Pancreatitis


Article Author:
Nabeeha Mohy-ud-din


Article Editor:
Suzanne Morrissey


Editors In Chief:
Marie Amma
Jennifer Barrow
Darcy Duncan


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
2/19/2019 4:14:57 PM

Introduction

Acute pancreatitis is an acute response to injury of the pancreas. Chronic pancreatitis can result in permanent damage to the structure and endocrine and exocrine functions of the pancreas. In the United States, about 200,000 hospital admissions annually are due to acute pancreatitis, and this number has been increasing.[1]

Etiology

The two most common causes of acute pancreatitis in the United States are gallstones (35% to 40% of cases) and alcohol use (30% of cases).[2] However, the causes are extensive and include, but are not limited to, the following: autoimmune pancreatitis, hypertriglyceridemia, post-endoscopic retrograde cholangiopancreatography (ERCP), genetic risk (gain of function mutations in PRSS1, mutations in CFTR and SPINK1 genes), pancreatic duct injury and medications. The drugs most strongly associated with acute pancreatitis are azathioprine, 6-mercaptopurine, didanosine, valproic acid, angiotensin-converting–enzyme inhibitors, and mesalamine. Other rare causes include biliary sludge and microlithiasis, biliary obstruction, hypercalcemia, infections (mumps, coxsackievirus, hepatitis B, cytomegalovirus amongst others), toxins, vascular disease-causing pancreatic ischemia, anatomic abnormalities such as choledochal cysts, and idiopathic causes.

The most recent American College of Gastroenterology guidelines recommend checking the triglyceride level in a patient who has no evidence of gallstones and no history of significant alcohol use.[3]  They recommend that this should be considered the cause if it is greater than 1000 mg/dl. The guidelines also state that for patients older than 40 years of age, consideration of a pancreatic tumor as the cause of pancreatitis should be made. Furthermore, genetic testing can be considered for those younger than 30 years of age if they have a family history of pancreatic disorders and no other cause of pancreatitis is identified.

The most common cause of chronic pancreatitis is ethanol abuse. Smoking is also an important risk factor. There are several other causes which include tropical pancreatitis, idiopathic pancreatitis, ductal obstruction (pancreas divisum, pseudocysts, stones, tumors, and trauma), mutations in cystic fibrosis genes, hereditary pancreatitis and systemic diseases such as systemic lupus erythematosus.

Epidemiology

Acute pancreatitis accounts for about 275 000 hospital admissions annually.[2] Eighty percent of patients admitted with pancreatitis usually have mild disease and can be discharged within a few days. Overall mortality of acute pancreatitis is approximately 2%.[2]  The relapse rate of acute pancreatitis is between 0.6% to 5.6%, and this depends on the etiology of pancreatitis. The relapse rate is highest when pancreatitis is due to alcohol use.[4]

Chronic pancreatitis has an annual incidence rate of 5 to 12 per 100,000 people. The prevalence of chronic pancreatitis is 50 per 100,000 people. The most common age group is 30 to 40 years, and it occurs more in men than women.[5]

Pathophysiology

The pathogenesis of acute pancreatitis can occur by the following mechanisms: pancreatic duct and acinar injury. In acute pancreatitis, digestive enzymes within the pancreas are not secreted properly, and this leads to auto-digestion and inflammation of the pancreas.

Alcohol can cause acute pancreatitis through direct toxicity and immunologic processes.[6] Gallstones can lead to temporary obstruction of the pancreatic duct, and this is also believed to be the mechanism of ERCP-induced pancreatitis.

Chronic pancreatitis can occur by repeated acute attacks which leads to inflammatory infiltrates and fibrosis within the pancreas. Over time, this leads to pancreatic insufficiency.

Histopathology

Histopathological characterization of acute pancreatitis depends on the severity of the disease, specifically the absence or presence of necrosis. The disease can be classified as:

  • Interstitial (or edematous) pancreatitis
  • Hemorrhagic-necrotizing pancreatitis

In acute pancreatitis, the pancreas can be edematous, necrotic and surrounded by fat stranding. In mild pancreatitis, fat necrosis is minimal; whereas, with severe pancreatitis, there are large foci of fat necrosis that have merged. This is associated with parenchymal destruction and focal hemorrhages.

Chronic pancreatitis is characterized by mononuclear infiltrates and fibrosis. There can be calcifications present within the pancreas as well.

History and Physical

Acute pancreatitis most commonly presents with abdominal pain, which usually occurs in the upper abdomen and radiates to the back. It is described as severe and is frequently associated with nausea and vomiting.

In regards to medical history, healthcare providers should ask the patient specifically about the previous history of gallbladder disease, history of hyperlipidemia, and previous episodes of pancreatitis. A detailed social history should be obtained including a history of alcohol use. Clinicians should ask patients about previous procedures such as ERCP, and they should obtain a list of medications that the patient is currently taking. Patients should also be asked about a family history of pancreatic disorders.

