Matthew DeLaney, MD, Assistant Professor, Department of Emergency Medicine, University of Alabama at Birmingham.
Carl Germann, MD, FACEP, Assistant Professor, Tufts University School of Medicine, Attending Physician, Maine Medical Center, Portland, ME.
Catherine A. Marco, MD, FACEP, Professor, Department of Emergency Medicine, Emergency Medicine Residency Program Director, University of Toledo College of Medicine and Life Sciences, Toledo, OH.
Pancreatitis is common disease that causes significant morbidity and mortality. In the United States, pancreatitis frequently leads to emergency department (ED) visits and subsequent hospitalization. It is estimated that more than 200,000 patients are admitted to the hospital with pancreatitis each year.1
Gallstones and excessive alcohol use are the two most common causes of acute pancreatitis. Patients at increased risk of developing gallstone pancreatitis include those older than the age of 60 years and those who have stones that are smaller than 5 mm.2,3 While gallstones are the most common cause of pancreatitis, only 4% of patients with gallstones will develop pancreatitis.4
Excessive alcohol use is the second most common cause of pancreatitis. Casual alcohol use is not a risk factor for pancreatitis. There is considerable debate about the role that alcohol plays in the development of pancreatitis. In patients who drink more than five drinks per day, alcohol is thought to have a dose-dependent relationship with the risk of pancreatitis. Other risk factors include smoking and HIV.5 Patients with HIV have a risk that is 35-800 times compared to otherwise healthy patients.4
Behind gallstones and alcohol, idiopathic pancreatitis is the third most common cause of inflammation. Patients in this category typically have no obvious explanation for their symptoms; however, recent data have suggested that these patients may have inflammation from microlithiasis, or non-visualized gallstones, within their biliary system.3 If this theory holds, this third category of patients may be combined with the larger subset of patients suffering from gallstone pancreatitis.
Post-operative pancreatitis can be caused by a variety of surgical procedures and can present a specific diagnostic challenge. Surgeries involving the hepatobiliary system are the most common cause of post-operative pancreatitis. In patients who have had recent surgery, it can be difficult to differentiate between typical post-operative pain and pain that may be caused by an episode of acute pancreatitis. In addition to abdominal surgeries, procedures such as cardiac valve surgery and renal transplant can increase the patient's likelihood of developing acute pancreatitis. Chung et al found that 5.9% of patients who underwent cardiac valve replacement developed acute pancreatitis.6 For reasons that are somewhat unclear, patients with post-operative pancreatitis tend to have more severe disease course and a higher rate of complications. Bragg et al reported that 53% of patients with post-operative pancreatitis developed significant complications, such as pseudocysts, abscesses, and fistulas.7
Certain medications increase the risk of acute pancreatitis. Corticosteroids and less widely used medications such as didanosine and pentamidine, used to treat HIV, are known to cause pancreatitis. Additionally, cases of pancreatitis have been attributed to the use of valproic acid, various chemotherapeutic agents, and assorted statin agents. Interestingly, estrogen has been linked to cases of pancreatitis and is thought to cause inflammation indirectly by increasing triglycerides.8
A recent study found diabetic patients who took glucagon-like peptide-1-based therapies such as exenatide and a dipeptidyl peptidase 4 inhibitor, sitagliptin, had twice the risk of hospitalization for acute pancreatitis when compared to a control group of diabetic patients who were not taking these agents. Many media outlets have reported on the results of this study, and patients taking these agents should be educated about the symptoms associated with acute pancreatitis and should be closely monitored.9
Genetic cases of pancreatitis are thought to be caused by defects in several genes. In these patients, trypsinogen is activated inappropriately and the pancreas undergoes auto-digestion.10
The remaining known causes for pancreatitis are varied and include autoimmune disorders such as systemic lupus erythematosus, hypertriglyceridemia, hypercalcemia, hyperparathyroidism, infection, and traumatic, iatrogenic, vascular, and environmental causes, including cases reported after bites from scorpions and Gila monsters.11 Two lesser known risk factors for developing pancreatitis are pregnancy and type 2 diabetes. In pregnancy, the risk of pancreatitis is thought to be related to an increase in the level of triglycerides. While the mechanism of pancreatitis is less clear in type 2 diabetics, these patients have a 2.8-times greater risk of developing acute pancreatitis when compared to non-diabetic patients.12
