Acute pancreatitis

Overview 
Theory 
Diagnosis 
Management 
Follow up 
Resources 

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

all patients

1st line – fluid resuscitation

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1st line –

fluid resuscitation

Early and adequate fluid replacement is the single most important step in initial treatment. Evidence suggests early fluid resuscitation reduces the risk of organ failure and death.[55][114][115]

Administer intravenous fluids to all patients with suspected or confirmed acute pancreatitis, even those with mild disease.[9][54] Failure to give enough fluids is a common error, particularly in patients who present with mild symptoms.[9][54]
Initial treatment aims are to limit the severity of inflammation, pancreatic necrosis and to provide supportive treatment.[104] For patients that are not hypovolaemic, an intravenous fluid bolus is not recommended. The aim is to correct hypovolaemia without causing overhydration.[105] Volume status should be reassessed at 12, 24, 48, and 72 hours to evaluate for hypovolaemia.[105]
Check local protocols for specific recommendations on fluid choice.There is debate, based on conflicting evidence, on whether there is a benefit in using normal saline or balanced crystalloid in critically ill patients.
- Be aware that large volumes of normal saline as the sole fluid for resuscitation may lead to hyperchloraemic acidosis. This has particular relevance in acute pancreatitis where low pH may trigger premature trypsinogen activation and exacerbate abdominal pain. If the patient has had a large volume of saline infused, it is important to monitor sodium and chloride.
Some guidelines specifically recommend use of Ringer’s lactate (a balanced crystalloid) for patients with acute pancreatitis.[9][54] There is weak evidence of an anti-inflammatory effect with Ringer’s lactate; however, high-quality evidence on choice of fluid specific to patients with acute pancreatitis is lacking.[25][111][112]

Start intravenous fluid therapy, titrating to one or more of the following indicators of end-organ perfusion[54][106][113]

Heart rate <120 bpm
Mean arterial pressure 65 to 85 mmHg
Urinary output >0.5 to 1 mL/kg/hour
Haematocrit 35% to 44%
Note that central venous pressure may be unreliable as an indicator of adequate resuscitation.[8][54]

Patients with acute severe pancreatitis should be catheterised to monitor urine output.

Practical tip

Note that use of lactate-containing fluid in a patient with impaired liver metabolism may lead to a spuriously elevated lactate level, so results need to be interpreted with other markers of volume status.

Practical tip

Beware systemic inflammatory response syndrome (SIRS) and/or multi-organ failure - these are the biggest risk to life in the first week.[9][54][56]

Pancreatic inflammation and the SIRS response can lead to third space fluid loss, resulting in profound hypovolaemia, hypoperfusion, and end-organ damage.
Assess for signs of organ dysfunction, particularly cardiovascular, respiratory, or renal.
Consider intensive care unit (ICU) transfer for any patient who has SIRS or early signs of organ failure.

Evidence: Choice of fluids

Evidence from two large randomised controlled trials (RCTs) suggests there is no difference between normal saline and a balanced crystalloid for critically ill patients in mortality at 90 days, although results from two meta-analyses including these RCTs point to a possible small benefit of balanced solutions compared with normal saline.

There has been extensive debate over the choice between normal saline (an unbalanced crystalloid) versus a balanced crystalloid (such as Hartmann’s solution [also known as Ringer’s lactate] or Plasma-Lyte®). Clinical practice varies widely, so you should check local protocols.

In 2021-2022, two large double-blind RCTs were published assessing intravenous fluid resuscitation in intensive care unit (ICU) patients with a balanced crystalloid solution (Plasma-Lyte®) versus normal saline: the Plasma-Lyte® 148 versus Saline (PLUS) trial (53 ICUs in Australia and New Zealand; N=5037) and the Balanced Solutions in Intensive Care Study (BaSICS) trial (75 ICUs in Brazil; N=11,052).[116][117]
- In the PLUS study, 45.2% of patients were admitted to ICU directly from surgery (emergency or elective), 42.3% had sepsis, and 79.0% were receiving mechanical ventilation at the time of randomisation.
- In the BaSICS study, almost half the patients (48.4%) were admitted to the ICU after elective surgery and around 68% had some form of fluid resuscitation before being randomised.
- Both found no difference in 90-day mortality overall or in prespecified subgroups for patients with acute kidney injury (AKI) or sepsis, or post-surgery. They also found no difference in the risk of AKI.
- Neither study included specific/subgroup information on patients with acute pancreatitis.
One meta-analysis of 13 RCTs (including PLUS and BaSICS) confirmed no overall difference, although the authors did highlight a non-significant trend towards a benefit of balanced solutions for risk of death.[118]
A subsequent individual patient data meta-analysis included 6 RCTs of which only PLUS and BaSICS were assessed as being at low risk of bias. There was no statistically significant difference in in-hospital mortality (Odd's ratio [OR] 0.96, 95% confidence interval [CI] 0.91, 1.02). However, the authors argued that using a Bayesian analysis there was a high probability that balanced solutions reduced in-hospital mortality, although they acknowledged that the absolute risk reduction was small.[119]
One 2025 network meta-analysis included 28 studies assessing the effectiveness of balanced crystalloids for fluid resuscitation in patients with sepsis and septic shock only. It showed a significant reduction in 90-day mortality (Risk ratio [RR] -0.89; 95% CI 0.81, 0.97) for sepsis patients receiving balanced crystalloids compared to those receiving normal saline.
Previous evidence has been mixed.
- One 2015 double-blind, cluster-randomised, double-crossover trial conducted in four ICUs in New Zealand (N=2278), the 0.9% Saline vs Plasma-Lyte® for ICU fluid Therapy (SPLIT) trial, found no difference for in-hospital mortality, acute kidney injury, or use of renal-replacement therapy.[120]
- However, a 2018 US multicentre unblinded cluster-randomised trial - the isotonic Solutions and Major Adverse Renal events Trial (SMART), among 15,802 critically ill adults receiving ICU care - found possible small benefits from balanced crystalloid (Ringer’s lactate or Plasma-Lyte®) compared with normal saline. The 30-day outcomes showed a non-significant reduced mortality in the balanced crystalloid group versus the normal saline group (10.3% vs. 11.1%; odds ratio [OR] 0.90, 95% CI 0.80 to 1.01) and a major adverse kidney event rate of 14.3% versus 15.4%, respectively (OR 0.91, 95% CI 0.84 to 0.99).[121]
One 2019 Cochrane review included 21 RCTs (N=20,213) assessing balanced crystalloids versus normal saline for resuscitation or maintenance in a critical care setting.[122]
- The three largest RCTs in the Cochrane review (including SMART and SPLIT) all examined fluid resuscitation in adults and made up 94.2% of participants (N=19,054).
- There was no difference in in‐hospital mortality (OR 0.91, 95% CI 0.83 to 1.01; high-quality evidence as assessed by GRADE), acute renal injury (OR 0.92, 95% CI 0.84 to 1.00; GRADE low), or organ system dysfunction (OR 0.80, 95% CI 0.40 to 1.61; GRADE very low).
There are very few high-quality studies on choice of fluid specifically for patients with acute pancreatitis. The 2018 American Gastroenterological Association (AGA) Institute guideline and the 2020 guideline from the UK National Institute for Health and Care Excellence (NICE) both concluded there is insufficient evidence to recommend one crystalloid over another.[8][106] Similarly, the 2019 World Society of Emergency Surgery (WSES) guidelines for the management of severe acute pancreatitis recommend isotonic crystalloids without specifying a preference for type of fluid; however, the WSES also states that Ringer’s lactate may be associated with anti-inflammatory effect, although evidence for superiority of Ringer’s lactate versus normal saline based on randomised trials is weak.[25]
A balanced crystalloid is recommended in preference to normal saline by both the 2024 American College of Gastroenterology (ACG) guideline and the 2013 International Association of Pancreatology/American Pancreatic Association (IAP/APA) guideline.[9][54]
- This is based on an RCT that found the incidence of SIRS was lower among acute pancreatitis patients treated with Ringer’s lactate compared with normal saline.
- The ACG also notes potential benefits linked to the better pH balance of Ringer’s lactate compared with normal saline, which could theoretically result in metabolic acidosis and make the pancreatic acinar cells more susceptible to further injury.