The physical examination should begin with the vital signs: pulse, blood pressure, respiratory rate, and temperature. The vital signs can also assess the patient’s hydration status. The presence of jaundice indicates biliary tree obstruction. An abdominal exam should be performed, and this may reveal abdominal tenderness/guarding and decreased bowel sounds if an ileus is present. Grey-Turner sign is present where there is ecchymosis in the flanks. Cullen's sign is present when there is ecchymosis around the umbilicus. These signs can signify pancreatic necrosis leading to blood in the abdomen.[7] A patient with severe pancreatitis may also present with mental status changes.

Chronic pancreatitis can present with abdominal pain, nausea, and vomiting. However, it can also be painless, and patients can present with steatorrhea and weight loss.

Evaluation

Current ACG guidelines recommend that a diagnosis of acute pancreatitis should include at least two of the following: abdominal pain consistent with acute pancreatitis, a serum lipase level at least three times the upper limit of the normal range, and findings of acute pancreatitis on abdominal imaging. These guidelines also state that imaging (including computed tomography scans and/or magnetic resonance imaging (MRI) need not be performed in every patient at the time of diagnosis, but in those whose symptoms fail to resolve or in whom the diagnosis remains in question 2 to 3 days after admission to hospital.[3]

Whenever a patient with acute pancreatitis is admitted to the hospital, an assessment of the initial severity of pancreatitis, including evidence of organ failure (particularly respiratory, cardiovascular or renal compromise) should be made. The recently revised Atlanta classification can be used to classify these patients as mild, moderately severe or severe cases of acute pancreatitis.[8]

Laboratory work ordered on admission should include a complete metabolic panel, complete blood count, serum lipase, lactate, serum triglycerides, and C-reactive protein (CRP) levels. The best assessment of evolvement of acute pancreatitis can be made using a rising blood urea nitrogen (BUN) level or a rising hematocrit level. [9]Systemic inflammatory response syndrome (SIRS) criteria can also be used to assess the clinical status of the patient.[9]

In patients with chronic pancreatitis, amylase/lipase levels can be elevated or normal. Fecal fat, stool elastase, and alpha-1-antitrypsin level can also be checked for these patients. An HbA1c level can provide an estimate of the possible endocrine dysfunction caused by chronic pancreatitis. Other tests including IgG4/ANA levels, genetic testing (CFTR, SPINK1, PRSS1) can be ordered if the patient is young or has a positive family history. Imaging studies including Magnetic resonance cholangiopancreatography (MRCP) or CT scans can be ordered. These imaging studies may reveal pancreatic calcifications, pancreatic ductal obstructions or dilations.

Treatment / Management

The most important step in the management of acute pancreatitis is aggressive fluid resuscitation. Current guidelines define this as 250 to 500ml per hour of isotonic crystalline fluids.[3] However, adjustments can be made if there is a concern for cardiovascular or renal comorbidities. One trial suggested the superiority of Ringer’s lactate as compared with normal saline in reducing inflammatory markers.[10] Fluid requirements should be frequently reassessed, and as stated above BUN and hematocrit levels can be used to assess the hydration status of the patient.

In regards to nutrition in acute pancreatitis, oral feedings can be started immediately if the patient can tolerate them. In severe pancreatitis, enteral feedings are preferred over parenteral feedings as there is decreased risk of infections, surgical interventions, and lower mortality. Analgesia is also an important aspect of management of pancreatitis and can include the use of intravenous (IV) opioids.

For patients with acute pancreatitis and acute cholangitis, a gastroenterology consult should be placed, and an urgent ERCP (within 24 hours) is recommended. For patients who have gallstones within the gallbladder, a cholecystectomy can be performed within the same admission. However, if there is a concern of necrotizing AP, surgery can be delayed until the surrounding inflammation has decreased.

For patients with acute pancreatitis caused by hypertriglyceridemia, current standard therapy involves placing the patient on an insulin drip (this activates lipoprotein lipase). Fibrates can also be prescribed for the patient and consideration for apheresis can be made. It is important to state, that there is no role for antibiotics in acute pancreatitis in the absence of infectious complications.

The treatment for chronic pancreatitis involves pain control, counseling regarding smoking and alcohol cessation and pancreatic enzyme replacement. Most importantly, patients should be encouraged to eat a low-fat diet in small meals. If patients fail medical therapy, surgery and extracorporeal shock wave lithotripsy (ESWL) for duct stones can be recommended.

