Evidence-Based Disposition of Acute Pancreatitis

Author: Jonathan Reeder, MD (EM Resident Physician, UTSW / Parkland) // Reviewed by: Michael J. Yoo, MD (EM Assistant Professor, San Antonio, TX); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Background

The pancreas is composed of both endocrine and exocrine cells.  The exocrine pancreas, which is of interest in acute pancreatitis, generates and releases enzymes that facilitate the degradation of large dietary macromolecules into smaller components that are absorbable by the small intestine. As a mechanism to prevent auto-digestion and self-injury to the organ, the pancreas produces proenzymes to include trypsinogen and chymotrypsinogen which are then converted in the duodenum to their active forms trypsin and chymotrypsin, respectively.  However, at times these layers of security are overwhelmed or simply fail, and acute pancreatitis results.  Specifically, when the pancreas sustains an inciting event, such as alcohol abuse or biliary obstruction, intra-acinar activation of proteases occurs, which leads to a cascade of destruction of acinar cells and release and activation of higher levels of proteases in a positive feedback system.  A wide range of injury patterns may occur, from localized, minor injury to activation of systemic inflammation via an exaggerated release of proinflammatory cytokines which can lead to shock and acute respiratory distress syndrome (ARDS).Of note, we believe that pancreatitis induced ARDS is driven by the large amounts of lecithinase released from destroyed acinar cells.  Lecithin is a major component of surfactant, and its destruction causes large scale pulmonary edema as alveoli collapse.2  Furthermore, the large-scale cytokine release in severe pancreatitis can lead to increased intestinal permeability, translocation of enteric organisms, bacteremia, and sepsis.3,4

 

Classification

The revised Atlanta criteria broadly classify acute pancreatitis into two main categories:

  • Interstitial edematous acute pancreatitis
  • Necrotizing acute pancreatitis

 

Interstitial edematous acute pancreatitis is defined as inflammation of pancreatic parenchyma and peripancreatic tissues but without evidence of pancreatic tissue necrosis.5

Necrotizing acute pancreatitis is characterized by pancreatic parenchymal necrosis and/or peripancreatic tissue necrosis.5

Furthermore, acute pancreatitis can be classified by severity:

  • Mild acute pancreatitis is characterized by the lack of organ failure or local or systemic complications
  • Moderate acute pancreatitis is characterized by less than 48 hours of organ failure, or local or systemic complications without organ failure
  • Severe acute pancreatitis is characterized by persistent (>48 hours) organ failure in one or more organ systems

 

Diagnostic Criteria

The diagnosis of acute pancreatitis is traditionally defined by the Atlanta criteria, requiring two of the following three criteria:

  1. Characteristic abdominal pain, usually described as mid-epigastric pain, sometimes radiating to the back.5
  2. Elevated serum biomarkers.  Amylase and lipase are two serum laboratory tests commonly considered, but lipase has greater sensitivity and specificity.  Values greater than 3 times the upper limit of normal are considered positive for meeting this criterion.5
  3. Imaging consistent with pancreatitis.  Contrast-enhanced computed tomography (CT), magnetic resonance imaging (MRI), or ultrasound are all modalities used to investigate the pancreas.5

 

Scoring Systems

Ranson’s and APACHE II

There are several scoring systems designed to predict mortality, necessity of intensive care, and pancreatitis severity. Ranson’s criteria and APACHE II are among the most well-known scoring systems for pancreatitis severity. These scoring tools rely on a combination of serum laboratory and clinical findings.  Unfortunately, neither tool has perfect test characteristics. A recent meta-analysis shows that Ranson has a sensitivity of 0-100% and a specificity of 14-97%, while APACHE II has a sensitivity of 68-100% and specificity of 21-96%.13  The complete Ranson score cannot be calculated until 48 hours post-admission.  However, an initial score >2 is often used as suggestive of admission (estimated mortality increases from 1% for scores 1-2 to 15% for a score of 3). APACHE II is used to predict mortality in the intensive care unit (ICU) using the worst laboratory values within the first 24 hours of admission but is often used in the ED to predict the necessity for an ICU admission.