Pancreatitis occurs as a result of an inflammatory process in the pancreas. Initially, trypsin, a proteolytic enzyme, is inappropriately activated within the pancreas. Typically this enzyme aids digestion in the duodenum, but when activated in the pancreas, it causes intrapancreatic inflammation and local cell damage.13 Next, the pancreas activates the inflammatory cascade, releasing cytokines that can spread the inflammatory process to other organ systems, including the kidneys and lungs. Ten percent to 15% of patients with pancreatitis develop systemic inflammatory response syndrome (SIRS).14 Patients with more severe cases of pancreatitis are at risk for developing acute respiratory distress syndrome (ARDS). This may occur when inflammatory mediators released by the pancreas cause vasodilatation and pulmonary inflammation, resulting in respiratory distress and potential respiratory failure. In addition, the patients with acute pancreatitis can develop overwhelming sepsis and multi-system organ failure.15 The mortality rate approaches 50% in patients with multi-organ failure and pancreatitis.16
There is typically an inciting event that triggers the release of trypsin from the pancreas. In gallstone pancreatitis, the biliary stones lodge within the common bile duct. As bile starts to accumulate behind the impacted stone, the intraductal pressure increases, which can lead to trypsin release. In cases of alcohol-induced pancreatitis, the trigger mechanism is not as well understood.
Cases of pancreatitis tend to fall into one of two categories: edematous and necrotizing. Edematous pancreatitis, which makes up approximately 80% of the cases, is typically a benign process and has a mortality of less than 1%. Necrotizing pancreatitis, which accounts for the remaining 20% of the cases, is much more severe and has a mortality rate of 10-24 %.17 During the initial assessment in the emergency department, it is difficult to distinguish between these two types.
Epigastric pain can be caused by disorders of the heart, esophagus, stomach, and aorta. Patients with any component of chest pain or epigastric discomfort may have acute coronary syndrome. Aortic dissection should be considered, particularly when there are symptoms such as a "tearing" or "ripping" pain that radiates to the back. Gastroesophageal reflux is a more benign cause of epigastric pain that can mimic pancreatitis. In some cases, pancreatitis can cause peri-umbilical or lower abdominal pain. In these patients, diseases such as appendicitis, diverticulitis, mesenteric ischemia, and other potentially dangerous intra-abdominal issues need to be considered.
Clinical Features. The classic presentation of pancreatitis involves a fairly abrupt onset of upper abdominal pain. Pain will typically reach a point of maximal intensity fairly suddenly, often within an hour, and will persist for more than 24 hours in a majority of cases.15 While the pain can present in the right or left upper quadrant, pain will often localize to the epigastric or peri-umbilical region. The pain is often associated with nausea and vomiting. The pain will radiate to the back in approximately 50% of patients; however, patients can also experience radiations to the lower abdomen and up into the chest.18
In mild cases, patients may have some mild abdominal tenderness to palpation and, as the severity of the disease progresses, this may develop into significant abdominal tenderness with guarding and rebound. In more severe cases, patients may become critically ill and develop hemodynamic instability in the form of fever, tachycardia, and hypotension.
Laboratory Tests. Amylase is secreted by the acinar cells in the pancreas and rises within 6-24 hours. Amylase will stay elevated for anywhere from 3-7 days.19 While an elevated amylase can be suggestive of pancreatitis, a significant number of patients with pancreatitis will have a normal amylase level in the ED. Up to 30% of patients who present with abdominal pain and have a normal amylase are actually suffering from pancreatitis.20 Amylase is a less reliable indicator of pancreatic inflammation in patients who are chronic, heavy drinkers.
Lipase is also released from the acinar cells in the pancreas. Serum lipase levels rise as early as 4-8 hours after the onset of disease, peak at around 24 hours, and remain elevated for up to 14 days. This early rise in serum lipase is helpful in patients who present early in their disease course. In addition, lipase stays elevated for a significantly longer period than amylase. Lipase is more sensitive for pancreatitis in patients who have inflammation from chronic alcohol abuse.21 Lipase is now the preferred laboratory test to use when evaluating patients for pancreatitis. Patients who have a lipase value that is three times the upper limits of normal very likely have pancreatitis, and a lipase level of greater than five times normal is almost 100% specific for acute pancreatitis.22
While lipase appears to be a superior test, both lipase and amylase can be used to identify pancreatitis in patients. Unfortunately, neither of these tests can be used to risk-stratify patients in terms of their risk of developing severe pancreatitis.
