Acute pancreatitis, an inflammatory disorder of the pancreas, is the leading cause of hospital admissions for gastrointestinal dysfunction in the United States and many other countries. Gallstones and alcohol abuse are long-established risk factors, but several new causes have emerged along with new aspects of pathophysiology that have increased the understanding of this disorder. The increased incidence of acute pancreatitis has reinforced the need for effective management of acute pancreatitis. In this article, compiled from the journal Lancet, Medical Pulse reviews how to manage patients with acute pancreatitis, with emphasis on diagnosis, differential diagnosis, complications, prognostic factors, treatment, and prevention of recurrence, as well as the transition from acute to chronic pancreatitis.
Morbidity rate
The annual incidence of acute pancreatitis ranges from 13 to 45/100,000 people. acute pancreatitis was the most common discharge diagnosis for gastrointestinal disorders and liver disease among patients treated in U.S. hospitals in 2009. The number of acute pancreatitis as the most predominant diagnosis was 30% higher than in 2000. In addition, acute pancreatitis was the second highest cause of total length of stay, contributed the most to total costs, and was the fifth most common cause of inpatient death.
Etiology
Gallstones and alcohol abuse are the main risk factors for acute pancreatitis. However, over the course of 20 to 30 years, the risk of biliary pancreatitis is unlikely to exceed 2% in patients with asymptomatic gallstones and the risk of alcoholic pancreatitis is unlikely to exceed 2 to 3% in heavy alcohol abusers. Other factors, possibly genetic, may play only a partial role. Drugs represent an additional etiology of acute pancreatitis (e.g., Figure 1).
Pathogenesis
Mechanism of cell injury (omitted)
Alcoholic pancreatitis (as shown in the figure)
Figure Effects of alcohol on pancreatic alveoli and stellate cells, based on experimental in vitro and in vivo evidence.
Classification
The Atlanta classification is the standard classification for the severity of acute pancreatitis. The recently published revised classification defines clinical and imaging severity for acute pancreatitis. The clinical severity of acute pancreatitis is divided into three categories: mild, moderate, and severe (Table 2).
Diagnosis
Major diagnostic methods
Clinicians are most interested in confirmation of the diagnosis and exclusion of the differential diagnosis. According to the revised Atlanta classification, acute pancreatitis is diagnosed if two of the following three criteria are met: abdominal pain (persistent acute onset, severe epigastric pain, usually radiating to the back); serum lipase (or amylase) activity higher than three times the upper limit of normal; or characteristic presentation of acute pancreatitis on contrast-enhanced CT, or MRI, or abdominal ultrasonography. Diagnostic imaging is essential in patients with mild enzyme elevations. Importantly, pancreatic enzyme concentrations at the time of presentation are not related to the severity of the disease. The disease may be severe or even fatal with only a slight increase in pancreatic enzymes (<3 times the normal value).
Laboratory tests
In addition to serum amylase and lipase, the following variables should be determined at admission: complete blood count without differences; electrolyte concentrations; blood urea nitrogen (BUN), creatinine, serum glutamate aminotransferase, serum glutamate oxalase, alkaline phosphatase, and glucose; coagulation status; and total protein. Arterial blood gas analysis, at oxygen saturation levels below 95% usually indicates that the patient is short of breath. The frequency of repeat tests depends on the clinical course.
Electrocardiogram and chest radiograph
≤50% of cases of ST-segment elevation were recorded, mainly in the posterior wall, without myocardial infarction. Chest radiographs in both planes may show pleural effusion and pulmonary infiltrates, both signs of severe disease. Abdominal surface tomograms (upright or left lateral recumbent) can also be used for diagnosis. Intestinal obstruction is demonstrated by an anterior circuit (isolated intestinal collaterals in the left upper or middle abdomen) or by a colonic cut-off sign (curvature of the left colon or absence of gas in the descending colon). Pancreatic calcification indicates evidence of acute pancreatitis – i.e., the patient has an acute episode superimposed on chronic pancreatitis, rather than a first episode of acute pancreatitis.