 

BISAP

The BISAP score was investigated in the early 2000s and was designed to be a simplified scoring system compared to Ranson’s and APACHE II.  A score of 5 was found to suggest a mortality rate of 22%, and a score of 3 or more is suggestive of severe acute pancreatitis.14 The elements are outlined below.8

  • BUN > 25 mg/dl
  • Impaired mental status
  • SIRS
  • Age > 60
  • Presence of pleural effusion

 

Systemic Inflammatory Response Syndrome (SIRS)

The SIRS criteria have been studied as a predictor of mortality in pancreatitis, and the presence of SIRS was found by investigators to correlate with a 25% mortality rate during the index admission vs 0% in patients who did not meet SIRS criteria.6  The presence of SIRS criteria likely suggests a combination of large volume fluid shifts resulting in hemodynamic compromise versus development of or presence of concomitant systemic infection. Intestinal bacterial translocation leading to bacteremia is a common occurrence in secondary to the inflammation caused by severe acute pancreatitis.4

 

CT Severity Score

Balthazar et. al. demonstrated that a CT severity score based on necrosis, local inflammation, and fluid collections is useful in predicting outcomes. In their study, mortality rates were 23% with any degree of necrosis and 0% without.7

Disposition

Acute pancreatitis clearly represents a large spectrum of disease that presents prognostic and disposition challenges.  Many of the severity scores that exist are only useful once a patient is admitted.  In addition to initial stabilization, our role as emergency physicians is to identify cases of acute pancreatitis that are at risk of decompensation.

 

Outpatient Management

Our first goal is to determine which patients may be safely discharged and managed on an outpatient basis.  While the following are not an exhaustive list, patients who are well appearing and meet the following may be considered for outpatient management.

  • Etiology of acute pancreatitis is not gallstone or secondary to biliary disease.
    • Patients with gallstone pancreatitis and cholangitis require admission for emergent endoscopic retrograde cholangiopancreatography (ERCP) due to concern for the development of biliary system infection (i.e. ascending cholangitis). However, even those patients with acute gallstone pancreatitis without cholangitis should be admitted for serial exams and labs to monitor for passage of the stone and improvement in symptoms.
  • If the etiology of acute pancreatitis is alcohol-related, the patient must not be at risk for complicated alcohol withdrawal. Look for signs of tongue fasciculations, tremors, or other clinical signs of withdrawal.  (A further discussion on this topic can be found here: https://www.emdocs.net/alcohol-withdrawal/)
  • Patient must be able to tolerate oral intake.
  • Pain is well controlled.
  • Vital signs are non-emergent.

 

Admission

Patients who do not meet the criteria for outpatient management should be risk stratified to determine the level of care.  The following criteria (several of which are major criteria from BISAP) are reasonable indicators that a patient is a high risk of decompensation and may require an ICU level of care:

  • SIRS criteria
  • Any evidence of pancreatic or peripancreatic necrosis on imaging
  • Acute renal failure
  • Signs of large volume third spacing:
    • Hemoconcentration on labs
    • Evidence of pleural effusions on CXR or abdominal CT (if obtained)
  • Newly elevated blood urea nitrogen (BUN) > 25 mg/dl

This list is not all-inclusive. Any vital sign or laboratory derangement that would generally require ICU levels of care applies equally to acute pancreatitis.

 

Disposition Pitfalls

Imaging

There is often a temptation to allow imaging to guide disposition of intra-abdominal pathologies.  However, in the case of acute pancreatitis, imaging is often low yield. The usual study of choice for emergency physicians is a contrasted CT of the abdomen and pelvis.  However, this study is insensitive in diagnosing acute pancreatitis, especially early in the disease process. Approximately 30% of early pancreatitis cases are missed on CT.10,11  Furthermore, CT is only useful in disposition decision making when evidence of necrosis or local complications are seen.  The degree of pancreatic and peri-pancreatic inflammation does not correlate to the severity of disease and should not be used in isolation to determine disposition.10 As such, in well-appearing patients with no evidence of SIRS or large volume third-spacing and clear evidence of pancreatitis without diagnostic uncertainty, clinicians should consider foregoing the CT imaging.  However, we continue to recommend imaging the biliary system with a right upper quadrant ultrasound to evaluate for gallstones, which if present, is likely to change acute management.