Despite the superior test characteristics of lipase over amylase, it is still common practice to order both tests for patients who present with abdominal pain. Studies have shown that adding an amylase value to a lipase value in the workup of a patient offers no diagnostic advantage over ordering a lipase.23,24 This simply adds unnecessary cost. Over the course of the year, eliminating amylase reduced departmental charges by $350,000.25
In patients with pancreatitis, low volume status has been shown to be a significant risk factor for death. A recent study found that a BUN of greater than 20 mg/dL was associated with an odds ratio of 4.6 for mortality. Patients with an elevated hematocrit had a more severe disease course.26 In patients with no signs of hemoconcentration and a hematocrit below 44%, the risk of developing pancreatic necrosis is lowered.27
In patients without a history of alcohol abuse, an alanine aminotransferase (ALT) value three times normal has a 95% positive predictive value for gallstone pancreatitis.28 While an elevated ALT can help identify patients with gallstone pancreatitis, a patient with biliary pancreatitis can have completely normal liver function tests. Up to 20% of patients with acute gallstone pancreatitis will have normal liver function tests.
Patients with acute pancreatitis may have low serum calcium. The exact mechanism behind this hypocalcemia is unclear but is due, in part, to the chelation of calcium by fatty acids released when the pancreas becomes inflamed. Patients with low calcium levels may complain of paresthesias and have hyper-reflexia and QT prolongation on their EKG. These patients should receive calcium replacement as clinically indicated.15,29
A CRP of greater than 130 mg/dL can be indicative of patients who are at increased risk of developing a complicated disease course. Typically this value is obtained at 72 hours, which limits its use in the emergency department. Additionally, CRP is fairly non-specific and can be elevated by other disease processes such as pneumonia or cholangitis.30 Given these limitations, CRP is not part of the ED workup.
Trypsinogen activation peptide (TAP) is typically elevated in patients with acute pancreatitis. TAP levels at the time of admission correlate with disease severity; however, this test is not available to most emergency department practitioners.31 Urine trypsinogen 2 is measured using a point-of-care urine dipstick. While more research is needed, early data show this urine dipstick outperforms CRP in its ability to predict cases of severe pancreatitis. Additional markers such as pro-calcitonin and interleukin have been studied in the evaluation of patients with possible pancreatitis.32
A computed tomography (CT) scan can help identify more severe cases of pancreatitis. Not all patients with acute pancreatitis need imaging during the ED workup; decisions to obtain these studies should be made on a case-by-case basis. Some patients may require emergent imaging to eliminate other potential causes of abdominal pain, while other patients may be appropriately treated and admitted without having any imaging performed.
Transabdominal ultrasound is readily available in most emergency departments and can evaluate patients for possible gallstone pancreatitis. Diagnosing common bile duct stones by ultrasound has a low sensitivity but a high specificity. The presence of common bile duct dilation without common bile duct stones lacks the sensitivity and specificity necessary to identify patients with biliary pancreatitis. Findings such as the presence of mobile gallstones or sludge in the gallbladder are suggestive of gallstone pancreatitis but lack the diagnostic accuracy necessary to confirm the diagnosis.33
In addition to evaluating the gallbladder, transabdominal ultrasound can be used to evaluate the pancreas itself. While views of the pancreas are often limited due to bowel gas, ultrasound can show pancreatic enlargement, echotextural changes, and fluid surrounding the pancreas.34 While not available to emergency practitioners, endoscopic ultrasound is emerging as a highly accurate means of identifying stones in the common bile duct. With increasing use of endoscopic ultrasound, patients who previously have been thought to have idiopathic pancreatitis are now being correctly diagnosed with having a biliary source to their inflammation.35
In the emergency department, practitioners should have a high index of suspicion for patients who present with acute pancreatitis and have no history of alcohol abuse. A reasonable approach would be to obtain a transabdominal ultrasound in these patients.