Evidence: Fluid volume and duration

The overall weight of evidence is converging towards a moderate goal-directed fluid replacement strategy for patients with acute pancreatitis.

There has been extensive debate over the relative benefits of an aggressive versus a more conservative approach to fluid resuscitation in acute pancreatitis. While, traditionally, early aggressive hydration was standard practice there was no evidence for this approach. More recent studies suggest that both overly aggressive and overly conservative fluid therapy can cause harm in acute pancreatitis, and that a moderate goal-directed fluid replacement strategy offers the best overall patient outcomes.[50][123]

Overly aggressive fluid replacement can lead to increased mortality due to fluid overload. Two randomised controlled trials (RCTs) from the same research group in 76 and 116 patients with acute severe pancreatitis found that aggressive non-targeted fluid therapy (10-15 mL/kg/hour) was associated with significantly higher rates of sepsis, abdominal compartment syndrome, need for mechanical ventilation, and death compared with more conservative fluid replacement (5-10 mL/kg/hour).[124][125]
Conversely, one RCT in 60 patients with predicted mild acute pancreatitis found that aggressive early fluid resuscitation (20 mL/kg bolus followed by 3 mL/kg/hour) was associated with better clinical outcomes at 36 hours than more conservative hydration (10 mL/kg bolus followed by 1.5 mL/kg/hour). Both groups had a goal-directed approach with haematocrit, blood urea nitrogen (BUN), and creatinine levels assessed every 12 hours.[126]
However, one subsequent larger RCT (249 patients) was halted when interim analysis showed a significant between-group difference in safety outcomes, with the aggressive early fluid resuscitation group (20 mL/kg bolus followed by 3 mL/kg/hour) experiencing a higher incidence of fluid overload without improvement in clinical outcomes compared with the moderate fluid resuscitation group (10 mL/kg bolus followed by 1.5 mL/kg/hour). In both groups, fluids were adjusted based on clinical assessment at 12, 24, 48, and 72 hours.[123]

Guidelines differ in their specific recommendations so you should check local protocols:

The guideline committee for the UK NICE guideline on pancreatitis (first published 2018) was unable to make a recommendation on the speed of fluid resuscitation due to the lack of clear evidence at that time. The committee recommended further research in this area.[8]
The 2018 AGA Institute and 2013 IAP/APA guidelines both recommend goal-directed fluid resuscitation, with the latter specifying a starting volume of 5 to 10 mL/kg/hour.[54][106]
The 2019 WSES guideline for the management of severe acute pancreatitis recommends that fluid volume be adjusted to the patient’s age, weight, and pre-existing renal and/or cardiac conditions, and states that the value of early goal-directed therapy in patients with acute pancreatitis remains unknown.[25]
These guideline recommendations were published before the subsequent, larger RCT (249 patients) findings discussed above.

Consider – supplemental oxygen

Plus – analgesia

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Plus –

analgesia

Treatment recommended for ALL patients in selected patient group

Pain is the predominant symptom. Ensure it is treated promptly and effectively.[50]

Failure to control pain can compromise breathing and contribute to haemodynamic instability.[56]

In mild cases, use a standard pain ladder approach to select, monitor, and adjust analgesia.[50]

Use a pain score to monitor the response to analgesia and adjust the dose and/or type of analgesic using local pain management protocols.
Opioids may be needed for effective pain control.[56][127] [ ] [Evidence C]
- A Cochrane review found that opioids are an appropriate option in acute pancreatitis and may decrease the need for supplementary analgesia. However, the quality of evidence for different analgesia approaches was low.[127]

Morphine is considered safe despite a theoretical risk of exacerbating pancreatic inflammation.[56][127]

Despite the theoretical risk that morphine may increase pressure on the sphincter of Oddi and therefore exacerbate pancreatitis, there is no good evidence that this is clinically significant. In practice morphine is considered a safe option [56][127]

Practical tip

An example of a suitable pain relief regimen would be to start with a non-steroidal anti-inflammatory drug (NSAID) such as ibuprofen. If pain relief is inadequate, use a low-potency opioid (e.g., codeine) alone or in combination with ibuprofen. If pain relief continues to be inadequate, a high-potency opioid (e.g., morphine) with or without an adjunctive treatment (e.g., an NSAID) may be required.
In practice, many patients will require a high-potency opioid immediately rather than using the standard pain ladder approach.
Check your local protocols for specific advice on choice of drugs and doses.

Primary options

ibuprofen: 300-600 mg orally (immediate-release) every 6-8 hours when required, maximum 2400 mg/day

codeine phosphate: 30-60 mg orally/intramuscularly every 4 hours when required, maximum 240 mg/day

ibuprofen: 300-600 mg orally (immediate-release) every 6-8 hours when required, maximum 2400 mg/day

and

codeine phosphate: 30-60 mg orally/intramuscularly every 4 hours when required, maximum 240 mg/day

morphine sulfate: 5-10 mg orally (immediate-release)/subcutaneously/intravenously/intramuscularly every 4 hours initially, adjust dose according to response

Consider – anti-emetic

Plus – nutritional support

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Plus –

nutritional support

Treatment recommended for ALL patients in selected patient group

Start a normal oral diet as soon as the patient can tolerate it (ideally within 24 hours).

Use a low/normal fat soft or solid diet for early feeding. A liquid diet is unnecessary.[9][50][106]

Oral nutrition should resume as soon as the pain and any nausea/vomiting begins to subside.

Enteral feeding (oral or by enteral tube if oral feeding is not tolerated) is thought to protect the gut-mucosal barrier, reducing bacterial translocation and thereby reducing the risk of infected necrosis and other serious outcomes.[50][54][106]

Undertake repeat trials of oral feeding if it cannot be achieved on the first attempt in patients with mild disease.[106]

Early oral feeding is not successful in all patients, owing to pain, vomiting, or ileus.
Avoid routine requesting of nil by mouth status; it is important to attempt repeat feeding trials in patients with mild disease.[8]
Most patients with mild disease can re-establish oral feeding within 24-48 hours.[9]

Evidence: Oral feeding

Early oral feeding promotes better outcomes.

