Hospital Medicine

Pancreatic abscess; Infections of the pancreas

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Pancreatic abscess; Infections of the Pancreas

I. What every physician needs to know.

Acute pancreatitis can be associated with infectious complications. Early in the course of acute pancreatitis it is often difficult to differentiate the systemic inflammatory response syndrome (SIRS) that occurs due to pancreatitis itself from that related to the development of infection. Infectious complications of acute pancreatitis typically occur in patients with associated pancreatic necrosis. Though it was previously thought that infectious complications are more likely to arise later in the disease course, recent evidence has suggested that infections of the pancreas can arise within 7-14 days of admission.

Infected necrosis represents a major cause of morbidity and mortality in patients with acute pancreatitis and can result from infection of either an acute necrotic collection (ANC) or an area of walled off necrosis (WON). Infected necrosis should be suspected in patients who fail to improve or deteriorate after 7-10 days of supportive treatment. There is no clear correlation between extent of necrosis and infection risk. Empiric antibiotic therapy should always be initiated when superimposed infection is suspected and continued until infection is definitively ruled out.

The original Atlanta classification system for pancreatitis previously used the term “pancreatic abscess” to describe the presence of a localized collection of purulent material (without significant necrosis) that resulted from an episode of acute pancreatitis. However, due to the scarcity of this finding and confusion surrounding the term, the revised 2012 classification guidelines no longer include the term “pancreatic abscess” as an infectious complication of the pancreas.

Infection of necrotic pancreatic tissue is thought to occur via colonic translocation of bacteria flora. For this reason, causative organisms are typically gram-negative gut flora, although gram-positive infections are also seen (most commonly Enterococcus). Although rare, infection with fungal, viral, and other less common bacterial pathogens does occur.

II. Diagnostic Confirmation: Are you sure your patient has a pancreatic infection?

A persistently elevated white blood cell count, fevers, worsening abdominal pain, positive blood cultures, and failure to improve despite appropriate initial management may all be suggestive of superimposed infection of the pancreas. However, none is specific for this condition. Computed tomography (CT) scan demonstrating gas within pancreatic tissue is highly suggestive of infected necrosis. Gram stain and cultures from CT-guided fine needle fluid aspiration of the fluid collection can be used to confirm the diagnosis.

A. History Part I: Pattern Recognition:

Patients at risk for pancreatic infection include those with acute pancreatitis complicated by pancreatic necrosis. Superimposed infection should be suspected in patients who fail to improve after 7-10 days of hospitalization and supportive care, and in those who rapidly deteriorate. Although development of SIRS can often be attributed to pancreatitis itself, an infectious evaluation should be undertaken and empiric antibiotic therapy initiated until infection has been ruled out.

B. History Part 2: Prevalence:

Pancreatic necrosis is the major predisposing risk factor for development of infectious pancreatic complications though extent of necrosis has not been clearly shown to correlate with risk of infection. Necrotizing pancreatitis occurs in approximately 20% of patients with acute pancreatitis. Development of infected pancreatic necrosis carries a mortality rate upwards of 30%. No genetic or gender differences in rates of infectious complications have been demonstrated.

C. History Part 3: Competing diagnoses that can mimic pancreatic infection.

Other differential considerations include pancreatic pseudocyts, pancreatic necrosis without associated infection, gastric ulcer, cholangitis, cholecystitis, mesenteric ischemia, bowel obstruction and a perforated viscus. Other hospital-acquired infections can also present similarly. Imaging is often required to differentiate among these conditions. However, in patients admitted with acute pancreatitis who follow an unexpectedly prolonged hospital course complicated by fevers and progressive symptoms, superimposed pancreatic infection should remain a primary consideration.

D. Physical Examination Findings.

Physical exam findings in patients with pancreatic infections generally parallel the symptoms of acute pancreatitis but are often more severe and occur after 7-10 days of hospitalization. Abdominal pain is located in the midepigastric region. An associated mass may or may not be present. In severe pancreatitis, patients are often markedly dehydrated on presentation. Hypotension and/or hypoxia may signal progression to shock. Fevers can result from underlying infection but also occur in the setting of ongoing pancreatic inflammation.

