Acute Pancreatitis


Article Author:
Jonathan Gapp


Article Editor:
Subhash Chandra


Editors In Chief:
Sherri Murrell


Managing Editors:
Avais Raja
Orawan Chaigasame
Khalid Alsayouri
Kyle Blair
Radia Jamil
Erin Hughes
Patrick Le
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Hassam Zulfiqar
Navid Mahabadi
Hussain Sajjad
Steve Bhimji
Muhammad Hashmi
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Sarosh Vaqar
Mark Pellegrini
James Hughes
Beenish Sohail
Hajira Basit
Phillip Hynes
Sandeep Sekhon


Updated:
2/28/2019 9:48:12 PM

Introduction

Acute pancreatitis is common and is the leading cause of hospitalization amongst gastrointestinal disorders in the United States. The severity of the disease varies widely, from mild disease needing conservative treatment to severe and complicated disease with high morbidity and mortality. The diagnosis of acute presentation is easy, but the major challenge is predicting progression of disease course and outcome. This is important to determine the level of care. [1][2][3]

Etiology

In the majority of cases, alcohol use, gallstones, and hypertriglyceridemia cause acute pancreatitis. The rate of occurrence of each etiology of acute pancreatitis varies across geographic regions and socio-economic strata. Common etiologies of acute pancreatitis are listed below.[3][4][5]

  • Alcohol use
  • Gallstones
  • Hypertriglyceridemia
  • Idiopathic
  • Drug-induced pancreatitis
  • Post-procedural (ERCP or abdominal surgery)
  • Ampullary stenosis is formerly known as sphincter of Oddi dysfunction type I
  • Autoimmune pancreatitis, type I (systemic IgG4 disease-related) and type II
  • Viral infection (Coxsackie, Cytomegalovirus, Echovirus, Epstein-Barr virus, Hepatitis A/B/C, HIV, Mumps, Rubella, Varicella)
  • Bacterial infection (Campylobacter jejuni, Legionella, Leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis, Mycoplasma)
  • Trauma
  • Smoking
  • Congenital anomalies (annular pancreas) 
  • Genetic disorders (hereditary pancreatitis, cystic fibrosis, alpha 1-antitrypsin deficiency) 
  • Hypercalcemia
  • Parasitic infections (Ascaris lumbricoides, Cryptosporidium, Clonorchis sinensis, Microsporidia)
  • Renal disease (Hemodialysis)
  • Toxins (Scorpion bites, organophosphate poisoning)
  • Vasculitis (Polyarteritis nodosa, Systemic lupus erythematosus)

Epidemiology

Overall, the frequency of acute pancreatitis has been noted to be rising in the United States and the rest of the world. Whether this trend is related to a true increase in incidence or simply increased detection is difficult to determine. The rise in incidence is considered, in part, due to increased hypertriglyceridemia and metabolic syndrome with multiple reports showing an increase in acute pancreatitis secondary to hypertriglyceridemia. Despite the increased incidence, mortality has decreased in the United States with most recent studies citing mortality of approximately 2%. The peak age of incidence of acute pancreatitis occurs in the fifth and sixth decades; however, mortality increases with age. Incidence has been thought to differ across geographic regions and socio-economic regions and is likely related to differences in use of alcohol and occurrence of biliary calculi, the two major causes of acute pancreatitis. In the United States, population incidence has been most recently cited as 600 to 700 per 100,000 people with 200,000 to 250,000 discharges occurring per year for acute pancreatitis. [6][7]

Pathophysiology

The pathophysiology of pancreatitis incorporates both the localized destruction in the pancreas and systemic inflammatory response. The inciting event is the premature activation of trypsinogen to trypsin within the acinar cell as opposed to in the duct lumen. It is postulated that this can be caused by elevated ductal pressures (such as in duct obstruction) as well as problems with calcium homeostasis and pH. Because calcium transport is an ATP driven process, particularly for sequestration in the smooth endoplasmic reticulum, it is suspected that many toxins responsible for pancreatitis (including alcohol) involve ATP depletion resulting in elevated intra-acinar calcium concentrations that stimulate early activation of trypsinogen to trypsin, which activates enzymes such as elastase and phospholipases. Early activation of these zymogens leads to localized tissue damage and release of Damage Associated Molecular Patterns (DAMPs). The release of DAMPs causes recruitment of neutrophils and initiation of the inflammatory cascade. This inflammatory cascade is responsible for the systemic manifestations of acute pancreatitis and can ultimately lead to increase capillary permeability and damage of endothelium with microvascular thrombosis that causes multiorgan dysfunction syndrome (MODS), the main cause of morbidity and mortality in acute pancreatitis.