Latest evidence demonstrates that enteral (ideally oral) feeding reduces the risk of infected pancreatic necrosis and other serious outcomes.[106][107]

Combined results from 11 RCTs on early versus delayed feeding found:[106]
- No difference in mortality
- Delayed feeding was associated with a significantly higher risk of needing intervention for pancreatic necrosis (2.47-fold higher risk with delayed vs. early feeding, 95% confidence interval [CI] 1.41 to 4.35)
- A trend towards a higher risk of other poor outcomes for delayed versus early feeding:
  - Infected necrosis (Odd's ratio [OR] 2.69, 95% CI 0.8 to 3.6)
  - Multiple organ failure (OR 2.00, 95% CI 0.48 to 8.22)
  - Total necrotising pancreatitis (OR 1.84, 95% CI 0.88 to 3.86).

Enteral nutrition

In patients who areunable to feed orally, use enteral tube feeding rather than parenteral nutrition.

Start this within 72 hours of presentation.[8]
Nasojejunal or nasogastric tube feeding are both safe options.[8][9][50][54][56][106]
Many patients with predicted severe/moderately severe acute pancreatitis or necrotising pancreatitis do end up needing nutrition support. Always offer enteral (rather than parenteral) nutrition to patients in this group unless it is contraindicated.[8][106]
Either a polymeric or elemental enteral nutrition formulation can be used.[54]
- No specific enteral nutrition formulation has been proven to be better than another in improving clinical outcomes.[128][129]

Evidence: Benefits of enteral feeding

Enteral feeding is associated with a lower risk of serious complications and death compared with parenteral.

The use of enteral nutrition is associated with a lower likelihood of harm compared with parenteral nutrition.

There is good evidence to support the benefits of enteral compared with parenteral feeding in patients with acute pancreatitis. Enteral nutrition (orally or by tube) was associated with a significantly lower risk of infected pancreatic necrosis (OR 0.28, 95% CI 0.15 to 0.51), single organ failure (OR 0.25, 95% CI 0.10 to 0.62), and multi-organ failure (OR 0.41, 95% CI 0.27 to 0.63) in a meta-analysis of 12 RCTs for the 2018 AGA Institute guideline group.[106]
An earlier Cochrane review of eight RCTs also found that enteral nutrition, compared with total parenteral nutrition, significantly reduced mortality (RR 0.50, 95% CI 0.28 to 0.91), multi-organ failure (RR 0.55, 95% CI 0.37 to 0.81), systemic infections (RR 0.39, 95% CI 0.23 to 0.65), and the need for surgical intervention (OR 0.44, 95% CI 0.29 to 0.67) in patients with (predicted) severe acute pancreatitis. There was also a trend towards a shorter hospital stay.[130]

Debate: Timing of enteral nutrition

The evidence on the optimum timing to start enteral nutrition in (predicted) severe acute pancreatitis is mixed and guidelines differ.

Guidance from the UK National Institute for Health and Care Excellence (NICE) recommends enteral nutrition within 72 hours of presentation for any patient with severe or moderately severe acute pancreatitis.[8]

NICE’s review of the evidence found no benefit from delaying nutrition whereas underfeeding is known to be an issue in clinical practice, with some patients waiting 5 to 7 days for nutritional support.

One 2017 literature review concluded that the latest evidence supports limiting tube feeding to those patients with predicted severe pancreatitis who are unable to achieve sufficient oral calorie intake after 3 to 5 days.[50]

This is based on two RCTs that found no beneficial effects on infection rates or mortality from early nasojejunal feeding.

However, the IAP/APA 2013 guideline cites one small RCT of 60 patients with severe acute pancreatitis that found outcomes were better when enteral nutrition was started within 48 hours rather than delayed for 7 days of fasting.[131]

Evidence: Nasojejunal versus nasogastric tube feeding

There is no clear evidence of any difference in outcomes from nasojejunal versus nasogastric tube feeding.

Three RCTs that have compared nasoenteral (nasojejunal or nasoduodenal) versus nasogastric tube feeding in acute pancreatitis have failed to find any evidence of a significant difference in mortality.[106]

The 2018 AGA Institute guideline, the 2024 ACG guideline, and the 2013 IAP/APA guideline all recommend that either nasojejunal or nasogastric tube feeding can be used.[9][54][106]

Nasogastric tube insertion is a ward-based procedure that is easier and cheaper than nasojejunal tube insertion, which requires access to radiology or endoscopy.[9][56][132]
- Two RCTs have suggested that at least 80% of patients with severe acute pancreatitis can tolerate the nasogastric route.[133][134]
In practice, however, safety concerns over the risk of aspiration with a nasogastric tube mean that nasojejunal feeding is sometimes preferred in patients with severe acute pancreatitis, although there is little evidence to support this approach.[8][106] One Cochrane review of five RCTs that compared nasojejunal versus nasogastric tube feeding in severe acute pancreatitis failed to find evidence of a significant difference in mortality.[135]
Nasojejunal feeding may also be more effective in patients with gastric outlet obstruction or other types of digestive intolerance.[8][136]
Gastric feeding may be more suitable for patients with no duodenal stenosis or oedema.[8]
- If nasogastric tube feeding is used, the patient should be put in an upright position and placed on aspiration precautions.[9]

Parenteral nutrition

Parenteral nutrition is associated with higher mortality. Only use parenteral nutrition for patients in whom enteral feeding is not feasible, not tolerated, or failing to meet calorie requirements.[9][54]

Parenteral nutrition is associated with higher mortality and a higher risk of organ failure and/or pancreatic necrosis than enteral feeding.[106][130]
Parenteral nutrition should be reserved for patients who do not tolerate enteral feeding or cannot tolerate the targeted nutritional requirements, or if there are contraindications to enteral feeding. Contraindications to enteral feeding may include bowel obstruction, abdominal compartment syndrome, prolonged paralytic ileus, and mesenteric ischaemia.[136]

Consider – empirical intravenous antibiotics (if infection is confirmed or strongly suspected)

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Consider –

empirical intravenous antibiotics (if infection is confirmed or strongly suspected)

Additional treatment recommended for SOME patients in selected patient group

Only give antibiotics if pancreatic or extra-pancreatic infection is proven or strongly clinically suspected.[8][9][50][54][106]

Suspect infection based on signs and symptoms such as fever, leukocytosis, and signs of organ dysfunction.

Extra-pancreatic infections (e.g., pneumonia, cholangitis, urinary tract infections, sepsis) are a major cause of mortality in the early phase of acute pancreatitis when SIRS is the main cause of death.
- Up to 20% of patients with acute pancreatitis will develop an extra-pancreatic infection.[137]

Suspected infection should be treated empirically and aggressively with intravenous antibiotics. The antibiotics should be discontinued if blood cultures are negative and no source of infection is identified.[9]

Choose an antibiotic that has good pancreatic penetration, such as a carbapenem (e.g., imipenem/cilastatin), a fluoroquinolone (e.g., ciprofloxacin), or metronidazole.[9] Imipenem/cilastatin is usually the first-line choice because it has good pancreatic penetration. Check local guidance on antibiotic stewardship.