Differential Diagnosis

The differential diagnosis of acute pancreatitis includes other causes of epigastric abdominal pain such as peptic ulcer disease, choledocholithiasis or cholangitis, cholecystitis, perforated viscus, mesenteric ischemia and intestinal obstruction amongst others. The diagnosis of AP can be differentiated from these conditions based on clinical features and laboratory values. However, when significant doubt exists, a contrast-enhanced abdominal computed tomography (CT) scan can be performed for further evaluation.

Differentials of chronic pancreatitis include acute pancreatitis, pancreatic malignancy, and chronic mesenteric ischemia among others.

Prognosis

Mortality from acute pancreatitis is about 2%.[2] After an episode of acute pancreatitis, endocrine and exocrine insufficiency can develop in about 20% to 30% of patients.[5][10][11] Risk factors for recurrent attacks include the etiology of the first attack, the severity of the initial attack, and the degree of pancreatic structural damage. There are several scoring systems that can stratify the severity of acute pancreatitis: Acute Physiology and Chronic Health Evaluation II (APACHE II), APACHE combined with scoring for obesity (APACHE-O), the Glasgow scoring system, the Harmless Acute Pancreatitis Score (HAPS), PANC 3, the Japanese Severity Score (JSS), Pancreatitis Outcome Prediction (POP), and the Bedside Index for Severity in Acute Pancreatitis (BISAP).[11] These scoring systems are not superior to frequent reassessment by clinicians and have been shown to have a high false-positive rate.

Complications

Complications of acute pancreatitis can be divided into local and systemic. Local complications include the following:

  • Pancreatic pseudocyst
  • Walled-off necrosis
  • Peri-pancreatic fluid collection
  • Acute necrotic collection

Peripancreatic fluid collections usually develop in less than 4 weeks after the initial presentation of pancreatitis whereas a pseudocyst and walled off necrosis more than 4 weeks after the onset of acute pancreatitis.

Systemic complications include the following:

  • Acute respiratory distress syndrome (ARDS)
  • Compartment syndrome
  • Acute kidney injury (AKI)
  • Disseminated intravascular coagulation(DIC)

Chronic pancreatitis has several complications including:

  • Formation of pseudocysts
  • Diabetes
  • Pseudoaneurysms
  • Splenic vein thrombosis
  • Recurrent acute pancreatitis
  • Risk of progression to pancreatic cancer

Deterrence and Patient Education

Patients admitted to hospital with pancreatitis should undergo aggressive counseling regarding the risks of readmission. This should include counseling regarding alcohol and smoking cessation. Dietary and lifestyle modifications including weight reduction, low-fat diet, and regular exercise should also be emphasized.

Pearls and Other Issues

  • Acute pancreatitis is a response to injury to the pancreas and results in inflammation of the pancreas. Chronic pancreatitis results in chronic changes within the pancreas including a mononuclear infiltrate and fibrosis of the pancreas.
  • Abdominal pain is the most common presenting complaint of AP and can occur with nausea and vomiting. Chronic pancreatitis can present with or without abdominal pain, nausea or vomiting. Patients with chronic pancreatitis can present with steatorrhea and weight loss.
  • The diagnosis of AP involves two of the following three: abdominal pain characteristic of pancreatitis, lipase greater than two-thirds of the upper limit of normal and imaging findings of acute pancreatitis. In chronic pancreatitis, patients can have a normal lipase and amylase level. Calcifications within the pancreas can point towards chronic pancreatitis.
  • Early aggressive intravenous hydration is the cornerstone of therapy for acute pancreatitis. Early enteral feeding can also be encouraged, and antibiotics in the absence of infectious complications should be avoided.
  • Complications of AP may be local such as peripancreatic fluid collection, pseudocyst or necrosis. Systemic complications may also occur such as ARDS, AKI, and DIC. Complications of chronic pancreatitis involve pseudocyst formation, diabetes, pseudoaneurysms, splenic vein thrombosis, and recurrent attacks.

 

Enhancing Healthcare Team Outcomes

The management of acute pancreatitis involves multi-disciplinary teams including hospitalists, gastroenterologists, surgeons, nurses, pharmacists, addiction specialists, and dietitians. The management of acute pancreatitis should involve specific counseling geared toward the etiology of pancreatitis. If a patient is noted to have several readmissions with pancreatitis, and the cause is known to be alcohol abuse, for instance, this should be specifically targeted via intensive counseling by the healthcare team. Before the patient is discharged from the hospital, it may be beneficial for a dietitian to meet with them and recommend dietary changes (such as low-fat diet) to patients with chronic pancreatitis. Medication reconciliation on admission and discharge should be emphasized so any medications that may be the cause of pancreatitis can be changed.


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Pancreatitis - Questions

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Which of the following types of necrosis is most common with pancreatitis?



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What is the most common cause of pancreatitis in North America?



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Which test is most specific for pancreatitis?