More recently, it has become apparent that there is also a genetic predisposition for pancreatitis in some individuals. These patients often suffer from recurrent acute pancreatitis and a progression to chronic pancreatitis. Not surprisingly, associated genes are involved in the activation of trypsin. The cystic fibrosis transmembrane conductance regulator (CFTR) gene involved in bicarbonate secretion into pancreatic ductules, cationic trypsinogen gene (PRSS1) gain of function mutations, mutations in pancreatic secretory trypsin inhibitor (SPINK1), and trypsin degrading enzyme, chymotrypsin C (CTRC), all play a role in recurrent pancreatitis. Furthermore, they are involved in the increasingly acknowledged spectrum of disease from acute to chronic pancreatitis.[2][8][9]

History and Physical

The patient will commonly describe moderate to severe abdominal pain located in the epigastrium with nausea and anorexia. The nature of the pain can vary, often depending on whether the etiology is a biliary obstruction or a metabolic/toxicologic cause. Biliary etiology is more often described as a sharper pain, which radiates through to the back with more of an acute onset; whereas, metabolic and toxicologic causes, such as alcohol, often have a more indolent onset with more dull and generalized pain. A thorough history regarding alcohol use and medications should be gathered, keeping in mind that over five years of heavy alcohol use is often needed to induce alcohol-related pancreatitis. Smoking history is also important as a risk factor for acute pancreatitis. Family history should be reviewed, particularly when more common etiologies appear less likely, as there are rare genetically related cases of familial pancreatitis. A physical exam is often significant for elevated temperature, tachycardia and in severe cases, hypotension. The abdominal exam will typically reveal epigastric tenderness with possible guarding and rigidity and decreased bowel sounds. In severe cases where retroperitoneal bleeding has occurred, Grey-Turners sign may be present, as ecchymosis at the flanks while Cullen's sign appears as periumbilical ecchymosis secondary to peritoneal hemorrhage.

Evaluation

The diagnosis of acute pancreatitis has been defined by the Revised Atlanta Classification and requires at least 2 of 3 criteria be met: 1) a lipase or amylase level that is three times the upper limit of normal 2) abdominal pain that is consistent with pancreatitis 3) abdominal imaging consistent with acute pancreatitis. Initial evaluation of suspected acute pancreatitis involves laboratory abnormalities are suggesting biliary cholestasis, hypercalcemia or severe hyperlipidemia will help in determining the etiology of pancreatitis. An abdominal ultrasound is recommended in all the patients to assess for choledocholithiasis and bile duct dilatation. A chest radiograph is also often obtained in moderate to severe cases to evaluate for pleural effusions, which is an indication of the higher severity of disease with elevated mortality. In cases where the diagnosis is equivocal, but pancreatitis is still suspected, computed tomography (CT) with intravenous contrast is obtained to establish or rule out the diagnosis. CT is also recommended in cases where the patient has failed to improve or to worsen despite appropriate fluid resuscitation over 48 hours to determine the presence of necrosis. 

When no cause for pancreatitis is forthcoming with the evaluation mentioned above, consultation of a gastroenterology specialist is often required for further evaluation with magnetic resonance cholangiopancreatography (MRCP), or endoscopic ultrasound (EUS). As MRCP is non-invasive, there is no perioperative risk. MRCP is non-invasive, doesn’t require contrast but lacks sensitivity for detection of biliary stones less than 3 mm and chronic pancreatitis and EUS is preferred. Diagnostic ERCP is reserved for recurrent episodes of acute pancreatitis.[10][11][12]

Treatment / Management

The foundation of management for acute pancreatitis remains early aggressive fluid resuscitation. Lactated Ringer's solution is the recommended fluid of with an initial bolus of 15 to 20 mL/kg and following rates of 3 mL/kg per hour (usually approximately 250 to 500 mL per hour) for the first 24 hours if no other contraindications are present. The fluid resuscitation is monitored with a combination of blood urea nitrogen, hematocrit, and urine output, monitoring every 4 to 6 hours in first 24 hours of resuscitation to adjust the fluid rate. Continued non-response indicates a high likelihood of ensuing MODS and is grounds for upgrading the level of care.[13][14][15]

Another important issue is nutrition. Common practice is to keep nothing by mouth until abdominal pain, nausea, vomiting, appetite, and ileus improve. Early feeding in mild pancreatitis is safe and does not exacerbate symptoms. Soft, low residue, low-fat diet is recommended for initial feeding and advanced to regular consistency as tolerated. In cases of severe pancreatitis or where peroral intake is not tolerated, nesojejunal feeding is superior to parenteral nutrition as it helps to minimize bacterial translocation by maintaining the intestinal barrier.