Systemic fluoroquinolone antibiotics may cause serious, disabling, and potentially long-lasting or irreversible adverse events. This includes, but is not limited to: tendinopathy/tendon rupture; peripheral neuropathy; arthropathy/arthralgia; aortic aneurysm and dissection; heart valve regurgitation; dysglycaemia; and central nervous system effects including seizures, depression, psychosis, and suicidal thoughts and behaviour.[156]

Prescribing restrictions apply to the use of fluoroquinolones, and these restrictions may vary between countries. In general, fluoroquinolones should be restricted for use in serious, life-threatening bacterial infections only. Some regulatory agencies may also recommend that they must only be used in situations where other antibiotics, that are commonly recommended for the infection, are inappropriate (e.g., resistance, contraindications, treatment failure, unavailability).
Consult your local guidelines and drug information source for more information on suitability, contraindications, and precautions.

Do not give prophylactic antibiotics in the absence of proven or highly suspected infection, regardless of predicted or actual disease severity, as there is no evidence to support their use.

There is no good evidence to support the use of prophylactic antibiotics to prevent infection in patients with acute pancreatitis, even among those with predicted severe disease or with sterile pancreatic necrosis. Major guidelines recommend against routine use of prophylactic antibiotics.[9][54][106]

Evidence: Prophylactic antibiotics

Prophylactic antibiotics have no benefits in reducing the risk of infected necrosis or death.

Three RCTs and two meta-analyses have failed to show any benefit from prophylactic antibiotics compared with placebo in reducing the risk of infection of pancreatic (or peri-pancreatic) necrosis or reducing the risk of death.[138][139][140][141][142]

Prophylactic antibiotics also have no impact on rates of organ failure or length of hospital stay.[106]
This lack of benefit from prophylactic antibiotics holds true for patients with predicted severe disease and those with sterile necrotising pancreatitis as well as those with milder disease, according to a meta-analysis conducted for the AGA Institute 2018 guideline group.[106]

Primary options

imipenem/cilastatin: 500-1000 mg intravenously every 6 hours

Secondary options

metronidazole: 500 mg intravenously every 8 hours

ciprofloxacin: 400 mg intravenously every 8-12 hours

Plus – severity assessment

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Plus –

severity assessment

Treatment recommended for ALL patients in selected patient group

Use SIRS criteria along with patient risk factors to assess severity in the first 48 hours.

Organ failure is of paramount importance in an early assessment of severity. Deaths in patients with acute pancreatitis occur in a biphasic pattern, with SIRS/multi-organ failure the main cause of death in the early phase (<2 weeks).
During the ongoing admission, assess severity based on persistent SIRS and the absence/presence of local complications. Local complications, in particular infected pancreatic necrosis, are the main cause of deaths in the late phase (>2 weeks).
Guidelines recommend using SIRS-based criteria rather than more complicated scoring systems such as APACHE II or Glasgow to assess severity.[9][54][106] For more information, see Risk stratification under Diagnosis Recommendations.

Never classify a patient as having mild disease until at least 48 hours after onset of symptoms. Many patients who go on to develop severe disease present without signs of organ failure or local complications.

Accurately assessing severity is challenging. Around 50% of patients will have predicted severe/moderately severe disease in the early period after presentation.[50] Only half of these patients will actually go on to develop severe/moderately severe pancreatitis.
Mortality among patients with predicted severe disease is around 10% compared with <1% in those with predicted mild disease.[50]

Immediately transfer to ICU any patient who meets the Atlanta Criteria for organ failure or who fulfills one or more of the below criteria:[54]

Heart rate <40 bpm or >150 bpm
Systolic arterial pressure <80 mmHg or mean arterial pressure <60 mmHg, or diastolic arterial pressure >120 mmHg
Respiratory rate >35 breaths/minute
Serum sodium <110 mmol/L or >170 mmol/L
Serum potassium <2 mmol/L or >7 mmol/L
pH <7.1 or >7.7
Serum glucose >44.4 mmol/L
Serum calcium >3.75 mmol/L
Anuria
Coma.

Consider – calcium replacement therapy

Consider – magnesium replacement therapy

gallstone pancreatitis: with cholangitis

Plus – endoscopic retrograde cholangiopancreatography (ERCP)

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Plus –

endoscopic retrograde cholangiopancreatography (ERCP)

Treatment recommended for ALL patients in selected patient group

Arrange emergency ERCP within 24 hours for any patient with acute gallstone pancreatitis who has concurrent cholangitis.[9][25][50][54] [ ]

There is clear evidence that ERCP within 24 hours of admission reduces morbidity and mortality in patients with acute gallstone pancreatitis complicated by cholangitis.[149]

Suspect cholangitis if Charcot’s triad is present:[50]

Jaundice
Fever and rigors
Right upper quadrant pain.

It is challenging to accurately diagnose cholangitis in patients who have SIRS, which is a common early phase complication in patients with (predicted) severe acute gallstone pancreatitis.

Several definitions have been proposed for cholangitis, including Charcot’s triad, expert opinion, and the updated TF13 Tokyo guidelines.[50][148] These use low thresholds for inflammation and cholestasis, both of which are commonly present in acute pancreatitis. This can lead to overdiagnosis of cholangitis in patients with acute pancreatitis, exposing patients to unnecessary and potentially risky ERCP procedures.[50]

gallstone pancreatitis: without cholangitis or bile duct obstruction

Plus – cholecystectomy

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Plus –

cholecystectomy

Treatment recommended for ALL patients in selected patient group

Arrange cholecystectomy for any patient with gallstones confirmed as the cause. It should be done during the initial admission for any patient with mild acute gallstone pancreatitis.[50][54][56][106]

Cholecystectomy is recommended to reduce the risk of recurrence of acute pancreatitis.
The optimum timing of cholecystectomy in different patient groups has been the subject of vigorous debate.[50][106]
Cholecystectomy should be undertaken during the initial hospital admission in any patient with mild acute pancreatitis, as soon as possible after the initial symptoms have resolved and certainly within 2 weeks.[50][54][56][106][143]
- Early cholecystectomy is favoured in mild disease because the risk of recurrent acute pancreatitis is directly related to the delay between the first attack and the timing of cholecystectomy.[144][145][146] The shorter the interval, the lower the risk.
- Even a few weeks delay in undertaking cholecystectomy is associated with a high risk (up to 80%) of recurrence and readmission for acute pancreatitis.[144]

In patients with more severe disease, it is common practice to delay cholecystectomy until the inflammation has resolved.[54][56]

In severe acute gallstone pancreatitis, cholecystectomy is often delayed until any organ dysfunction and/or intra-abdominal inflammation has resolved.[50][56] However, this is based on expert consensus rather than solid evidence.

Evidence: Timing of cholecystectomy

Same-admission cholecystectomy improves outcomes in mild disease.

