eMedicine Specialties > Gastroenterology > Pancreas

Pancreatitis, Acute: Follow-up

Author: Timothy B Gardner, MD, Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of Pancreatic Disorders, Section of Gastroenterology, Dartmouth-Hitchcock Medical Center
Coauthor(s): Brian S Berk, MD, Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of End Stage Liver Disease, Section of Gastroenterology, Dartmouth Hitchcock Medical Center; Paul Yakshe, MD, Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview University Medical Center
Contributor Information and Disclosures

Updated: Jun 10, 2008

Follow-up

Further Inpatient Care

  • Further inpatient care depends on whether any of the complications of severe pancreatitis develop and how well patients respond to treatment. This ranges from a few days to several months of intensive care.
  • Patients can be discharged when their pain is well controlled with oral analgesia, they are able to tolerate an oral diet that maintains their caloric needs, and all complications have been addressed adequately.

Further Outpatient Care

  • Once the patient is stable enough to be discharged from the hospital, routine clinical follow-up care is needed to monitor for potential complications of the pancreatitis, especially pseudocysts.
  • No evidence-based guidelines have been established for outpatient follow-up care. Generally, a reasonable time to see the patient is within 7-10 days from the date of hospital discharge to evaluate how he or she is doing and to check for signs or symptoms of complications. If the pancreatitis was moderate to severe and associated with peripancreatic fluid collections, subsequent imaging studies are indicated to determine if a pseudocyst has developed.

Transfer

  • No evidence-based guidelines have been established to indicate when a patient should be transferred to a more experienced or skilled medical center. Nevertheless, if severe acute pancreatitis is suggested by the Atlanta Criteria or by a CRP level greater than 10 mg/dL, a Ranson score of 4 or greater, or an APACHE II score of 9 or greater, it is appropriate to consider transfer to an institution where an intensivist staffs the critical care unit and an interested subspecialist experienced in the diagnosis and treatment of pancreatitis is available.

Deterrence/Prevention

  • When the cause of pancreatitis can be determined, prevention depends on preventing the etiologic agent from causing subsequent episodes.
    • In patients with documented gallstone pancreatitis, and probably in those with idiopathic recurrent pancreatitis, a cholecystectomy is required.
    • In patients who abuse alcohol, a dedicated person (eg, physician, psychologist, addiction counselor) who can help the patient overcome the addiction to alcohol is required.
    • When an uncommon cause of pancreatitis is identified, the path of prevention is specific to the etiology.

Complications

  • Acute fluid collections
    • These commonly occur early in the course of acute pancreatitis.
    • They are primarily detected by imaging studies and not physical examination.
    • Because they lack a defined wall and usually regress spontaneously, most acute fluid collections require no specific therapy.
  • Pseudocyst
    • This is a collection of pancreatic fluid enclosed by a wall of granulation tissue and requires 4 or more weeks to develop.
    • While they are sometimes palpable on physical examination, they are usually detected with abdominal ultrasonography or CT scanning.
  • Intra-abdominal infections
    • Within the first 1-3 weeks, fluid collections or pancreatic necrosis can become infected and jeopardize clinical outcome.
    • From 3-6 weeks, pseudocysts may become infected or a pancreatic abscess may develop. A pancreatic abscess is a circumscribed intra-abdominal collection of pus, within or in proximity to the pancreas. It is believed to arise from localized necrosis, with subsequent liquefaction that becomes infected.
    • Intestinal florae are the predominant source of bacteria causing the infection. The usual suspects are Escherichia coli (26%), Pseudomonas species (16%), Staphylococcus species (15%), Klebsiella species (10%), Proteus species (10%), Streptococcus species (4%), Enterobacter species (3%), and anaerobic organisms (16%).
    • Fungal superinfections may occur weeks or months into the course of severe necrotizing pancreatitis.
  • Pancreatic necrosis
    • This is a nonviable area of pancreatic parenchyma that is often associated with peripancreatic fat necrosis and is principally diagnosed with the aid of dynamic spiral CT scans.
    • Distinguishing between infected and sterile pancreatic necrosis is an ongoing clinical challenge.
    • Sterile pancreatic necrosis is usually treated with aggressive medical management, whereas almost all patients with infected pancreatic necrosis require surgical debridement or percutaneous drainage if they are to survive.