Contrast-enhanced CT is the standard imaging technique used to identify acute pancreatitis.36 CT scans in patients with acute pancreatitis serve two purposes. First, the CT findings can be used to predict disease severity. Additionally, a CT scan can help identify complications that arise from pancreatic inflammation.33
Balthazar et al have developed a CT Severity Index (CTSI) to categorize the severity of acute pancreatitis using CT findings. The CTSI looks at two categories. First, the severity of the pancreatic inflammation is given a grade of A through E, which corresponds to scores of 0 to 4. The second half of the CTSI looks for the presence of pancreatic necrosis. The extent of necrosis is described as none, less than one-third of the tissue, one-half, or greater than one-half. These four categories are given scores of 0, 2, 4, and 6. The extent of inflammation and the evaluation of necrosis are combined and patients are given a cumulative score ranging from 0 to 10.37 Patients with a CTSI score of greater than 5 have an associated mortality rate that is 15 times higher than patients who have a score of less than 5. In addition to this increased mortality rate, patients who scored greater than 5 had a higher rate of complications and a longer hospital length of stay when compared to patients with a lower score.38 In an observational study, CTSI was found to predict complications and mortality more reliably than the Ranson's criteria.39 (See Table 1.)
One of the limitations of CTSI is that it is based on CT findings on scans performed 72 hours after admission. Patients who are scanned earlier in the course of their disease may not have reached the most severe point in their disease and may not have reached the full extent of pancreatic inflammation or necrosis. While these patients may have lower scores than they would receive if evaluated at 72 hours, a recent study has shown a correlation between the CTSI and the rate of mortality and complications when patients are evaluated at 48 hours.40
In the emergency department, the majority of patients who present with acute pancreatitis do not need a CT scan. Flezler et al evaluated the role that CT plays during the emergency department assessment of patients with acute pancreatitis. In their study group, patients who underwent CT scanning had a longer emergency department length of stay and a prolonged stay in the hospital.41 However, CT scan can be useful in patients with acute pancreatitis who appear severely ill. If severe inflammation, early necrosis, or other complications are seen, these patients may require admission to an intensive care unit or transfer to a facility that has readily available gastroenterology and surgery. In addition, CT can be useful in identifying other disease processes in patients when the source of their abdominal pain is somewhat unclear.
The majority of patients with pancreatitis have a very low rate of morbidity and mortality; however, approximately 20% of patients will have more severe complications. Often it is difficult to identify this at-risk subset of patients based on their presentation in the emergency department. Various authors have developed scoring systems that attempt to identify patients who are at increased risk of having a bad outcome during their episode of pancreatitis. While most of these scoring systems can be difficult to apply during the patient's initial evaluation in the emergency department, recently several scores have been proposed that are applicable for emergency practitioners.
Ranson's criteria (see Table 1) risk-stratify patients by several factors, both at the time of admission and then again during the initial 48 hours of the patient's evaluation.42 The need to obtain data after admission severely limits the applicability of these criteria in the emergency department. The Acute Physiology and Chronic Health Evaluation (APACHE II) scale was derived to evaluate patients who are critically ill, and includes arterial blood gas values and the patient's past medical history as components of the score. Emergently, it can be difficult to obtain a comprehensive past medical history necessary to properly derive an APACHE II score. In addition to the practical limitations of calculating Ranson's and APACHE II scores, neither of these clinical scoring systems has been shown to accurately predict mortality or length of hospitalization in patients with acute pancreatitis.38
The Atlanta Classification of Severe Acute Pancreatitis was developed in an effort to take elements from various scoring systems and radiographic studies and reach a definition of what determines the severity of a course of pancreatitis. The initial criteria, developed in 1992, used the Ranson's criteria, APACHE II scale, and the presence of various CT findings.43 The Atlanta criteria were revised in 2008 and the process of acute pancreatitis was divided into an acute phase and a subsequent phase. The acute phase refers to the first week of disease. During this time frame, the criteria focus on the presence or absence of multi-system organ dysfunction. After the first week, during the subsequent phase, more emphasis is placed on the morphologic CT findings. Patients were categorized as having "mild" or "severe" pancreatitis. These revised criteria proved to be somewhat problematic.44
In 2012, a determinant-based classification system was developed. This system used the presence of pancreatic necrosis and the degree of organ dysfunction as the two major data points that were necessary to categorize the severity of a patient's pancreatitis. CT scan findings were used in addition to laboratory data, physical exam findings, and clinical gestalt to help place patients in one of four categories. Patients were defined as having mild, moderate, severe, or critical acute pancreatitis.45 While these consensus criteria have a very limited role in the emergency department, they do emphasize the risk associated with multi-organ system dysfunction and pancreatic necrosis in patients who present with acute pancreatitis. Emergency practitioners should identify patients with these two findings as being at significantly increased risk of having an adverse outcome.