CT
An unenhanced CT scoring system assesses the extent of pancreatic and peripancreatic inflammatory changes (Balthazar score or Pancreatic Size Index), or two types of peripancreatic inflammatory changes and extra-pancreatic complications (mesenteric edema and ascites score, extra-pancreatic score, and extra-pancreatic inflammatory score on CT). Both CT scores require intravenous contrast to determine the presence and extent of pancreatic parenchymal necrosis. Contrast-enhanced CT is the gold standard for diagnostic imaging and helps to determine the severity of disease (includes axial-enhanced CT pancreatic scans, performed at admission, day 1, 10, and 20 in patients with acute pancreatitis).
Prognostic variables
Existing scoring systems appear to maximize prediction of persistent organ failure in acute pancreatitis. Complex combinations of prediction rules are more accurate but cumbersome, as clinical use is limited and new methods are urgently needed clinically.
Treatment
Patient management begins in the emergency room, where acute pancreatitis has been confirmed, with the initiation of risk classification and basic treatment. Treatment includes early rehydration support, analgesia, and nutritional support. Patients undergoing hemodynamic resuscitation should have the head of the bed elevated and receive continuous pulse oximetry along with supplemental oxygenation.
As to what should be infused, the American College of Gastroenterology (ACG) recommendations and the International Pancreatic Association (IPA)/American Pancreatic Association (APA) guidelines are very similar: the ACG indicates that lactate Ringer’s solution may be the first choice for isotonic crystalloid replacement fluid, while the IAP/APA states that lactate Ringer’s solution should not be given to a small number of patients with hypercalcemia at the time of initial rehydration support. These two sets of guidelines also differ in terms of infusion rate, with the ACG recommending 250 to 500 mL/h and the IAP/APA supporting 5 to 10 mL/kg per hour. If the ACG recommendation is at an assumed patient weight of 70 kg, the IAP/APA guidelines would result in much higher infusion rates of 50 to 700 mL/h. Only the ACG firmly recommends that infusion should be initiated within the early initial 12 to 24 hours, when intravenous rehydration is most beneficial, with little benefit beyond this time.
Management of local complications
Necrosis
Prophylactic application of antibiotics is not indicated. Surgical resection of pancreatic necrosis can be performed by open laparoscopy or by necrotic tissue resection (open – or closed – continuous lavage). These approaches are not competing, but complementary to other techniques. There are no guidelines or consensus on whether surgical intervention should be performed in late episodes of pancreatitis, at least 2 weeks later.
Pseudocysts
Prognostic factors for progression of pseudocysts alcohol abuse and initial severe disease. Spontaneous resolution occurs in patients with pseudocysts, and this discriminating prognostic factor is the absence or mild symptoms and the absence of <4 cm pseudocysts in diameter. Symptomatic pseudocysts can be successfully decompressed using endoscopic gastric anastomosis [drainage] of pancreatic cysts.
Catheter rupture
Duct rupture may result in unilateral pleural effusion, pancreatic ascites, or amplified effusion. If the rupture is focal, placement of a bridging stent by endoscopic retrograde cholangiopancreatography will promote duct healing. When the duct rupture is extensive in area of necrosis, optimal management requires a multidisciplinary team of endoscopists, interventional radiologists, and surgeons.
Peripancreatic vascular complications
Splenic vein thrombosis has been reported to be found in 20% of patients with acute pancreatitis who undergo imaging. The risk of bleeding gastric varices is less than 5%, and splenectomy is not recommended. Pseudoaneurysms are rare, but cause serious complications in 4 to 10% of cases. Mesenteric angiography with catheter artery embolization is the first-line treatment.
Management of extra-pancreatic complications
Extrapancreatic infections, such as bloodstream infections, pneumonia, and urinary tract infections, occur in up to 24% of patients with acute pancreatitis and can double the mortality rate. If sepsis is suspected, it is reasonable to start antibiotics while awaiting blood culture results. If cultures are negative, antibiotics should be discontinued to reduce the risk of fungemia or C. difficile infection.