E. What diagnostic tests should be performed?

Laboratory markers to assess the severity of pancreatitis and blood cultures should be sent on all patients. Imaging studies are also required when a patient fails to improve despite 48-72 hours of supportive treatment and/or pancreatic infection is suspected.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

A number of laboratory tests can be sent if pancreatic infection is suspected, though none are specific for this condition. On initial presentation, hematocrit, chemistry panel, liver function tests, lactate dehydrogenase, and C-reactive protein (CRP) should be sent to help assess severity of underlying pancreatitis. A CRP level of greater than 150 mg/L has been shown to be associated with the presence of necrosis (sensitivity >80%, specificity >80%) with peak values typically occurring 36-72 hours after admission. An admission hematocrit of greater than 44% is another clearly identified risk factor for underlying pancreatic necrosis. Please see detailed section on acute pancreatitis for further details regarding severity and scoring systems.

For those patients in whom development of pancreatic infection is suspected, blood cultures should be sent. If imaging suggests the presence of an infected ANC or WON, fine needle aspiration with gram stain and culture should be considered to help guide antibiotic therapy.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Abdominal CT scan with contrast or contrast-enhanced magnetic resonance imaging (MRI) are both options for assessment of pancreatic necrosis though CT is more commonly used. In patients with renal failure who cannot receive contrast, a nonenhanced MRI can still detect underlying pancreatic necrosis and is the preferred imaging option. The presence of extraluminal gas in the pancreatic and/or peripancreatic tissues on imaging is consistent with underlying infection.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Ultrasound should only be considered if CT or MRI cannot be performed. Overlying bowel gas often limits visualization and ultrasound cannot reliably identify pancreatic necrosis. Following initial diagnosis, serial lipase and amylase measurements are of limited clinical utility in monitoring the course of acute pancreatitis. The degree of lipase and amylase elevation does not correlate with disease severity, disease course, or clinical outcomes. However, persistently elevated serum amylase and/or lipase values over a period of weeks can raise concern for ongoing pancreatic inflammation, pseudocyst, and other pancreatic complications.

III. Default Management

If pancreatic abscess or infection is suspected, CT scan or MRI should immediately be performed. Routine use of antibiotics or antifungal agents is no longer recommended for prevention of infection in cases of severe pancreatitis or sterile necrosis. However, if infected necrosis is suspected, CT-guided fine needle aspiration (FNA) should be considered and/or empiric antibiotic therapy begun. Though CT-guided FNA has been shown to be safe and effective there is debate as to whether this should be pursued in all patients with suspected pancreatic infection. If FNA is pursued, empiric antibiotics can be started while awaiting culture results with antibiotics later discontinued if sterile necrosis is confirmed. Initiation of empiric antibiotic therapy without FNA is also reasonable, reserving FNA for those who fail to respond to antibiotic therapy or in whom an underlying fungal etiology is suspected.

Antibiotic regimens should include those with adequate penetration into necrotic tissue. Favored empiric antibiotics include the carbapenems, quinolones, and metronidazole. Should infectious work-up yield the presence of gram-positive bacteria, vancomycin should also be added pending final culture results.

Intravenous fluids and nutritional support should be continued as in any case of severe pancreatitis. Although there is not a clear consensus on the exact amount of fluid resuscitation required, failure to adequately correct hemoconcentration can predispose patients to development of pancreatic necrosis. General recommendations include fluid boluses as needed to maintain hemodynamic stability, then continuing a maintenance rate of crystalloid at 250-500 ml/hr for the first 12-24 hours and for up to 48 hours. Patients must be closely monitored for development of associate respiratory distress and/or hypoxia during this time period.

A. Immediate management.

Emergency management of suspected pancreatic infection includes close monitoring, prompt imaging, and consideration of empiric antibiotic therapy. CT-guided FNA should be considered. If concurrent hemodynamic instability is noted, surgery should be consulted as urgent debridement may be necessary.

