst and pseudoaneurysms can be treated with angiographic embolization.48 Endoscopic drainage can be used in symptomatic collections. It is important to assess the ductal anatomy in these cases since transpapillary drainage should be performed if the pseudocyst is communicating with the main pancreatic duct or there is pancreatic duct disruption. Otherwise, transgastric or transduodenal approaches should be sufficient.
Both acute pancreatic necrosis and walled-off necrosis can become infected and have high mortality necessitating antibiotics and debridement. Previously, early surgical approach was the only option available for these patients, but transgastric endoscopic necrosectomy has been increasingly performed since 2000 with excellent results. It has dramatically changed the way we now treat symptomatic patients with walled-off necrosis.49 Drainage procedures (endoscopic, interventional radiology, or surgical) should be avoided in the first 4 weeks until a well-defined wall develops around these collections. A direct correlation exists between success of endoscopic intervention and degree of encapsulation,50 and early intervention is associated with poor outcomes.51 Multiple studies have now shown that endoscopic debridement is superior to open necrosectomy,52,53 due to lower morbidity and mortality rates.54 But it is very important to recognize that not all patients with necrotizing pancreatitis will need necrosectomy. Hence, a step-up approach has been proposed in managing these patients. In one of the largest prospective cohort studies on patients with necrotizing pancreatitis, it was shown that up to two-thirds of the patients with necrotizing pancreatitis can be managed conservatively with aggressive intensive care support. In those who develop infected necrosis, one-third can be managed by simple catheter drainage without debridement (either transcutaneous or endoscopic), while those who fail drainage require necrosectomy.3
The therapy for patients with severe acute pancreatitis must be individualized and decisions must be made in a multidisciplinary fashion including gastroenterologist/pancreatologist, critical care physician, surgeon, and interventional radiologist to ensure the best outcome.
Aboulian A, Chan T, Yaghoubian A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. 2010; 251(4):615-619.
Bakker OJ, van Santvoort HC, van Brunschot S, et al. Endoscopic transgastric vs surgical necrosectomy for infected necrotizing pancreatitis: a randomized trial. JAMA. 2012;307(10):1053-1061.
Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62(1):102-111.
Halangk W, Lerch MM, Brandt-Nedelev B, et al. Role of cathepsin B in intracellular trypsinogen activation and the onset of acute pancreatitis. J Clin Invest. 2000;106(6):773-781.
Petrov MS, Kukosh MV, Emelyanov NV. A randomized controlled trial of enteral versus parenteral feeding in patients with predicted severe acute pancreatitis shows a significant reduction in mortality and in infected pancreatic complications with total enteral nutrition. Dig Surg. 2006;23(5-6):336-345.
Sadr-Azodi O, Andrén-Sandberg Å, Orsini N, Wolk A. Cigarette smoking, smoking cessation and acute pancreatitis: a prospective population-based study. Gut. 2012;61(2):262-267.
Tenner S, Baillie J, DeWitt J, Vege SS. American College of Gastroenterology Guideline: management of acute pancreatitis. Am J Gastronterol. 2013;108(9):1400-1416.
van Santvoort HC, Bakker OJ, Bollen TL, et al. A conservative and minimally invasive approach to necrotizing pancreatitis improves outcome. Gastroenterology. 2011;141(4):1254-1263.
van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010;362(16):1491-1502.
Villatoro E, Mulla M, Larvin M. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database of Systematic Reviews 2010, Issue 5. Art. No.: CD002941. DOI: 10.1002/14651858.CD002941.pub3.