Prophylactic antibiotics are not needed. If infection is suspected, empirical antibiotics are appropriate until cultures results are back. Indication for antibiotic is limited to presence of infected necrosis.

Further management depends upon the etiology of pancreatitis. In gallstone pancreatitis, early cholecystectomy is strongly recommended. Early ERCP (within 24 hours of presentation) is of benefit in cases of concurrent cholangitis and obvious biliary obstruction. In cases of mild or spontaneously resolving biliary pancreatitis, ERCP is reserved for distal biliary filling defect on intraoperative cholangiogram during cholecystectomy. In the setting of hypertriglyceridemia, the goal of specific treatment is to bring down and maintain triglyceride level to less than 500 mg/dL. The options to achieve this goal include apheresis and insulin drip with or without glucose.

Local complications of pancreatitis include early (less than 4 weeks, peripancreatic fluid collection and pancreatitic/peripancreatic necrosis) and late (more than 4 weeks, pancreatic pseudocyst and walled-off necrosis). Acute peripancreatic fluid collection resolves spontaneously in most cases, and less than 10% result in pancreatic pseudocyst. Most of these pseudocysts resolve with observation alone with periodic follow-up using CT or MRI. Drainage is only recommended in symptomatic, infected or rapidly enlarging pseudocysts. The drainage modalities include endoscopic (transmural or transpapillary) or percutaneous, the endoscopic approach being the preferred modality.

Necrotic collection management remains challenging. The sterile collection is intervened if it caused symptoms such as persistent abdominal pain, nausea, vomiting, gastric outlet obstruction, bowel obstruction and disrupted pancreatic duct. One-third of this necrosis become infected. Infection results in clinical deterioration, lengthen the recovery, has high mortality. Antibiotics are initiated on earliest suspicion. The preferred antibiotic regimen includes a carbapenem alone, or combination of a quinolone, ceftazidime, or cefepime with metronidazole. Diagnosis of infected necrosis is established in the presence of gas bubbles in it on imaging and CT-guided percutaneous aspiration culture. Surgical necrosectomy is needed in patients continue to deteriorate clinically despite antibiotics. In stable patients, antibiotics are continued for 4 to 6 weeks and necrosectomy performed after the wall matures. The initial approach includes less invasive modalities which include endoscopic and percutaneous drainage and surgical debridement is reserved in unsuccessful cases.[16][17]

Differential Diagnosis

The differentials for acute pancreatitis include the overall differential for abdominal pain and can often be greatly narrowed with a good history and physical as described above. Differential diagnoses include but is not limited to the following:

  • Peptic ulcer disease
  • Cholangitis
  • Cholecystitis
  • Bowel perforation
  • Bowel obstruction
  • Mesenteric ischemia
  • Acute hepatitis
  • Diabetic ketoacidosis
  • Basilar pneumonia
  • Myocardial infarction
  • Renal colic
  • Aortic dissection

In many of these cases, an elevated lipase level 3 times the upper limit of normal will allow for determination of pancreatitis as the source of abdominal pain due to its high specificity. Abdominal ultrasound will help to differentiate cholecystitis whereas CT angiogram can be used when mesenteric ischemia is high on the differential. In high-risk patients, the cardiac source should be concurrently ruled out as pain can present atypically as epigastric. Progressing aortic dissection should be considered due to its particularly urgent nature, though the pain is often more severe and tearing than for those with acute pancreatitis.

Prognosis

Overall mortality of acute pancreatitis is approximately 1% to 2%; however, severe acute pancreatitis carries a much higher but undetermined mortality rate.

Severity assessment and prognostication is important to determine the level of care. Multiple clinical prediction scales have been developed and validated. Most are cumbersome to calculate and need 48-hour data. The Bedside Index for Severity in Acute Pancreatitis (BISAP) is a relatively recent addition to this list. This index has good predictive performance for both severe acute pancreatitis and mortality and has been validated prospectively, is simple and easy to calculate from initial presentation data. Use of the CT Severity Index (CTSI) can also aid in predicting mortality with the detection of any necrosis on CT imaging being a predictor of high mortality.