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A 32 year old female with HIV is admitted with a diagnosis of acute pancreatitis. Her history is remarkable for cryptococcal pneumonia and Mycobacterium avium-intracellulare. Medications include trimethoprim-sulfamethoxazole, fluconazole, clarithromycin, rifabutin, ethambutol, and efavirenz/tenofovir/emtricitabine. CD4 count is 35. The patient recovers. What should not be done about her discharge medications?



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A 35-year-old female with a history of alcohol use disorder presents to the emergency department with sudden onset abdominal pain, severe nausea and multiple episodes of vomiting. A lipase level is checked and elevated at 800 U/L. She is diagnosed with acute pancreatitis and admitted. Which of the following is an appropriate diet order for the patient?



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A 9-year-old female is playing field hockey and hit over the abdomen with a hockey stick. She is fine after about ten minutes, but over the next day she develops abdominal pain radiating to the back, fever, and persistent emesis. The exam shows diffuse abdominal tenderness, greatest at the epigastrium with guarding and decreased bowel sounds. Select the most appropriate test.



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Which condition often causes elevation of serum lipase level?



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What disease is diagnosed with an elevated lipase level?



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A 35-year-old female presents to the hospital with complaints of epigastric abdominal pain radiating to the back, nausea, and vomiting for one day. Her vitals are a blood pressure of 110/70 mmHg, heart rate of 84 bpm, oxygen saturation of 99% on room air, and she is afebrile. Physical exam reveals tenderness in the epigastrium. CT of the abdomen and pelvis reveals marked pancreatic edema and diffuse peripancreatic stranding. Laboratory values are remarkable for lipase of 1800 U/L, and she was diagnosed with acute pancreatitis. She does not drink alcohol, and there was no evidence of gallstones on the CT scan. What laboratory tests should be ordered for this patient in order to work up the etiology of her pancreatitis?



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A 40-year-old male with a past medical history of chronic abdominal pain presents to the emergency room with complaints of epigastric pain radiating to the back. His laboratory work reveals a lipase of 40 U/L, alanine aminotransferase (ALT) of 20 U/L, aspartate aminotransferase (AST) of 35 U/L, total bilirubin of 0.8 mg/dl, alkaline phosphatase of 80 U/L, BUN of 20 mg/dl. A CT scan of the abdomen shows calcifications within the pancreas. What is the most appropriate management of this patient?



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A 42-year-old female with a past medical history of depression and hypothyroidism has been admitted for acute pancreatitis. On the second day in the hospital, which of the following laboratory tests in addition to clinical evaluation will help predict the severity of this patients' pancreatitis?



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Pancreatitis - References

References

Fagenholz PJ,Castillo CF,Harris NS,Pelletier AJ,Camargo CA Jr, Increasing United States hospital admissions for acute pancreatitis, 1988-2003. Annals of epidemiology. 2007 Jul;     [PubMed]
Forsmark CE,Vege SS,Wilcox CM, Acute Pancreatitis. The New England journal of medicine. 2016 Nov 17;     [PubMed]
Tenner S,Baillie J,DeWitt J,Vege SS, American College of Gastroenterology guideline: management of acute pancreatitis. The American journal of gastroenterology. 2013 Sep;     [PubMed]
Lankisch PG,Breuer N,Bruns A,Weber-Dany B,Lowenfels AB,Maisonneuve P, Natural history of acute pancreatitis: a long-term population-based study. The American journal of gastroenterology. 2009 Nov;     [PubMed]
Yadav D,Lowenfels AB, The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology. 2013 Jun;     [PubMed]
Apte MV,Pirola RC,Wilson JS, Mechanisms of alcoholic pancreatitis. Journal of gastroenterology and hepatology. 2010 Dec;     [PubMed]
Banks PA,Bollen TL,Dervenis C,Gooszen HG,Johnson CD,Sarr MG,Tsiotos GG,Vege SS, Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013 Jan;     [PubMed]
Yang CJ,Chen J,Phillips AR,Windsor JA,Petrov MS, Predictors of severe and critical acute pancreatitis: a systematic review. Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2014 May;     [PubMed]
Wu BU,Hwang JQ,Gardner TH,Repas K,Delee R,Yu S,Smith B,Banks PA,Conwell DL, Lactated Ringer's solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2011 Aug;     [PubMed]
Mounzer R,Langmead CJ,Wu BU,Evans AC,Bishehsari F,Muddana V,Singh VK,Slivka A,Whitcomb DC,Yadav D,Banks PA,Papachristou GI, Comparison of existing clinical scoring systems to predict persistent organ failure in patients with acute pancreatitis. Gastroenterology. 2012 Jun;     [PubMed]
Mookadam F,Cikes M, Images in clinical medicine. Cullen's and Turner's signs. The New England journal of medicine. 2005 Sep 29     [PubMed]

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