Order set for when pancreatic infection is suspected:

- CBC with differential

- Blood cultures, 2 sets

- CT scan with contrast or MRI with gadolinium, MRI without gadolinium can be obtained in those unable to receive contrast due to renal failure

- Empiric antibiotics for positive culture or systemic signs of infection

- Consider interventional radiology consult for CT-guided FNA if fluid collection visualized on imaging and infection is suspected

- Surgical consult for possible urgent debridement if the patient becomes hemodynamically unstable

- For stable patients with symptomatic infected necrosis, minimally-invasive methods of necrosectomy are preferred over open necrosectomy due to improved clinical outcomes

When possible, culture results should be used to tailor therapy. For empiric therapy, recommendations are as follows:

Carbapenems may be used alone:

- Imipenem 500 mg IV q8 (drug of choice based on available data)

- Ertapenem 1 g IV q24

- Meropenem 1 g IV q8

- Doripenem 500 mg IV q8

OR, combination therapy with fluoroquinolones and metronidazole is a reasonable alternative:

- Ciprofloxacin 400 mg IV q8

- Levofloxacin 500 mg IV q24

- Moxifloxacin 400 mg IV q24

- Plus, metronidazole 500 mg IV q6-8

When culture results are available, other antibiotics with good penetration include:

- Ceftazidime 1-2 g IV q8-12

- Cefepime 2 g IV q8-12

- Clindamycin 1.2-2.7 g/day in 2-4 divided doses (maximum dose: 4.8 g/day)

B. Physical Examination Tips to Guide Management.

Resolution of fevers, tachycardia and hypotension, as well as improvement in any associated abdominal pain are all potential markers of clinical improvement in this condition, although none are specific to this diagnosis.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Daily CBCs should be followed to ensure leukocytosis resolves. For those with confirmed pancreatic infection and associated bacteremia, serial blood cultures should be followed to confirm eventual clearance of infection. If the original pancreatic aspirate cultures are negative but infectious symptoms persist, recurrent aspiration every 5-7 days can be considered to identify ongoing or evolving infection.

D. Long-term management.

Prior to discharge, the underlying etiology of the pancreatitis should be established in an effort to decrease risk of recurrence. Please see section on acute pancreatitis for specific management of the underlying causes of acute pancreatitis. Discharge can be considered when patients no longer exhibit signs or symptoms of underlying infection, have adequately controlled pain and are able to adequately maintain hydration and nutritional intake. For those who cannot eat due to persistent pain or other complications, a feeding tube may be required. For confirmed infections, duration of therapy should be tailored accordingly. In stable patients with known infected necrosis, surgical, radiologic, and endoscopic drainage should be delayed for more than 4 weeks if possible. Such interventions are preferably delayed to allow time for liquefaction of the contents of the necrotic area and the development of WON.

E. Common Pitfalls and Side-Effects of Management.

IV. Management with Co-Morbidities.

A. Renal Insufficiency.

Imaging modality may be affected by degree of renal insufficiency. If renal failure is present, CT and MRI with contrast agents are contraindicated. However, MRI without contrast can be used in the detection of pancreatic necrosis.

Imipenem should not be used in individuals with significantly reduced creatinine clearance, unless they will receive dialysis within 48 hours of administration. Those weighing less than 30 kg with impaired renal function should also not receive imipenem due to increased risk of seizures and thrombocytopenia in these patient populations. Ciprofloxacin and levofloxacin require dosage reductions with renal impairment, while moxifloxacin does not. Consider dosage reductions of metronidazole in patients with significantly impaired creatinine clearance.

B. Liver Insufficiency.

Dosage reductions of metronidazole are required in severe liver disease.

C. Systolic and Diastolic Heart Failure.

Exercise caution with fluid resuscitation. Otherwise, no change in standard management.

D. Coronary Artery Disease or Peripheral Vascular Disease.

No change in standard management.

E. Diabetes or other Endocrine issues.

No change in standard management.

F. Malignancy.

No change in standard management.

G. Immunosuppression (HIV, chronic steroids, etc.).

No change in standard management, although a low threshold for empiric antibiotic therapy should be utilized in patients with a history of immunosuppression.

H. Primary Lung Disease (COPD, Asthma, ILD).

No change in standard management.

I. Gastrointestinal or Nutrition Issues.

No change in standard management.

J. Hematologic or Coagulation Issues.

No change in standard management.

K. Dementia or Psychiatric Illness/Treatment.

No change in standard management.

V. Transitions of Care.

A. Sign-out considerations While Hospitalized.

Follow vital signs at least every 4 hours. If evidence of decompensation or sepsis arises, initiate empiric antibiotic therapy. Exercise a low threshold to transfer to the intensive care unit for closer monitoring.

B. Anticipated Length of Stay.

The average length of stay for complicated pancreatitis varies greatly but can last for weeks, depending on the severity of pancreatitis on initial presentation and on whether associated complications arise.