Complications

  • Sepsis
  • Necrotic pancreas
  • Hemorrhagic pancreatitis
  • ARDS
  • Renal failure
  • Pancreatic duct disruption
  • Pseudocysts
  • Infected pancreatic necrosis
  • Pancreatic abscess

Consultations

General surgeon

Radiologist

Gastroenterologist

Critical care specialist

Pulmonologist

Endocrinologist

Pearls and Other Issues

  • The pathophysiology of acute pancreatitis is based on the premature activation of the zymogen, trypsinogen, with resulting local pancreatic destruction leading to activation of the inflammatory cascade which causes the systemic inflammatory response syndrome (SIRS) often associated with acute pancreatitis. Systemic inflammation can lead to multiorgan dysfunction syndrome (MODS).
  • Diagnosis of acute pancreatitis is defined by the Revised Atlanta Criteria which states that acute pancreatitis requires at least 2 of the following 3 criteria: 1) lipase or amylase levels 3 times the upper limit of normal, 2) physical exam consistent with pancreatitis, and 3) imaging (CT, MRI, ultrasound) findings that are consistent with acute pancreatitis.
  • Use of the Bedside Index Severity in Acute Pancreatitis (BISAP) score can aid in triaging patients for the level of care. TThis index has good predictive performance for both severe acute pancreatitis and mortality and has been validated prospectively, is simple and easy to calculate from initial presentation data.
  • The most important stage of management of acute pancreatitis is the first 12 to 24 hours of admission. It is during this time that appropriate fluid resuscitation can greatly reduce complications and mortality. Close observation of vitals and basic labs to ensure adequate fluid resuscitation are key.
  • The incidence of idiopathic pancreatitis remains as high as 10% to 20% of acute pancreatitis cases and causes a particular diagnostic and management dilemma. Recent studies continue to address the best use of EUS and ERCP in the evaluation of these cases with a more tempered approach to ERCP due to its relatively high rate of inducing post-procedural pancreatitis.

Enhancing Healthcare Team Outcomes

Acute pancreatitis is a serious disorder and the most effective way to manage the disorder is with a team of healthcare professionals that includes a surgeon, radiologist, endocrinologist, pulmonologist, intensivist, gastroenterologist, pharmacist, nurse, and addiction specialist. The three major causes of acute pancreatitis are gallstones, alcohol, and medications. The emphasis today is on prevention. The nurse and pharmacist are in the prime position to educate the patient on lowering their risks of acute pancreatitis by abstaining from alcohol, losing weight, eating a low-fat diet and lowering their lipid profile. In addition, the pharmacist can re-evaluate all the medications and recommend discontinuation of those associated with pancreatitis.[18][19][20] (Level V)

Outcomes

Acute pancreatitis is a serious disorder which still carries a mortality of 5-15%, depending on the cause, patient age and comorbidity. In general patients with gallstone pancreatitis tend to have higher mortality than patients with alcoholic pancreatitis. In addition, the presence of type 2 diabetes significantly increases the risk of complications and death. In patients with multiorgan involvement, the mortality can be as high as 20%. Most deaths are due to multiorgan failure and hypotensive shock. Various classifications have been developed to assess the prognosis of patients with acute pancreatitis, but most are cumbersome for practical use. [21][22][23](Level V) 


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Acute Pancreatitis - Questions

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A 43-year-old male with alcoholism is found to have acute pancreatitis. He is in the intensive care unit with multi-organ failure. Which of the following pancreatitis complications is associated with the highest mortality rate?



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A patient has been diagnosed with acute pancreatitis. Which of the following about this medical condition is false?



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A 54-year-old is seen in the emergency department with mid abdominal pain, low-grade fever, and nausea. The exam reveals a distended tender abdomen with bluish discoloration on the flanks. The urinary trypsinogen activation peptide and serum trypsinogen 2 values are elevated. Which of the following statements about this medical disorder is false?



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Abdominal pain of sudden onset accompanied by peritoneal fluid accumulation and high amylase in blood are typical signs of which disease?



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A 65-year-old female is admitted to the intensive care unit for acute pancreatitis with a Bedside Index of Severity for Acute Pancreatitis (BISAP) score of five. A CT of the abdomen shows a 2-centimeter by 3-centimeter by 1-centimeter focus of pancreatic necrosis. Which of the following is least likely to be a resulting complication of her condition?



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Which of the following is least likely associated with a pathogenesis of acute pancreatitis?



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Which of the following medications used to treat diabetes mellitus type 2 is most likely to cause acute pancreatitis?



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A male presents to the emergency department with sudden onset of abdominal pain. The examination reveals peritoneal signs, and blood work reveals high amylase. Which of the following conditions might this patient have developed?



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Which of the following statements regarding acute pancreatitis is true?



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Which of the following is false about acute pancreatitis staging?