There are two scoring systems that are applicable in the emergency department. The Bedside Index for Severity of Acute Pancreatitis (BISAP) (see Table 3) and the Harmless Acute Pancreatitis Score (HAPS) (see Table 4) were designed in an effort to identify high-risk patients with pancreatitis during their initial evaluation. The BISAP has five components. Patients are given one point per variable: blood urea nitrogen greater than 25 mg/dL; the presence of the systemic inflammatory response syndrome (SIRS); age greater than 60 years; pleural effusion seen on imaging; and altered mental status, defined as a Glasgow Coma Score of less than 15.46 Patients with scores of 3,4, and 5 have corresponding mortality of 5.3%, 12.7%, and 22.5%. In addition to predicting mortality, the BISAP has been validated to predict the risk of persistent organ failure in patients with acute pancreatitis.47 As with all of the scoring systems for acute pancreatitis, the BISAP is not intended to fully risk-stratify patients, as patients with acute pancreatitis and a low BISAP score are not deemed low risk enough to be discharged home. Patients with an elevated BISAP score are at increased risk of a bad outcome and should receive close monitoring and management.
The HAPS uses even simpler clinical criteria. Patients are evaluated for the following three features: the absence of rebound tenderness and/or guarding, normal hematocrit, and normal serum creatinine. Patients who had all three elements of the score were thought to have a "non-severe" disease course, with 98% positive predictive value.48 As with the BISAP, HAPS is not intended to identify patients that can be appropriately discharged home.
While the HAPS and BISAP can be used to risk-stratify patients in the emergency department with pancreatitis, it is not clear that these scoring systems guide initial therapy or provide any information that would not be apparent to the physician at the bedside. For most emergency practitioners, patients who have high scores in any of the scoring systems would likely be identified as "sick." As with any other "sick patients," common treatments such as fluid resuscitation, airway management, pain management, and admission to an appropriate level of care are reasonable for patients with acute pancreatitis.
Despite the benign course that is seen with most patients, no good data exist that suggest that any subset of patients can be treated as outpatients. The main goals of hospitalization are to reduce the morbidity and mortality associated with acute pancreatitis. Patients with severe disease need to be identified and treated, while less severe cases require pain management, adequate nutrition, and proper consultation by specialists. (See Table 5.) In patients who develop severe disease, the role for treatments such as ERCP, MRCP, and possible surgical intervention is somewhat unclear. In addition, treatments such as enteral feeding, broad spectrum antibiotics, and pain management have all been studied in an attempt to decrease the morbidity and mortality associated with acute pancreatitis.