Prognosis

  • Clinical assessment and prognostication
    • Identifying patients in greatest need of aggressive medical treatment by differentiating their disease severity as mild or severe is recommended.
    • In mild disease, the pancreas exhibits interstitial edema, an inflammatory infiltrate without hemorrhage or necrosis, and, usually, minimal or no organ dysfunction.
    • In severe disease, the inflammatory infiltrate is severe, associated with necrosis of the parenchyma, often accompanied by evidence of severe gland dysfunction, and it may be associated with multiorgan system failure.
    • Several clinical scoring systems (eg, Ranson criteria, Glasgow, Imrie) are available. The APACHE II scoring system, though cumbersome, appears to be the best validated.
  • Biological markers
    • The most widely available marker is the hematocrit value. Admission hemoconcentration to a hematocrit value greater than 47% had been reported as a sensitive marker to predict pancreatic necrosis at admission. However, subsequent study has revealed admission hematocrit to be useful only as a negative predictor for necrosis in patients without hemoconcentration.
    • CRP, an acute-phase reactant released in response to interleukin-6, is a useful marker at 36-48 hours.
    • Interleukin-6 levels begin to rise in the first several hours of pancreatitis, stimulating the release of CRP. Early studies appear promising, indicating that this may be a reliable indicator of severity. This is not yet validated and not yet commercially available for clinical use.
  • Genetic markers: Polymorphisms in the chemokine monocyte chemotactic protein 1 (MCP-1) gene may play a role in predisposing patients to severe acute pancreatitis, although this marker is still under investigation and is not used clinically.

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • Serum amylase and lipase levels can be elevated in patients with brain injury (eg, cerebrovascular accident, brain trauma).
    • These patients are generally cared for in an intensive care unit and require mechanical ventilation.
    • Pancreatic enzyme elevations may rise and fall dangerously over many days to weeks. The elevation is believed to result from the hyperstimulation of the pancreas from a central mechanism, but no evidence of acute pancreatitis is present on imaging studies.
  • Failure to identify disease severity can be an area of medical/legal hazard. Recognizing patients with severe acute pancreatitis as soon as possible is critical to achieving optimal outcomes.
  • Patients should not have ERCP in the setting of acute pancreatitis unless they (1) are clinically worsening and have suspected gallstone pancreatitis, or (2) have increasing obstructive liver tests with known choledocholithiasis.  Otherwise, ERCP should be avoided in all patients with acute pancreatitis.
  • Autoimmune pancreatitis is a rare condition.  Corticosteroids should not be used to treat this condition in the short term in patients who are suspected of having autoimmune pancreatitis and who present with acute pancreatitis.

Special Concerns

  • Recurrent acute pancreatitis can be a challenging clinical problem. First, seek to determine the etiology using modalities that subject the patient to the least risk while simultaneously assessing for treatable causes.
    • Abdominal CT scanning is a reasonable first approach. If neoplasia or chronic pancreatitis is found, it must be addressed and treated accordingly.
    • If the CT scan is not diagnostic, order MRCP. If this shows developmental abnormalities, strictures, or evidence of chronic pancreatitis, remember that endoscopic or surgical treatment may be of benefit in a subset of patients.
    • If the MRCP findings are normal, further evaluation by EUS is indicated. This has a better sensitivity for detecting biliary sludge and microlithiasis, which are probably the most common causes of recurrent idiopathic pancreatitis. EUS may also help detect periampullary lesions missed by abdominal CT scanning or MRCP.
    • If prior studies showed evidence of microlithiasis or biliary sludge, a cholecystectomy is indicated. If the patient has already had a cholecystectomy or if pancreatitis recurs, further evaluation by ERCP is indicated. This may reveal papillary stenosis, in which case a pancreatic and, possibly, biliary sphincterotomy are indicated.
    • The role of genetic testing is emerging, and whether testing for cationic trypsinogen mutations, SPINK1 mutations, or CFTR mutations should be performed remains unclear, because no effective treatment currently exists for these diseases.
    • If recurrent pancreatitis continues, ERCP with sphincter of Oddi manometry is indicated. This is placed last in the evaluation because patients with suspected SOD (especially resulting from sphincter of Oddi dyskinesia) have a very high rate of post-ERCP pancreatitis, and creating more iatrogenic complications than cures of recurrent pancreatitis is a concern.
 


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References
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Further Reading

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Keywords

pancreas, pancreatic enzymes, pancreastasis, pancreatic autodigestion, abdominal pain, elevated pancreatic enzyme levels, inflammation of the pancreas, endoscopic retrograde cholangiopancreatography, ERCP, magnetic resonance cholangiopancreatography, MRCP, endoscopic ultrasound, zymogen granules, alcohol abuse, alcohol dependence, alcoholism, alcoholics, biliary disease, biliary tract disease

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Contributor Information and Disclosures

Author

Timothy B Gardner, MD, Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of Pancreatic Disorders, Section of Gastroenterology, Dartmouth-Hitchcock Medical Center
Timothy B Gardner, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, American Pancreatic Association, and American Society of Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Coauthor(s)

Brian S Berk, MD, Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of End Stage Liver Disease, Section of Gastroenterology, Dartmouth Hitchcock Medical Center
Brian S Berk, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, and American Gastroenterological Association
Disclosure: Nothing to disclose.

Paul Yakshe, MD, Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview University Medical Center
Paul Yakshe, MD is a member of the following medical societies: American College of Gastroenterology, American Pancreatic Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Tushar Patel, MB, ChB, Professor of Medicine, Director of Hepatology, Ohio State University Medical Center
Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Noel Williams, MD, Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada
Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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