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A 55-year-old female was admitted to the hospital 48 hours ago for acute pancreatitis. In calculating her predicted mortality, which of the following values would contribute to a poorer prognostic score?



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A 65-year-old female is admitted to the hospital for treatment of acute pancreatitis. Which of the following is a possible etiology of her acute pancreatitis?



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In a patient with acute pancreatitis and a Ranson criteria score of six, what is the expected mortality?



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Which of the following are not risk factors associated with acute pancreatitis?



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What is the most common cause of acute pancreatitis in the United States?



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A 16-week female who is pregnant presents with severe nausea, vomiting, and midepigastric abdominal pain radiating to the back. She is rocking and has her knees drawn to her chest. She has mildly elevated transaminases and a significantly elevated amylase. What is the most likely diagnosis?



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A 65-year-old female complains of acute onset, severe epigastric abdominal pain. There is associated emesis and radiation to the back. Serum amylase and lipase are elevated. What is the most likely etiology of her pain?



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A 38-year-old male with no significant past medical history presents to the emergency department with complaints of severe epigastric pain which he describes as "radiating to my back." What is the most likely diagnosis?



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A 45-year-old male is admitted to the hospital after presenting with epigastric pain with nausea and vomiting and initial laboratories showing an elevated lipase consistent with a diagnosis of acute pancreatitis. A further review of laboratory values shows aspartate aminotransferase of 75 units/L, alanine aminotransferase of 270 units/L, alkaline phosphatase of 202 international units/L, and total bilirubin of 2.1 mg/dL. Which of the following is the most likely cause of his pancreatitis?



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Which of the following is not known to cause acute pancreatitis?



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A 52-year-old female is brought to the emergency department with severe upper abdominal pain, radiating to the back. She reports the pain is sharp and had sudden onset. She has had three episodes of bilious emesis without relief. The patient is otherwise healthy but has had several episodes of right upper quadrant pain after meals that resolve in a few hours. She is on no medications. On exam, vital signs are heart rate 120 beats/min, blood pressure 90/55 mmHg, respiratory rate 22 breaths/min, temperature 37.8 degrees C, SaO2 89 percent on room air. Her body mass index is 31 kg/m2. Lungs show scattered crackles and dullness to percussion at the bases. Abdominal exam shows tenderness to palpation at the upper quadrants without rebound, masses, or hepatosplenomegaly. Bowel sounds are hypoactive. Amylase and lipase are markedly elevated. Transaminases are four times normal. Alkaline phosphatase is 280 U/L, creatinine 2.0 mg/dL, hematocrit 42 percent, white blood cell count is 12,500/microL with 87 percent neutrophils, and arterial blood gas shows a pH of 7.30, Paco2 30 mmHg, and a Pao2, of 60 mmHg. Ultrasound shows dilation of the common bile duct and edema with enlargement of the pancreas. Which of the following statements about this scenario is inaccurate?



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A 47-year-old male presents to the emergency department complaining of severe epigastric pain radiating to the back and associated nausea and vomiting. He has a prolonged history of alcohol use disorder and states that he often drinks 500 mL of vodka per day with many failed attempts at quitting. The patient appears to be in distress and using accessory muscles to breathe. His vitals show a temperature of 38.5 C, heart rate 115 beats/min, blood pressure 90/45 mmHg, and respiratory rate 42. Laboratory studies are significant for lipase of 5534 units/L and mildly elevated transaminases with aspartate aminotransferase greater than alanine aminotransferase. Hematocrit is 42%. A chest x-ray is obtained and shows bilateral, patchy opacities throughout the lung fields. Which of the following indicates a poor prognosis?



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You are working in the local urgent care center and a normally healthy 37-year-old male presents with abdominal pain that he describes as epigastric and worsening when leaning forward with associated nausea and vomiting. You are highly considering acute pancreatitis in your differential diagnosis simply based upon this provided history. Based on the epidemiology of acute pancreatitis, the most suspected etiology would be which of the following in the United States?



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What is the best test to diagnose acute pancreatitis?



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A 50-year-old male with alcohol use disorder is admitted with acute pancreatitis. He admits to drinking a fifth of vodka daily and is having epigastric pain, nausea, and has vomited once but denies hematemesis or hematochezia. Vital signs are pulse 115 beats/min, respirations 16 breaths/min, and blood pressure 160/80 mmHg. The abdomen reveals decreased bowel sounds and is tympanic. There is tenderness to palpation at the mid epigastrium without rebound, masses, or splenomegaly. The liver is 16 cm at the midclavicular line. Lipase is 1200 units/L, amylase 550 units/L, alanine aminotransferase 140 units/L, aspartate aminotransferase 270 units/L, alkaline phosphatase 90 units/L, and albumin 2.5 grams/L. What is the best management of this patient?