Early cholecystectomy is favoured in mild disease because the risk of recurrent acute pancreatitis is directly related to the delay between the first attack and the timing of cholecystectomy.[144][145][146]

The shorter the interval, the lower the risk. Even a few weeks delay in undertaking cholecystectomy is associated with a high risk (up to 80%) of recurrence and readmission for acute pancreatitis.[144]
One RCT found that same-admission cholecystectomy was associated with significant reductions in a composite outcome of mortality and gallstone-related complications (OR 0.24, 95% CI 0.09 to 0.61), readmission for recurrence (OR 0.25, 95% CI 0.07 to 0.90), and pancreatobiliary complications (OR 0.24, 95% CI 0.09 to 0.61) when compared with later cholecystectomy.[147]

In patients who are unfit for surgery, consider endoscopic biliary sphincterotomy to reduce the risk of recurrence.

Patients with mild acute gallstone pancreatitis who are unable to have cholecystectomy because of frailty and/or comorbid disease may benefit from biliary sphincterotomy.[9] Evidence suggests that this can effectively reduce the risk of recurrent acute pancreatitis, although cholecystitis may still occur.[25]

Endoscopic retrograde cholangiopancreatography (ERCP) is not indicated in mild acute gallstone pancreatitis without cholangitis. The risks of the procedure outweigh any potential benefits in this group[25][50][54]

One meta-analysis of eight RCTs carried out for the AGA Institute 2018 guideline group found that urgent ERCP has no impact on mortality, multi- or single-organ failure, infected pancreatic necrosis, or total rate of pancreatic necrosis when compared with conservative management.[106]

ERCP is probably not indicated in severe acute gallstone pancreatitis without cholangitis or bile duct obstruction.

There is ongoing debate about the balance of risks and benefits of urgent ERCP (within 24 hours) in patients with (predicted) severe acute gallstone pancreatitis without concurrent cholangitis and without evidence of bile duct obstruction.[50]
- The 2019 WSES guideline states that ERCP cannot be currently recommended for this patient group.[25]
- The 2018 AGA Institute guideline recommends against its use.[106]
- The 2013 IAP/APA guideline says it is “probably” not indicated.[54]
- The 2024 ACG guideline concluded that current evidence does not support ERCP in this patient group.[9]

Evidence: ERCP in severe gallstone pancreatitis

There is conflicting evidence on the role of ERCP in severe gallstone pancreatitis.

Several RCTs and meta-analyses have reached different conclusions on the role of ERCP in severe gallstone pancreatitis.[50]

The quality of evidence is poor, with some trials failing to exclude patients with cholangitis (in whom the procedure is certainly indicated) and others using varied definitions of gallstone pancreatitis.[50]
Results are awaited from the APEC trial, a large multicentre RCT looking at whether early ERCP with sphincterotomy reduces complications and mortality in (predicted) severe acute gallstone pancreatitis without cholangitis.[151]

gallstone pancreatitis: with bile duct obstruction

Consider – endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy

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Consider –

endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy

Additional treatment recommended for SOME patients in selected patient group

ERCP is probably indicated in gallstone pancreatitis with common bile duct obstruction.[54] [ ]

One meta-analysis of seven RCTs including 757 patients found support for the use of ERCP in patients with gallstone obstruction although there were too few patients to study hard clinical outcomes such as mortality.[152]
Ongoing derangement of LFTs is an important sign of possible bile duct stones.

Arrange bile duct imaging with endoscopic ultrasound (EUS) if available (or magnetic resonance cholangiopancreatography [MRCP] if not) if bile duct obstruction is suspected in the absence of cholangitis. This imaging-first approach can help prevent unnecessary ERCP procedures.[9][50][54]

More widespread use of EUS to detect common bile duct stones is emerging as a useful strategy to guide a decision on the need for ERCP in severe acute gallstone pancreatitis without cholangitis.
MRCP is an alternative option for detecting common bile duct stones and is more widely available than EUS. However, EUS is superior to MRCP for detecting small stones (<5 mm).
- A negative MRCP does not rule out the presence of small common bile duct stones (<5 mm), which are known to cause gallstone pancreatitis [54]

Evidence: EUS-first strategy

Many ERCP procedures can be avoided by prior bile duct imaging.

A meta-analysis comparing an EUS-first strategy with diagnostic ERCP in patients with acute gallstone pancreatitis found that 71% of ERCP procedures could be avoided without any negative impact on clinical outcomes by employing an EUS-first approach.[153]

Where bile duct stones are identified in the absence of cholangitis, it is reasonable to wait 48 hours to see if there is spontaneous improvement of gallstone obstruction before undertaking ERCP.[54]

There is no specific evidence available to guide the optimal timing of ERCP in patients with bile duct obstruction but no cholangitis and this remains a controversial issue.

Evidence: Timing of ERCP

There is only weak evidence to support decisions on the timing of ERCP.

A meta-analysis of seven RCTs including 757 patients with bile duct obstruction found no statistically significant effect from performing ERCP within 24 hours compared with within 72 hours. However, none of the RCTs included was designed specifically to study this [54]

alcohol-related pancreatitis

Plus – vitamin replacement

Plus – alcohol abstinence programme

Back

Plus –

alcohol abstinence programme

Treatment recommended for ALL patients in selected patient group

Arrange a brief alcohol counselling intervention during the same admission.[106]

There is sparse evidence available to support decisions on the most effective approach to alcohol counselling for patients with alcohol-related acute pancreatitis.
Patients should be encouraged to abstain from alcohol for 6 to 12 months (regardless of whether or not the acute pancreatitis was alcohol-related).[56]

Evidence: Alcohol abstinence counselling

Weak evidence supports some benefits from same-admission counselling.

A literature review conducted for the AGA Institute 2018 guideline group found a single RCT comparing a single intervention during the initial admission with 6-monthly outpatient interventions for 2 years. There was a strong trend towards a reduction in total hospital admission rates for the single intervention during admission and there were no significant differences in risk of a recurrent attack of acute pancreatitis.[106]

Patients with an alcohol-related cause may need alcohol withdrawal prophylaxis.

A benzodiazepine is generally used as the first-line agent.[154] Choice of drug and dose regimen depends on various factors including the indication (e.g., alcohol withdrawal seizures, delirium tremens) and patient-specific factors (e.g., hepatic impairment, ability to take oral medication).

See Alcohol withdrawal.

ONGOING

deteriorating or failing to improve after 5-7 days

1st line – contrast-enhanced computed tomography (CECT)

Back

1st line –

contrast-enhanced computed tomography (CECT)

Request CECT for any patient who fails to improve after 5 to 7 days of initial treatment to check for the presence of local complications.[54]

This is particularly important for any patient with ongoing signs of SIRS or organ failure.[56]
- Acute pancreatitis has early and late phases and deaths occur in a biphasic pattern:
  - Early phase (<2 weeks)- early mortality is caused by SIRS/multi-organ failure.
  - Late phase (>2 weeks) - late mortality is caused by local complications, in particular infected pancreatic necrosis.
Local complications include pancreatic necrosis and pancreatic/peri-pancreatic fluid collections, including pseudocysts.

Do not request CECT scanning to detect local complications within the first 3 to 4 days after presentation.