C. When is the Patient Ready for Discharge.

Discharge should be considered when hemodynamic stability has been ensured, adequate pain control achieved with oral medications and the patient can maintain oral nutrition and hydration independently. For patients who are unable to meet nutritional needs with oral nutrition, feeding tubes are often necessary.

D. Arranging for Clinic Follow-up.

1. When should clinic follow up be arranged and with whom.

Follow-up with both a gastroenterologist and primary care physician should occur within 1-2 weeks of discharge. For those who required surgical intervention while hospitalized, surgery follow-up should also be arranged within a few weeks of discharge depending on the type and extent of procedure performed.

2. What tests should be conducted prior to discharge to enable best clinic first visit.


3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

Repeat labs including a CBC with differential and comprehensive chemistry panel should be sent to ensure stability and are required if patients remain on long-term antibiotic therapy.

E. Placement Considerations.

Peripherally inserted central catheter (PICC) placement is indicated for patients requiring long-term antibiotic therapy and should be placed prior to discharge. Feeding tubes may also be required for patients who remain unable to maintain adequate nutrition and hydration orally. For those with a prolonged hospitalization, rehabilitation centers offering acute rehabilitation or subacute nursing should be strongly considered. Referrals should be placed early once hemodynamic stability has been ensured and discharge is anticipated.

F. Prognosis and Patient Counseling.

The hospital mortality rate of severe acute pancreatitis approaches 20%. The mortality rate rises to upwards of 30% in the presence of infected pancreatic necrosis. Patient counseling should be tailored to help prevent recurrent episodes of pancreatitis when appropriate (i.e., alcohol cessation counseling for alcoholic pancreatitis, surgery consultation for cholecystectomy in gallstone pancreatitis).

VI. Patient Safety and Quality Measures.

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Appropriate referrals should be made to prevent recurrent episodes of pancreatitis when appropriate. For example, referral for cholecystectomy in gallstone pancreatitis and alcohol cessation counseling for alcohol-related pancreatitis. Please see section on acute pancreatitis for further details.

VII. What's the evidence?

Arvanitakis, M, Koustiani, G, Gantzarou, A.. "Staging of severity and prognosis of acute pancreatitis by computed tomography and magnetic resonance imaging - a comparative study". Dig Liver Dis. vol. 39. 2007. pp. 473-82.

Baillargeon, JD, Orav, J, Ramagopal, V. "Hemoconcentration as an early risk factor for necrotizing pancreatitis". Am J Gastroenterol. vol. 93. 1998. pp. 2130-4.

Banks, PA, Bollen, TL, Dervenis, C. "Classification of acute pancreatitis-2012: revision of the Atlanta classification and definitions by international consensus". Gut. vol. 62. 2013. pp. 102-111.

Banks, PA, Freeman, ML. "Practice Guidelines in Acute Pancreatitis". Am J Gasteroenterol. vol. 101. 2006. pp. 2379-2400.

Beger, HG, Rau, BM.. "Severe acute pancreatitis: Clinical course and management". World J Gastroenterol. vol. 13. 2007. pp. 5043-51.

Dionigi, R, Rovera, F, Dionigi, G. "Infected pancreatic necrosis". Surg Infect (Larchmt). vol. 7. 2006. pp. S49-52.

Gardner, TB, Vege, SS, Pearson, RK. "Fluid Resuscitation in Acute Pancreatitis". Clin Gastroenterol Hepatol. 2008. pp. 6L1070-1076.

Lenhart, DK, Balthazar, EJ.. "MDCT of acute mild (nonnecrotizing) pancreatitis: abdominal complications and fate of fluid collections". AJR Am J Roentgenol. vol. 190. 2008. pp. 643-9.

Solomkin, JS, Mazuski, JE, Bradley, JS. "Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America". Surg Infect (Larchmt). vol. 11. 2010. pp. 79-109.

Tenner, S, Baillie, J, DeWitt, J, Vege, SS.. "American College of Gastroenterology guideline: management of acute pancreatitis". Am J Gastroenterol. vol. 108. 2013. pp. 1416-15.

Whitcomb, D.. "Acute Pancreatitis". N Engl J Med. vol. 354. 2006. pp. 2142-50.

Quinlan, J.. "Acute pancreatitis". Am Fam Physician. vol. 90. 2014 Nov 1. pp. 632-639.

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