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A 48-year-old female presents with epigastric pain radiating through to the back and on physical exam has epigastric tenderness. She denies any use of alcohol or tobacco products. Her heart rate is 115 beats/min, respirations 16 breaths/min, blood pressure 130/85 mmHg, and oxygen saturation 98% on room air. Her lipase is elevated to 13,800 units/L. It has been decided to admit her to the hospital. Which of the following is true concerning her prognosis at this time?



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Which of the following diagnoses does not increase the risk of acute pancreatitis?



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Which of the following is a common cause of acute pancreatitis?



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Which of the following is indicated by epigastric pain radiating to the back with hypotension and tachycardia?



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A young male patient presents with sharp abdominal pain. The patient is diagnosed with acute pancreatitis after exam and laboratories. Which of the following is least likely to be the etiology?



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A 12-year-old female presents to the emergency department after sustaining an injury where she fell off her bike and landed on her handlebars 5 hours prior to arrival. She is complaining of nausea and epigastric pain that radiates to her back. She has urinated since the accident, and it was clear. Which of the following findings is not consistent with this patient's presentation?



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A 13-year-old female presents to the emergency department with complaints of abdominal pain, nausea, and emesis after sustaining blunt abdominal trauma. Her WBC count is 18,000 cells/mm3 and her lipase is 1250 units/L. Which of the following is false regarding this patient?



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A 49-year-old female with a history of alcohol use disorder presents with 8 hours of progressive epigastric pain radiating to her back. The pain is worse when lying down. At presentation, the patient is hypotensive, tachycardic, and has a low-grade fever. What test(s) would be most helpful in establishing a diagnosis?



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A 72-year-old female who lives independently is brought in by emergency medical services after being found down at home by a friend who became suspicious when the patient had not arrived for their weekly book club. On initial assessment, the patient is tachycardic and hypotensive and is on supplemental oxygen via nasal cannula at 5 L. She is moaning and uncomfortable, non-verbal, but opens her eyes to command and moves all extremities. An exam reveals abdominal tenderness and ecchymosis around the umbilicus. Which of the following conditions is associated with periumbilical ecchymosis?



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You are an emergency medicine resident and are working with a medical student in the evaluation of a 43-year-old male who presents with epigastric pain radiating to the back, nausea, and vomiting. Laboratory results show an elevated lipase of 2000 units/L. The patient appears uncomfortable and complains of 8 out of 10 pain during the exam. You and the medical student agree that this appears to be a case of acute pancreatitis and the student asks you, "Should we order a CT scan of the abdomen to see if he has pancreatitis?". What is the correct response?



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A 58-year-old male presents to the emergency department with epigastric pain that has been worsening over the past week and is admitted to the hospital. He appears jaundiced and uncomfortable. CT of the abdomen reveals the presence of a pancreatic mass. "Groove pancreatitis" is considered in the differential diagnosis. Which of the following would be consistent with this diagnosis?



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Which of the following is associated with Grey Turner or Cullen's sign?



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In which medical disorder can Scarpa fascia be show bruising secondary to hemorrhage?



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A 16-year-old male was desert-exploring with his friends in the middle east. He was exploring a cave when a scorpion emerged from under the rocks and stung him on his right leg. The next day he developed nausea, vomiting and mid-epigastric abdominal pain. What complication is the patient likely to develop if he doesn't get treated?



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A male presents with complaints of dull, steady pain in the abdomen which started 24 hours ago. The pain is constant and also occurs in the back. He is nauseated and has no appetite. On exam, he has a temp of 101 F, BP 90/65 mm Hg, P 120 bpm, and RR 20/min. The abdomen is diffusely tender, and the bowel sounds are diminished. There is guarding but no rebound pain. The abdominal film is shown. While the blood work is pending, what diagnostic study will be ordered next?

(Move Mouse on Image to Enlarge)
  • Image 6059 Not availableImage 6059 Not available
    Image Courtesy S Bhimji
Attributed To: Image Courtesy S Bhimji



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Which of the following is not true about severity assessment and predicting outcome in acute pancreatitis?



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An adult male is admitted with acute pancreatitis. Which of following findings are associated with the worst outcome?