Pancreatic necrosis often takes >72 hours to develop so early CECT is unreliable for detecting any fluid collections and determining the extent of any necrosis.[25][50][80][109]

Pancreatic and/or peri-pancreatic necrosis develops in around 20% of patients with acute pancreatitis.[8]

Pancreatic necrosis is defined as diffuse or focal areas of non-viable pancreatic parenchyma >3 cm in size or >30% of the pancreas.[9]
Necrosis is usually associated with moderately severe or severe disease.[106] It may be:
- Sterile or infected. Necrotic collections become infected in around one third of patients.[50] This is thought to occur as a result of bacterial translocation from the gut.[50]
- Diffuse (typically <4 weeks) or walled off (>4 weeks). Early in the course of the disease, pancreatic necrosis is a diffuse solid/semi-solid inflammatory mass. After approximately 4 weeks, a fibrous wall develops around the necrosis, making it easier to remove with drainage or necrosectomy/debridement.[9]

Pancreatic/peri-pancreatic fluid collections often resolve spontaneously whereas pseudocysts persist.

Acute fluid collections are those that occur within the first 4 weeks and lack a defined wall. They are usually asymptomatic and resolve spontaneously within 20 days.
Pseudocysts are fluid collections that have persisted beyond 2 weeks (usually more than 4 weeks) and developed a defined wall.

Refer to a specialist pancreatic centre any patient:[54]

Who has severe acute pancreatitis
Who is being considered for intervention (drainage or necrosectomy/debridement).

Plus – ongoing supportive treatment

Plus – ongoing nutritional support

Back

Plus –

ongoing nutritional support

Treatment recommended for ALL patients in selected patient group

Enteral nutrition

In patients who are unable to feed orally, use enteral rather than parenteral nutrition.

Start this within 72 hours of presentation.[8]
Nasojejunal or nasogastric tube feeding are both safe options.[8][9][50][54][56][106]
Many patients with predicted severe/moderately severe acute pancreatitis or necrotising pancreatitis do end up needing nutrition support. Always offer enteral (rather than parenteral) nutrition to patients in this group unless it is contraindicated.[8][106]
Either a polymeric or elemental enteral nutrition formulation can be used.[54]
- No specific enteral nutrition formulation has been proven to be better than another in improving clinical outcomes.[128][129]

Evidence: Benefits of enteral feeding

Enteral feeding is associated with a lower risk of serious complications and death compared with parenteral.

The use of enteral nutrition is associated with a lower likelihood of harm compared with parenteral nutrition.

There is good evidence to support the benefits of enteral compared with parenteral feeding in patients with acute pancreatitis. Enteral nutrition (orally or by tube) was associated with a significantly lower risk of infected pancreatic necrosis (OR 0.28, 95% CI 0.15 to 0.51), single organ failure (OR 0.25, 95% CI 0.10 to 0.62), and multi-organ failure (OR 0.41, 95% CI 0.27 to 0.63) in a meta-analysis of 12 RCTs for the 2018 AGA Institute guideline group.[106]
An earlier Cochrane review of 8 RCTs also found that enteral nutrition, compared with total parenteral nutrition, significantly reduced mortality (RR 0.50, 95% CI 0.28 to 0.91), multi-organ failure (RR 0.55, 95% CI 0.37 to 0.81), systemic infections (RR 0.39, 95% CI 0.23 to 0.65), and the need for surgical intervention (OR 0.44, 95% CI 0.29 to 0.67) in patients with (predicted) severe acute pancreatitis. There was also a trend towards a shorter hospital stay.[130]

Debate: Timing of enteral nutrition

The evidence on the optimum timing to start enteral nutrition in (predicted) severe acute pancreatitis is mixed and guidelines differ.

NICE’s review of the evidence found no benefit from delaying nutrition whereas underfeeding is known to be an issue in clinical practice, with some patients waiting 5 to 7 days for nutritional support.

A 2017 literature review concluded that the latest evidence supports limiting tube feeding to those patients with predicted severe pancreatitis who are unable to achieve sufficient oral calorie intake after 3 to 5 days.[50]

This is based on two RCTs that found no beneficial effects on infection rates or mortality from early nasojejunal feeding.

Evidence: Nasojejunal versus nasogastric tube feeding

There is no clear evidence of any difference in outcomes from nasojejunal versus nasogastric tube feeding.

The 2018 AGA Institute guideline, the 2024 ACG guideline, and the 2013 IAP/APA guideline all recommend that either nasojejunal or nasogastric tube feeding can be used.[9][54][106]

Nasogastric tube insertion is a ward-based procedure that is easier and cheaper than nasojejunal tube insertion, which requires access to radiology or endoscopy.[9][56][132]
- Two RCTs have suggested that at least 80% of patients with severe acute pancreatitis can tolerate the nasogastric route.[133][134]
In practice, however, safety concerns over the risk of aspiration with a nasogastric tube mean that nasojejunal feeding is sometimes preferred in patients with severe acute pancreatitis, although there is little evidence to support this approach.[8][106]
Nasojejunal feeding may also be more effective in patients with gastric outlet obstruction.[8]
Gastric feeding may be more suitable for patients with no duodenal stenosis or oedema.[8]
- If nasogastric tube feeding is used, the patient should be put in an upright position and placed on aspiration precautions.[9]

Parenteral nutrition

Parenteral nutrition is associated with higher mortality and a higher risk of organ failure and/or pancreatic necrosis than enteral feeding.[106][130]
Parenteral nutrition should be reserved for patients who do not tolerate enteral feeding or cannot tolerate the targeted nutritional requirements, or if there are contraindications to enteral feeding. Contraindications to enteral feeding may include bowel obstruction, abdominal compartment syndrome, prolonged paralytic ileus, and mesenteric ischaemia.[136]

Consider – fine needle aspiration (FNA) and culture

Back

Consider –

fine needle aspiration (FNA) and culture

Additional treatment recommended for SOME patients in selected patient group

Do not use routine percutaneous FNA and culture to confirm or exclude the presence of infection. Only consider it if a patient with pancreatic necrosis but no clear clinical or imaging signs of infection fails to improve after several weeks.[54]

FNA with culture can be used to confirm infection but has poor sensitivity for diagnosing infection. False negative rates of up to 25% have been reported in infected pancreatic necrosis.[54][159]

Debate: FNA

Guidelines differ on the role of FNA to distinguish infected from sterile necrosis.

There is ongoing debate about the appropriate role of FNA to distinguish infected from sterile necrosis and guidelines differ on this.