Patients with pancreatitis often have pain that requires narcotic analgesia. Traditionally, practitioners have been taught to limit the use of morphine out of concern that morphine and its analogs may cause a spasm of the sphincter of Oddi, which could lead to a worsening of the patient's symptoms. In an effort to avoid this potential worsening, meperidine became a popular agent used to treat patients' pain. Multiple studies have shown meperidine to have questionable efficacy and a problematic safety profile. Additionally, more recent studies have shown that morphine has a minimal impact on the sphincter of Oddi and is a suitable agent to use for pain control in the setting of pancreatitis.49 Other opioids such as fentanyl and hydromorphone, as well as nonsteroidal anti-inflammatories, can be used. Once the patient is admitted, techniques such as thoracic epidural analgesia can be used to provide further pain control and to limit the potential for systemic effects that are common with traditional pain medications.50
Patients with acute pancreatitis often require aggressive fluid resuscitation. Cytokines and other inflammatory mediators released from the pancreas cause vasodilatation and decrease intravascular volume, which can lead to end-organ hypoperfusion. Studies have found that patients who receive inadequate fluid resuscitation have an increased morbidity and mortality. In the emergency department, most patients with acute pancreatitis should receive a bolus of 1-2 liters. After this initial bolus, patients should be placed on an infusion with a rate of 250-300 mL/hr. Fluid therapy can be adjusted to maintain a urine output of 0.5 mL/kg/hr. There is no consensus on the most appropriate type of IV fluid to use in patients during the initial resuscitation. While most patients need aggressive fluid resuscitation, therapy should be adjusted for each individual patient. Patients who show signs of volume overload such as hypoxia, jugular venous pulsations, or crackles on lung exam may require a less aggressive approach to fluid resuscitation.19
Traditionally it was thought that feeding these patients would cause additional stimulation to the pancreas and would worsen the course of the disease. In the emergency department, patients should be made NPO during their initial workup and treatment, and further decisions regarding nutrition should be made in consultation with the admitting service. Even in the most well-appearing patients, there are few data to suggest that patients with acute pancreatitis can tolerate early oral intake, however. Approximately 20% of patients will have a relapse of pancreatitis when they resume eating.51
Patients with acute pancreatitis who experience pancreatic necrosis have a significant increase in mortality. Numerous studies have evaluated the role that antibiotics play in the prevention of pancreatic necrosis. In 2001, a meta-analysis found that in patients with acute necrotic pancreatitis, using prophylactic antibiotics reduced the rates of sepsis, caused a decrease in the need for surgical intervention, and led to an overall mortality benefit.52 A more recent double-blinded, randomized, controlled trial compared patients treated with a placebo to patients given ciprofloxacin and metronidazole and showed no significant difference in the rate of complications, infection, or overall mortality. While the benefit from antibiotics in the treatment of pancreatitis is unclear, there are well-documented complications from antibiotic therapy, including adverse drug reactions and emerging rates of drug-resistant pathogens. Emergency practitioners should not use antibiotics for the treatment of acute pancreatitis without a clear consideration of potential risks and benefits.53
Endoscopic retrograde cholangiopancreatography (ERCP) has been used to treat acute pancreatitis thought to be secondary to gallstones. The initial theory behind this procedure was that removing obstructions within the biliary tree would relieve the upstream pressure and reduce the degree of inflammation in the pancreas. Removing these gallstones is also thought to lower the risk of associated cholangitis. Typically, ERCP is performed within the first 48-72 hours of the hospital course.
The data on the benefits of performing ERCP are somewhat varied. A 2004 Cochrane review evaluated outcomes in patients with pancreatitis who underwent ERCP. Patients with severe disease who underwent ERCP were found to have a lower rate of complications when compared to patients who were managed with more conservative non-invasive therapy. While complication rates were lower in the ERCP group, these patients had no reduction in mortality. In patients with mild pancreatitis, there was no difference in the rate of complications or the rate of mortality between the two groups.54 While the Cochrane review failed to show a mortality benefit, later studies have shown a survival benefit in a select group of patients with severe gallstone pancreatitis.55
Approximately 10% of patients who undergo ERCP will have a complication from this procedure. The most common complication is the development of post-ERCP pancreatitis. While less common, other complications such as bleeding, infection, and biliary perforation are well-documented risks associated with the procedure.56
For emergency practitioners, it is important to consider the need for ERCP in all patients who present with acute pancreatitis. Only a small subset of these patients will actually need to have this procedure performed, but there is a subset of patients who will benefit. Patients with presumed biliary pancreatitis who show signs of biliary sepsis, cholangitis, worsening jaundice, or elevated bilirubin may benefit significantly from an ERCP.