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A 49-year-old female presents with 8 hours of progressive epigastric pain that worsens when recumbent and with radiation to her back with associated nausea. The patient is well known at your institution and has a well-documented history of alcohol abuse. On your evaluation, the patient’s vitals show temperature of 100.6 F, heart rate of 123 beats per minute, blood pressure of 95/60 mmHg, respiratory rate of 16 breaths per minute and saturating at 90% on ambient air. The physical exam reveals an uncomfortable and ill-appearing patient from whom it is difficult to elicit a history as she drifts off between sentences. Breath sounds are slightly diminished over the left posterior lung fields, and she displays epigastric tenderness with guarding but without rigidity or rebound tenderness. Bowel sounds are decreased but present. The patient’s laboratory results show hemoglobin of 17.0 g/dL, hematocrit of 58.0%, white blood cell count of 17 x 10^9/microL and platelets of 135,000/microL. The metabolic shows alanine aminotransferase (ALT) 62 U/L, aspartate aminotransferase (AST) 128 U/L, and alkaline phosphatase of 135 U/L with blood urea nitrogen of 34 mg/dL, and serum creatinine of 1.20 mg/dL. Lipase is 2524 U/L. The chest x-ray is significant for mild to moderate left pleural effusion without visualization of free air under the diaphragm and abdominal ultrasound without dilatation of the common bile duct or presence of any stones in the visualized biliary ducts but is unable to visualize the pancreas due to overlying bowel gas. What is the next best step in the management of this patient?



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A young male is admitted to the hospital with mid-epigastric pain and emesis for 24 hours. The diagnosis is acute pancreatitis. The surgeon says that two causes account for the majority of cases of acute pancreatitis. They include which of the following? Select all that apply.



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Which of the following has been linked to drug-induced pancreatitis? Select all that apply.



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A client has been admitted to a medical-surgical unit with a diagnosis of acute pancreatitis. Pain associated with this disorder has which of the following characteristics? Select all that apply.



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A professor is lecturing on acute pancreatitis. The nursing students are frantically taking notes and trying to sort through what is essential knowledge for the upcoming end of semester exam. What important points should the students commit to memory for the upcoming exam? Select all that apply.



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A surgeon has just admitted a patient with a presumed diagnosis of acute pancreatitis. What blood work may be ordered by the provider? Select all that apply.



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Acute Pancreatitis - References