Post-illness recuperation
Resume eating
Basic treatment of acute pancreatitis should be continued until the patient demonstrates distinct clinical improvement (absence of pain, normal temperature and abdominal examination). There are no recommendations for the presence of severe acute pancreatitis; this decision depends on an individual basis. With mild acute pancreatitis, transoral feeding will be resumed as soon as possible, as recommended by the European guidelines for parenteral enteral nutrition. When and how feeding will be resumed has not been determined. The initiation of re-feeding does not depend on the normalization of lipase. This decision may be left to the patient himself – that is, when they are hungry is they eat.
Imaging
Patients with unexplained acute pancreatitis should undergo ultrasound to rule out stones in the gallbladder or bile ducts. Intraluminal ultrasound or magnetic resonance cholangiopancreatography presentation may rule out tumors. Tumor-associated acute pancreatitis may appear to resolve before reoccurring.
Transient secretory and endocrine pancreatic insufficiency
Transient secretory and endocrine pancreatic insufficiency can occur during the healing process. Therefore, pancreatic function should be monitored after 3 months of treatment for acute pancreatitis. Pancreatic enzyme replacement is usually not necessary, but can be used temporarily after severe episodes. Endocrine pancreatic function should be checked after 3 months (by fasting and postprandial glucose concentrations, or by measuring HbA1C). Severe acute pancreatitis is often followed by diabetes.
Transition to chronic pancreatitis
In a German study, over the course of almost 8 years, only alcoholics progressed to chronic pancreatitis, independent of the severity of the first acute pancreatitis and the discontinuation of alcohol and nicotine. Ductal scarring can be observed by endoscopic retrograde cholangiopancreatography, and even after healing, scarring leads to the diagnosis of chronic pancreatitis and pancreatic enzyme replacement.
Prevention
A study showed that medical staff intervention (through nurse communication with patients about how to eat and drink in moderation) intermittently for 6 months significantly reduced the recurrence of alcohol-induced pancreatitis over 2 years. In patients with mild cholestatic acute pancreatitis, cholecystectomy should be completed before hospital discharge. Patients with acute pancreatitis of necrotizing biliary origin should delay cholecystectomy to prevent infection until active inflammation subsides or fluid collections resolve or stabilize. In patients who cannot undergo surgery, recurrence rates are reduced by endoscopic sphincterotomy.
Prophylactic stent placement and pre-cut sphincterotomy are recommended for pancreatitis after transendoscopic retrograde cholangiopancreatography. Indomethacin inhibits prostaglandin production in vivo and is a potent inhibitor of serum phospholipase A2 activity within acute pancreatitis. more than 30 years ago, we found that indomethacin administration after an episode of acute pancreatitis reduced mortality in mice. Later, indomethacin suppositories were applied to patients with acute pancreatitis to reduce the frequency and intensity of pain. And then this good efficacy of indomethacin was forgotten until routine rectal administration of the recommended 100 mg diclofenac or indomethacin before and after endoscopic retrograde cholangiopancreatography. In contrast, the prophylactic use of conventional nitroglycerin, ceftazidime, growth inhibitors, gabapentin, ustekin, glucocorticoids, antioxidants, heparin, interleukin 10, hexoketocine, semamod and recombinant platelet-activating factor acetylhydrolase is not recommended. A network meta-analysis showed that rectal NSAIDs were superior to pancreatic duct stents for pancreatitis after endoscopic retrograde cholangiopancreatography.
Summary
For the clinical management of acute pancreatitis, the Atlanta Classification has been revised and will stand the test of clinical application. The new prognostic variables used to assess the severity of pancreatitis appear to have been exhausted. The hope brought by the new HPAS, by comparing it with existing variables, can identify patients with mild pancreatitis who do not need intensive treatment. Over the past few years, researchers have become very interested in patient transfer criteria, rehydration and nutritional approaches, and treatment of infections. Now, they are focusing their attention on recurrent episodes of pancreatitis caused by alcohol, and the prevention of pancreatitis after endoscopic retrograde cholangiopancreatography.