Magnetic retrograde cholangiopancreatography (MRCP) is a noninvasive test that can be used to evaluate patients for possible biliary obstruction. Known as the "pancreatogram," MRCP provides views similar to the ERCP. Unlike the ERCP, which can be both diagnostic and therapeutic, MRCP does not allow for any interventions. MRCP is also limited in its ability to detect small biliary stones and ductal strictures, which are seen more easily on ERCP. While it is not needed in every patient who presents with pancreatitis, when available, MRCP may provide an alternative diagnostic test in patients with possible biliary pancreatitis who are unable to undergo an ERCP.57
Endoscopic ultrasound is an emerging technology that may benefit select patients. Endoscopic ultrasound is helpful in identifying biliary stones and tumors and has been used to identify patients who might benefit from an ERCP.58
Patients who present with gallstone pancreatitis need urgent evaluation by a surgery team. Up to 50% of patients with gallstone-induced pancreatitis will have a recurrence of pancreatitis within two months unless they undergo a cholecystectomy. While cholecystectomy will eliminate the source of future gallstones, patients with retained gallstones may have recurrent pancreatitis after having their gallbladder removed. Patients with retained stones may benefit from ERCP. Cholangiography allows the provider to evaluate the biliary system for retained stones, and is similar to ERCP and endoscopic ultrasound in terms of its accuracy in identifying biliary obstructions.59 A recent randomized, controlled trial evaluating patients with gallstone pancreatitis found that early cholecystectomy reduced hospital length of stay by approximately 1.5 days.60
Apart from performing cholecystectomy and cholangiography, there is a limited role for surgical intervention in the treatment of acute pancreatitis. Patients with significant pancreatic necrosis may benefit from surgical debridement. Patients who have infected pancreatic necrosis and show signs of clinical deterioration may need urgent surgical intervention. For patients who are thought to have sterile necrosis, there is little role for urgent instrumentation. Malangoni et al found that delaying or foregoing surgical debridement for patients with sterile necrosis resulted in a decreased mortality rate. Likewise, patients who underwent surgical intervention had a significantly higher rate of nosocomial infection. In addition, patients who undergo hepatobiliary surgery are at risk of developing worsening pancreatitis. Procedures such as pancreatic biopsy and interventions on the common bile duct run a higher risk of causing post-operative pancreatitis, but most other intra-abdominal procedures do carry a risk of causing worsening pancreatitis.35 While not all patients with suspected gallstone pancreatitis will need emergent intervention, it is prudent to consult both gastroenterology and surgery services during the intitial workup for co-management and consideration for procedural intervention.
Chronic Pancreatitis. Patients with chronic pancreatitis pose an interesting, and at times frustrating, challenge for emergency practitioners. The etiology of chronic pancreatitis is unclear, and to date there are no readily available diagnostic tests used to identify this subset of patients. In addition, patients with chronic pancreatitis are heavy users of health care resources. These patients often require significant pain medications.
Chronic pancreatitis is thought to be caused by progressive and often increasing levels of inflammation in the pancreas. Typically, patients have several years of recurrent episodes of acute pancreatitis before developing chronic pancreatitis. In a study of chronic pancreatitis in Europe, the average patient was 50-70 years of age when they were diagnosed with chronic disease. Despite this predominance, there are case reports of patients developing chronic pancreatitis between the ages of 20 and 30 years.61 Ongoing alcohol abuse is thought to be the causative factor of ongoing inflammation in up to 70% of patients with chronic pancreatitis. As with acute pancreatitis, alcohol is responsible for most of the cases of chronic pancreatitis; however, conditions such as autoimmune disease, hypertriglyceridemia, and ongoing pancreatic duct obstruction can cause a patient to develop chronic pancreatitis. Notably, up to 30% of patients who develop chronic pancreatitis are diagnosed as having idiopathic pancreatitis and have no clear etiology identified.62
For patients with chronic pancreatitis, pain is often the predominant initial symptom.63 Amman et al identified these two subsets of patients and found that patients with short painful episodes were at low risk of developing complications and had essentially no need for surgical intervention. Patients with constant pain were at increased risk of developing structural changes, including pseudo-cyst formation, biliary strictures, and pancreatic stones, all of which might improve with surgical intervention.64 It is thought that as the chronic changes progress, patients will have a reduction in the severity and frequency of their pain; however, research in this area is limited.65
It is difficult to identify patients with chronic pancreatitis. To date, no readily available laboratory tests show enzymatic changes suggestive of chronic pancreatic dysfunction. Thirty percent to 50% of patients with chronic pancreatitis will develop diabetes from endocrine dysfunction. In addition, patients with chronic pancreatitis may develop malabsorption due to a deficiency of enzyme release due to chronic changes. It is estimated that patients must lose 90% of their pancreatic function before they develop any demonstrable loss of enzyme function.66
As with acute pancreatitis, there is poor correlation between laboratory values and the severity of disease in patients with chronic pancreatitis. Patients may report having a "burned out" pancreas that, while capable of producing pain, is not capable of elevating the levels of amylase and lipase.