Risky Discharges

Although most acute pancreatitis risk stratifying systems were designed for inpatient use rather than ED populations, this does not mean that we should not pay attention to the individual elements to help guide our disposition. In a retrospective study performed by Whitlock et. al., readmission after discharge for acute pancreatitis was found to occur at rates approaching 20%.12  The most significant risk factors were found to be:

  • Gastrointestinal symptoms, specifically nausea, vomiting, or diarrhea12
  • A less than solid diet at discharge12
  • Moderate to severe alcohol use12

While these findings relate to inpatient discharges, these symptoms and risk factors remain relevant in patients in the ED and may further guide disposition.  Given that the mainstay of treatment for acute pancreatitis is appropriate volume fluid resuscitation, patients who are experiencing persistent GI volume losses (diarrhea, vomiting) or are unlikely to remain PO tolerant are also unlikely to be successful outpatient candidates.  Furthermore, the additional challenges posed by alcohol use disorder complicate discharges, as there is a concern for alcohol abstinence and adherence to dietary and hydration recommendations and likelihood to follow return precautions.  Subsequently, these patients may warrant admission to monitor for the resolution of acute pancreatitis symptoms while concomitantly monitoring for alcohol withdrawal complications.

 

Conclusion

Acute pancreatitis is a commonly encountered etiology of abdominal pain in the ED. Despite its ubiquity, the spectrum of disease severity is broad, posing many diagnostic and disposition challenges for the emergency physician.  Keep in mind the following:

  1. Try to establish the etiology of the pancreatitis.  Without this knowledge, our ability to predict the disease course, and therefore disposition may be limited.
  2. Imaging is not necessary but may be helpful in a particularly acute patient or in one with high levels of diagnostic uncertainty.  Uncovering evidence of necrosis or localized complications will change the disposition.
  3. No single scoring tool is perfect.  They should not be used in isolation nor override clinical judgement.  However, look for key markers that may help predict morbidity/mortality:
    1. SIRS criteria
    2. Older age
    3. Evidence of large-volume fluid shifts, refractoriness to fluid repletion

 

Further Reading

 

References

  1. Steer ML. Pathogenesis of acute pancreatitis. Digestion. 1997;58 Suppl 1:46-49.
  2. Tenner S, Sica G, Hughes M, et al. Relationship of necrosis to organ failure in severe acute pancreatitis. Gastroenterology. 1997;113(3):899-903.
  3. Schmid SW, Uhl W, Friess H, Malfertheiner P, Büchler MW. The role of infection in acute pancreatitis. Gut. 1999;45(2):311-316.
  4. Kazantsev GB, Hecht DW, Rao R, et al. Plasmid labeling confirms bacterial translocation in pancreatitis. Am J Surg. 1994;167(1):201-207.
  5. Bradley EL 3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch Surg. 1993;128(5):586-590.
  6. Mofidi R, Duff MD, Wigmore SJ, Madhavan KK, Garden OJ, Parks RW. Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis. Br J Surg. 2006;93(6):738-744.
  7. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990;174(2):331-336.
  8. Wu BU, Johannes RS, Sun X, Tabak Y, Conwell DL, Banks PA. The early prediction of mortality in acute pancreatitis: a large population-based study. Gut. 2008;57(12):1698-1703.
  9. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology. 2013;13(4 Suppl 2):e1-e15.
  10. Mortele KJ, Ip IK, Wu BU, Conwell DL, Banks PA, Khorasani R. Acute pancreatitis: imaging utilization practices in an urban teaching hospital–analysis of trends with assessment of independent predictors in correlation with patient outcomes. Radiology. 2011;258(1):174-181.
  11. Koo BC, Chinogureyi A, Shaw AS. Imaging acute pancreatitis. Br J Radiol. 2010;83(986):104-112.
  12. Whitlock TL, Repas K, Tignor A, et al. Early readmission in acute pancreatitis: incidence and risk factors. Am J Gastroenterol. 2010;105(11):2492-2497.
  13. Di MY, Liu H, Yang ZY, Bonis PA, Tang JL, Lau J. Prediction Models of Mortality in Acute Pancreatitis in Adults: A Systematic Review. Ann Intern Med. 2016;165(7):482-490.
  14. Gao W, Yang HX, Ma CE. The Value of BISAP Score for Predicting Mortality and Severity in Acute Pancreatitis: A Systematic Review and Meta-Analysis [published correction appears in PLoS One. 2015;10(10):e0142025]. PLoS One. 2015;10(6):e0130412. Published 2015 Jun 19.

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