References

Valverde-López F,Wilcox CM,Redondo-Cerezo E, Evaluation and management of acute pancreatitis in Spain: A systematic review. Gastroenterologia y hepatologia. 2018 Aug 24     [PubMed]
Kahaleh M, Management of pancreatitis and pancreatic: fluid collections. Revista de gastroenterologia del Peru : organo oficial de la Sociedad de Gastroenterologia del Peru. 2018 Apr-Jun     [PubMed]
Bazerbachi F,Haffar S,Hussain MT,Vargas EJ,Watt KD,Murad MH,Chari S,Abu Dayyeh BK, Systematic review of acute pancreatitis associated with interferon-α or pegylated interferon-α: Possible or definitive causation? Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]. 2017 Sep 21     [PubMed]
Sepúlveda EVF,Guerrero-Lozano R, Acute pancreatitis and recurrent acute pancreatitis: an exploration of clinical and etiologic factors and outcomes. Jornal de pediatria. 2018 Jul 31     [PubMed]
Barbara M,Tsen A,Rosenkranz L, Acute Pancreatitis in Chronic Dialysis Patients. Pancreas. 2018 Sep     [PubMed]
de Pretis N,Amodio A,Frulloni L, Hypertriglyceridemic pancreatitis: Epidemiology, pathophysiology and clinical management. United European gastroenterology journal. 2018 Jun     [PubMed]
Kirkegård J,Cronin-Fenton D,Heide-Jørgensen U,Mortensen FV, Acute Pancreatitis and Pancreatic Cancer Risk: A Nationwide Matched-Cohort Study in Denmark. Gastroenterology. 2018 May     [PubMed]
Johnstone C, Pathophysiology and nursing management of acute pancreatitis. Nursing standard (Royal College of Nursing (Great Britain) : 1987). 2018 Jun 28     [PubMed]
Constantinoiu S,Cochior D, Severe Acute Pancreatitis - Determinant Factors and Current Therapeutic Conduct. Chirurgia (Bucharest, Romania : 1990). 2018 May-Jun     [PubMed]
Choi HW,Park HJ,Choi SY,Do JH,Yoon NY,Ko A,Lee ES, Early Prediction of the Severity of Acute Pancreatitis Using Radiologic and Clinical Scoring Systems With Classification Tree Analysis. AJR. American journal of roentgenology. 2018 Aug 30     [PubMed]
Mandalia A,Wamsteker EJ,DiMagno M, Recent advances in understanding and managing acute pancreatitis. F1000Research. 2018     [PubMed]
Smeets XJNM,Litjens G,Gijsbers K,Prokop M,Drenth JPH,Hermans J,van Geenen EJM, The Accuracy of Pancreatic Perfusion Computed Tomography and Angiography in Predicting Necrotizing Pancreatitis: A Systematic Review. Pancreas. 2018 Jul     [PubMed]
Barrie J,Jamdar S,Smith N,McPherson SJ,Siriwardena AK,O'Reilly DA, Mis-use of antibiotics in acute pancreatitis: Insights from the United Kingdom's National Confidential Enquiry into patient outcome and death (NCEPOD) survey of acute pancreatitis. Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]. 2018 May 24     [PubMed]
Reynolds PT,Brady EK,Chawla S, The utility of early cross-sectional imaging to evaluate suspected acute mild pancreatitis. Annals of gastroenterology. 2018 Sep-Oct     [PubMed]
Sellers ZM,Abu-El-Haija M,Husain SZ,Morinville V, New Management Guidelines for Both Children and Adults With Acute Pancreatitis. Gastroenterology. 2018 Jul     [PubMed]
Arvanitakis M,Dumonceau JM,Albert J,Badaoui A,Bali MA,Barthet M,Besselink M,Deviere J,Oliveira Ferreira A,Gyökeres T,Hritz I,Hucl T,Milashka M,Papanikolaou IS,Poley JW,Seewald S,Vanbiervliet G,van Lienden K,van Santvoort H,Voermans R,Delhaye M,van Hooft J, Endoscopic management of acute necrotizing pancreatitis: European Society of Gastrointestinal Endoscopy (ESGE) evidence-based multidisciplinary guidelines. Endoscopy. 2018 May     [PubMed]
Abu-El-Haija M,Kumar S,Quiros JA,Balakrishnan K,Barth B,Bitton S,Eisses JF,Foglio EJ,Fox V,Francis D,Freeman AJ,Gonska T,Grover AS,Husain SZ,Kumar R,Lapsia S,Lin T,Liu QY,Maqbool A,Sellers ZM,Szabo F,Uc A,Werlin SL,Morinville VD, Management of Acute Pancreatitis in the Pediatric Population: A Clinical Report From the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition Pancreas Committee. Journal of pediatric gastroenterology and nutrition. 2018 Jan     [PubMed]
Gódi S,Erőss B,Gyömbér Z,Szentesi A,Farkas N,Párniczky A,Sarlós P,Bajor J,Czimmer J,Mikó A,Márta K,Hágendorn R,Márton Z,Verzár Z,Czakó L,Szepes Z,Vincze Á,Hegyi P, Centralized care for acute pancreatitis significantly improves outcomes. Journal of gastrointestinal and liver diseases : JGLD. 2018 Jun     [PubMed]
Branquinho D,Ramos-Andrade D,Elvas L,Amaro P,Ferreira M,Sofia C, Drug-Induced Acute Pancreatitis and Pseudoaneurysms: An Ominous Combination. GE Portuguese journal of gastroenterology. 2016 Nov-Dec     [PubMed]
Srinivasan G,Venkatakrishnan L,Sambandam S,Singh G,Kaur M,Janarthan K,John BJ, Current concepts in the management of acute pancreatitis. Journal of family medicine and primary care. 2016 Oct-Dec     [PubMed]
Jin T,Jiang K,Deng L,Guo J,Wu Y,Wang Z,Shi N,Zhang X,Lin Z,Asrani V,Jones P,Mittal A,Phillips A,Sutton R,Huang W,Yang X,Xia Q,Windsor JA, Response and outcome from fluid resuscitation in acute pancreatitis A Prospective Cohort Study. HPB : the official journal of the International Hepato Pancreato Biliary Association. 2018 Aug 28     [PubMed]
Amas Gómez L,Zubia Olaskoaga F, Results of the modification of an acute pancreatitis management protocol in Intensive Care medicine. Medicina intensiva. 2018 Jul 30     [PubMed]
Garret C,Péron M,Reignier J,Le Thuaut A,Lascarrou JB,Douane F,Lerhun M,Archambeaud I,Brulé N,Bretonnière C,Zambon O,Nicolet L,Regenet N,Guitton C,Coron E, Risk factors and outcomes of infected pancreatic necrosis: Retrospective cohort of 148 patients admitted to the ICU for acute pancreatitis. United European gastroenterology journal. 2018 Jul     [PubMed]

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