It can be difficult to treat patients with chronic pancreatitis. One of the obstacles to treating patients with chronic pancreatitis is the overlap between substance abuse and the development of a chronically painful condition. By definition, patients who develop chronic pancreatitis due to ongoing alcohol abuse have a predilection toward abusing addictive substances. To treat chronic pancreatitis, patients typically receive narcotic analgesia, which has a well-documented and significant risk of causing desensitization and a need for increasing doses to obtain adequate levels of pain control. In addition, patients who are prone to addiction may be at increased risk of developing addiction to other substances.67 Up to 70% of patients with chronic pancreatitis have problems with alcohol abuse. As a result, a significant portion of patients with chronic pancreatitis are at increased risk of becoming addicted to other substances, including the medications used to treat their chronic disease state. This risk of co-dependency is poorly studied; however, providers should be cognizant of this risk when treating patients who present with chronic pancreatitis and a history of substance abuse.
The mainstay of treatment for chronic pancreatitis is to limit exposure to the offending agent. Patients are advised to avoid dietary fat and alcohol in an effort to limit ongoing inflammation and pancreatic damage. Pancreatic enzyme supplementation has been studied in patients with chronic pancreatitis, but to date, the data to support their use are limited.68
Despite these attempts to reduce pain, patients frequently require narcotic analgesia to treat their symptoms. Given the risk of addiction associated with narcotics, patients with chronic pain may be best managed in a pain clinic. In addition to narcotic analgesia, patients with chronic pain may be treated with non-narcotic modulators of chronic pain such as gabapentin and selective serotonin inhibitors like paroxetine. While these agents have well-established efficacy in the treatment of chronic pain, their use is beyond the scope of practice of most emergency practitioners.
Disposition Decision. Well-appearing patients who present with frequent episodes of alcohol-induced pancreatitis can be particularly difficult to manage in the emergency department. Often these patients will have a history of alcohol use, abdominal pain, and a slightly elevated lipase, but will otherwise have a benign appearance. The difficulty with this approach is that, to date, there is almost no literature to support outpatient management of any patient who presents with pancreatitis. Despite significant efforts to risk-stratify patients with acute pancreatitis, there are no historical elements, physical exam findings, laboratory values, or imaging studies that can reliably identify a subset of patients that is safe to discharge from the emergency department.
Sphincter of Oddi Dysfunction. Patients with sphincter of Oddi dysfunction represent a different subset of patients who present with chronic upper abdominal pain and may complain of symptoms consistent with chronic pancreatitis. These patients have typically undergone a cholecystectomy and have chronic episodes of upper abdominal pain with no other signs of gastrointestinal distress. This poorly defined patient population is thought to have a functional biliary disorder. Patients will typically have undergone extensive hepatobiliary testing, including ERCP and HIDA scan, and will have an essentially normal workup. In the emergency department it is important to recognize the existence of these chronic pain patients, treat their pain adequately, while at the same time ensuring that no other emergent disease process is causing their symptoms. Beyond their course in the emergency department, these patients can be difficult to identify and manage, and their treatment often involves a multidisciplinary approach.69
Pancreatitis is a common cause of abdominal pain in patients who present to the emergency department. The majority of patients with acute pancreatitis will have a benign clinical course; however, it is difficult to identify the small subset of patients who are at increased risk of having a complicated course and an adverse outcome. In the emergency department, the primary goals of treatment include providing adequate analgesia, limiting oral intake, and admitting the patient to the appropriate level of care. Tests such as ultrasound, CT scan, and emergent ERCP may be helpful in some patients, but are not a necessary part of the workup for the large majority of patients.
- Russo MW, Wei JT, Thiny MT, et al. Digestive and liver diseases statistics, 2004. Gastroenterology 2004;126:1448-1453.
- Mitchell RM, Byrne MF, Baillie J. Pancreatitis. Lancet 2003;361:1447-1455.
- Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med 2006;354:2142-2150.
- Mayumi T, Takada T, Kawarada Y, et al. Management strategy for acute pancreatitis in the JPN Guidelines. J Hepatobiliary Pancreat Surg 2006;13:61-67.
- Sadr-Azodi O, et al. Cigarette smoking, smoking cessation and acute pancreatitis: A prospective population-based study. Gut 2012;61:262.
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