The IAP/APA 2013 guideline recommends that because of the high false negative rate, FNA should only be undertaken in patients who fail to improve clinically after several weeks of necrotising pancreatitis where there are no clear clinical or imaging signs of infection.[54]
The ACG 2024 guideline recommends considering an FNA whenever infection is suspected, on the basis that patients with sterile as well as infected necrosis can appear similar in terms of leukocytosis, fever, and organ failure markers.[9]

infected pancreatic necrosis

Plus – intravenous antibiotics

Back

Plus –

intravenous antibiotics

Treatment recommended for ALL patients in selected patient group

Give immediate intravenous antibiotics to any patient with confirmed or highly suspected infected necrosis.[54]

In most cases, antibiotics are used alongside supportive care to delay the need for further intervention with catheter drainage or necrosectomy/debridement until the necrosis has become walled off.[50][54]

Suspect infected necrosis on the basis of clinical and/or imaging signs.[54]

Clinical signs (persistent fever, increasing inflammatory markers, new/persistent organ failure) and/or imaging signs (the presence of gas within the necrosis on CECT) are accurate indicators that pancreatic necrosis has become infected.[54]

Choose an antibiotic that has good pancreatic penetration, such as a carbapenem (e.g., imipenem/cilastatin), a fluoroquinolone (e.g., ciprofloxacin), or metronidazole.[9]

Imipenem/cilastatin is usually the first-line choice because it has good pancreatic penetration.
Check local guidance on antibiotic stewardship.

Prescribing restrictions apply to the use of fluoroquinolones, and these restrictions may vary between countries. In general, fluoroquinolones should be restricted for use in serious, life-threatening bacterial infections only. Some regulatory agencies may also recommend that they must only be used in situations where other antibiotics, that are commonly recommended for the infection, are inappropriate (e.g., resistance, contraindications, treatment failure, unavailability).
Consult your local guidelines and drug information source for more information on suitability, contraindications, and precautions.

Many patients with infected pancreatic necrosis will need intervention with drainage or necrosectomy/debridement.[50]

However, some studies have had high success rates from treating infected pancreatic necrosis solely with antibiotics.[160][161][162] One meta-analysis of 8 studies involving 409 patients found 64% could be managed by conservative antibiotic treatment with 12% mortality.[163]

The risk of death in patients with infected necrosis is as high as 30%.[9][54][157]

Infected necrosis tends to develop in the late phase of the disease (>14 days) although one review found 27% of cases occurred within the first 14 days.[158]

Primary options

imipenem/cilastatin: 500-1000 mg intravenously every 6 hours

Secondary options

metronidazole: 500 mg intravenously every 8 hours

ciprofloxacin: 400 mg intravenously every 8-12 hours

Consider – catheter drainage (percutaneous or endoscopic)

Back

Consider –

catheter drainage (percutaneous or endoscopic)

Additional treatment recommended for SOME patients in selected patient group

Drainage is indicated in infected necrosis when there is ongoing clinical deterioration or the patient fails to improve despite antibiotics and supportive care.[9][50][54]

The step-up approach to intervention is the best option even for patients with multi-organ failure.[54] This starts with catheter drainage (percutaneous retroperitoneal or endoscopic transluminal), with necrosectomy reserved for those patients who fail to respond.
Percutaneous catheter drainage is technically feasible in >95% of patients.[54]
Reduction in collection size of ≥75% after the first 10 to 14 days of percutaneous drainage correctly predicts successful treatment with this technique.[54][165]

Evidence: Step-up approach to infected necrosis

A step-up approach reduces the risk of both short- and long-term complications.

A multicentre RCT of 88 patients with infected necrosis showed that a step-up approach starting with percutaneous catheter drainage reduced both short-term complications (multi-organ failure) and long-term complications (endocrine insufficiency) when compared with open necrosectomy.[160]

35% of patients with infected necrosis were successfully managed with solely catheter drainage and did not require necrosectomy.
The step-up approach reduced the composite endpoint of death or major complications from 69% to 40% (RR 0.57, 95% CI 0.38 to 0.87).

Subgroup analysis of severity in one multicentre RCT found the step-up approach was beneficial regardless of whether or not patients had multi-organ failure.[160]

Ideally the intervention should be delayed until the necrotic collection is fully walled off (usually 4-5 weeks).[9][54]

Current guidelines recommend delaying intervention with catheter drainage (or necrosectomy/debridement) until the necrosis has become fully walled off (usually 4-5 weeks after the onset of acute pancreatitis).[9][54][56]
The rationale for this is that intervening once the necrosis has become walled off is presumed to carry a lower risk of bleeding and less likelihood of needing a second intervention.[50]

Evidence: Timing of intervention

Early necrosectomy is associated with worse outcomes but the evidence on timing of catheter drainage is less clear cut.

Evidence does suggest that open necrosectomy is associated with worse outcomes (including higher death rates) if performed early.[161][165][170][171][172] However, some commentators have queried the case for a delay in the case of catheter drainage.[173]

Results are awaited from the multicentre POINTER trial, an RCT that is comparing immediate versus postponed drainage in patients with infected pancreatic necrosis.

Intervention must not be delayed in a subgroup of patients who have an intra-abdominal catastrophe (e.g., ongoing acute bleeding, perforation, abdominal compartment syndrome).[54]

In cases where percutaneous catheter drainage cannot be safely delayed until >4 weeks, ideally necrosectomy should still not be undertaken until the collection has become walled off.[54]

Always consult a specialist pancreatic team about any patient being considered for intervention.[54][56]

The decision on timing of intervention(s) and choice of approach requires input from a specialist pancreatic centre.[54]

Consider – necrosectomy/debridement

Back

Consider –

necrosectomy/debridement

Additional treatment recommended for SOME patients in selected patient group

Minimally invasive or open necrosectomy is only indicated for patients who fail to respond to catheter drainage.[54] Minimally invasive necrosectomy is probably safer than open surgery.[8][54][166]

There are no head-to-head RCTs comparing minimally invasive versus open techniques for necrosectomy/debridement.[50]
However, retrospective studies suggest a lower risk of complications and death with minimally invasive techniques.[167][168]
Minimally invasive approaches include percutaneous, laparoscopic, endoscopic, and video-assisted retroperitoneal techniques.[169]
For around 60% to 70% of patients with infected pancreatic necrosis, the preferred intervention will depend on whether the necrosis is associated with the posterior wall of the stomach (endoscopic approach) or the postero-lateral abdominal wall (percutaneous approach).[8]
The UK NICE guideline recommends an endoscopic approach as the preferred first-line option when it is anatomically possible. This is based on evidence suggesting the endoscopic approach is more acceptable to patients than percutaneous catheter drainage and is associated with lower complication rates and shorter hospital stay. However, endoscopic procedures are high-risk and require referral to a specialist pancreatic centre.[8]

Delay the intervention until the necrosis has become walled off if at all possible.

Current guidelines recommend delaying intervention with catheter drainage or necrosectomy/debridement until the necrosis has become fully walled off (usually 4-5 weeks after the onset of acute pancreatitis).[9][54][56]
The rationale for this is that intervening once the necrosis has become walled off is presumed to carry a lower risk of bleeding and less likelihood of needing a second intervention.[50]
In cases where percutaneous catheter drainage cannot be safely delayed until >4 weeks (e.g., because of an intra-abdominal catastrophe), ideally necrosectomy should still not be undertaken until the collection has become walled off.[54]

Evidence: Timing of intervention

Early necrosectomy leads to worse outcomes.

Evidence suggests that open necrosectomy is associated with worse outcomes (including higher death rates) if performed early.[161][165][170][171][172]

Always consult a specialist pancreatic team about any patient being considered for intervention.[54][56]

The decision on timing of intervention(s) and choice of approach requires input from a specialist pancreatic centre.[54]

sterile pancreatic necrosis

Consider – catheter drainage or necrosectomy

Back

Consider –

catheter drainage or necrosectomy

Additional treatment recommended for SOME patients in selected patient group

Most patients with sterile necrosis can be managed conservatively.[54]

Asymptomatic sterile necrosis will often resolve over time without catheter drainage/necrosectomy, regardless of size, location, and extension [9][54][72]

Closely monitor patients with sterile necrosis as they can develop organ failure.[9]

Although the presence of infection in the necrosis increases the risk of organ failure, patients with sterile necrosis can also develop organ failure.[9]

Do not give prophylactic antibiotics to patients with necrosis who have no proven or clinically suspected infection.[8][9][50][54][106]

There is no evidence to support prophylactic antibiotics for sterile necrosis.[8][9][50][54][106]

Evidence: Prophylactic antibiotics

Prophylactic antibiotics do not reduce the risk of infected necrosis or death.

Prophylactic antibiotics also have no impact on rates of organ failure or length of hospital stay.[106]
This lack of benefit from prophylactic antibiotics holds true for patients with predicted severe disease and those with sterile necrotising pancreatitis as well as those with milder disease, according to a meta-analysis conducted for the AGA Institute 2018 guideline group.[106]

Indications for radiological, surgical, or endoscopic intervention in sterile necrosis include:[9][54]

Ongoing gastric outlet, intestinal, or biliary obstruction due to the mass effect of walled-off necrosis (normally 4 to 8 weeks after the onset of acute pancreatitis).
Symptoms (e.g., pain, ‘persistent unwellness’) that continue beyond 8 weeks after the onset of acute pancreatitis.
Disconnected duct syndrome with persistent symptomatic collections beyond 8 weeks after the onset of acute pancreatitis.

Delay the intervention until the necrosis has become walled off if at all possible.

Current guidelines recommend delaying intervention with catheter drainage or necrosectomy/debridement until the necrosis has become fully walled off (usually 4-5 weeks after the onset of acute pancreatitis).[9][54][56]
The rationale for this is that intervening once the necrosis has become walled off is presumed to carry a lower risk of bleeding and less likelihood of needing a second intervention.[50]

infected pseudocyst (abscess)

Plus – drainage (endoscopic, radiological, or surgical) and intravenous antibiotics

Back

Plus –

drainage (endoscopic, radiological, or surgical) and intravenous antibiotics

Treatment recommended for ALL patients in selected patient group

Pseudocysts do not appear until at least 2 weeks (usually more than 4 weeks) after the onset of an episode of acute pancreatitis.

Manage an infected pseudocyst as an abscess, with immediate antibiotics and catheter drainage.

Imipenem/cilastatin is usually the first-line choice because it has good pancreatic penetration.[25] Alternative options include metronidazole or a fluoroquinolone (e.g., ciprofloxacin).
Check local guidance on antibiotic stewardship.

Prescribing restrictions apply to the use of fluoroquinolones, and these restrictions may vary between countries. In general, fluoroquinolones should be restricted for use in serious, life-threatening bacterial infections only. Some regulatory agencies may also recommend that they must only be used in situations where other antibiotics, that are commonly recommended for the infection, are inappropriate (e.g., resistance, contraindications, treatment failure, unavailability).
Consult your local guidelines and drug information source for more information on suitability, contraindications, and precautions.

Pseudocysts can be drained percutaneously, surgically, or endoscopically. Endoscopic techniques have largely replaced surgical and percutaneous approaches.[64][175]

Primary options

imipenem/cilastatin: 500-1000 mg intravenously every 6 hours

Secondary options

metronidazole: 500 mg intravenously every 8 hours

ciprofloxacin: 400 mg intravenously every 8-12 hours

symptomatic sterile pseudocyst

Plus – drainage (endoscopic, radiological, or surgical)

Back

Plus –

drainage (endoscopic, radiological, or surgical)

Treatment recommended for ALL patients in selected patient group

Pseudocysts do not appear until at least 2 weeks (usually more than 4 weeks) after the onset of an episode of acute pancreatitis.

Manage asymptomatic, sterile pseudocysts conservatively regardless of size. Many pseudocysts resolve spontaneously.[64][174]

Arrange catheter drainage of symptomatic pseudocysts.

Pseudocysts can become painful, or cause early satiety and weight loss when their size affects the stomach and bowel.
Drainage of these pseudocysts is recommended for symptom relief.[64]
Pseudocysts can be drained percutaneously, surgically, or endoscopically. Endoscopic techniques have largely replaced surgical and percutaneous approaches.[64][175]
- The UK National Institute for Health and Care Excellence recommends endoscopic ultrasound-guided drainage or endoscopic transpapillary drainage as the preferred intervention for symptomatic pancreatic head pseudocysts.[8]

Use of this content is subject to our disclaimer

Acute pancreatitis

Treatment algorithm

all patients

fluid resuscitation

Practical tip

Practical tip

Evidence: Choice of fluids

Evidence: Fluid volume and duration

supplemental oxygen

analgesia

Practical tip

Primary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

anti-emetic

Primary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

nutritional support

Evidence: Oral feeding

Enteral nutrition

Evidence: Benefits of enteral feeding

Debate: Timing of enteral nutrition

Evidence: Nasojejunal versus nasogastric tube feeding

Parenteral nutrition

empirical intravenous antibiotics (if infection is confirmed or strongly suspected)

Evidence: Prophylactic antibiotics

Primary options

Secondary options

These drug options and doses relate to a patient with no comorbidities.

Primary options

Secondary options

Drug choice, dose and interactions may be affected by the patient's comorbidities. Check your local drug formulary.

Primary options

Secondary options

severity assessment

calcium replacement therapy

magnesium replacement therapy

endoscopic retrograde cholangiopancreatography (ERCP)

cholecystectomy

Evidence: Timing of cholecystectomy

Evidence: ERCP in severe gallstone pancreatitis

endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy

Evidence: EUS-first strategy

Evidence: Timing of ERCP

vitamin replacement

alcohol abstinence programme

Evidence: Alcohol abstinence counselling

deteriorating or failing to improve after 5-7 days

contrast-enhanced computed tomography (CECT)

ongoing supportive treatment

ongoing nutritional support

Enteral nutrition

Evidence: Benefits of enteral feeding

Debate: Timing of enteral nutrition

Evidence: Nasojejunal versus nasogastric tube feeding

Parenteral nutrition

fine needle aspiration (FNA) and culture

Debate: FNA

intravenous antibiotics

Primary options

Secondary options

catheter drainage (percutaneous or endoscopic)

Evidence: Step-up approach to infected necrosis

Evidence: Timing of intervention

necrosectomy/debridement

Evidence: Timing of intervention

catheter drainage or necrosectomy

Evidence: Prophylactic antibiotics

drainage (endoscopic, radiological, or surgical) and intravenous antibiotics

Primary options

Secondary options

drainage (endoscopic, radiological, or surgical)