Acute pancreatitis

Diagnostic approach

• ABCDE approach
• Focused clinical evaluation
• Serum lipase
• Serum amylase
• CBC
• CMP
• LDH
• CRP
• Procalcitonin
• Triglycerides
• ABG
• Ultrasound abdomen
• CECT abdomen if there is diagnostic uncertainty

Diagnostic criteria

≥ 2 of the following:

• Characteristic abdominal pain (i.e., constant, severe epigastric pain that radiates toward the back)
• Lipase or amylase ≥ 3× ULN
• Characteristic findings of acute pancreatitis on cross-sectional imaging

Management checklist

• Two large-bore IVs
• Goal-directed IV fluid therapy for acute pancreatitis
• Oxygen therapy as needed
• Electrolyte repletion as needed
• Management of ARDS as needed
• Analgesics (e.g., NSAIDs) and antiemetics as needed
• Consult GI or IR for therapeutic ERCP for patients with biliary pancreatitis.
• Consult general surgery for suspected severe or necrotizing pancreatitis.

Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by gallstones or alcohol use in adults and biliary disease and medications in children. The typical manifestation includes sudden, severe epigastric pain that radiates to the back, nausea and vomiting, and epigastric tenderness on palpation. Elevation of serum lipase or amylase ≥ 3× ULN and/or characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., abdominal ultrasound, contrast-enhanced CT abdomen) confirm the diagnosis. Clinical scores (e.g., Ranson criteria, APACHE II) are used to predict the severity and prognosis of pancreatitis. Initial management is primarily supportive and includes fluid resuscitation, analgesia, antiemetics, and early enteral nutrition as tolerated. The underlying cause should be identified and managed to prevent recurrence (e.g., cholecystectomy for biliary pancreatitis, long-term lipid-lowering therapy for hypertriglyceridemia-induced pancreatitis). Localized complications of pancreatitis include necrosis (necrotizing pancreatitis), which may become infected, pancreatic pseudocysts, and walled-off necrosis. Systemic complications include sepsis, ARDS, organ failure, and shock. Complications of pancreatitis are associated with significant morbidity and mortality.

Most common causes ^[1]

• Biliary pancreatitis (∼ 40% of cases; mostly caused by gallstones)
• Alcohol-induced (∼ 20% of cases)
• Idiopathic (∼ 25% of cases)

Other causes ^[1]

• Hypertriglyceridemia-induced pancreatitis: caused by severe hypertriglyceridemia (> 1,000 mg/dL)
• Hypercalcemia
• Post-ERCP
• Drug-induced pancreatitis
  • Steroids
  • Azathioprine
  • Sulfonamides
  • Loop and thiazide diuretics
  • Estrogen
  • Protease inhibitors
  • NRTIs
  • Anticonvulsants (e.g., valproate)
  • Metronidazole
• Scorpion stings
• Viral infections (e.g., coxsackievirus B, mumps)
• Trauma (especially in children)
• Autoimmune and rheumatological disorders (e.g., Sjögren syndrome)
• Pancreas divisum
• Hereditary (e.g., mutation of PRSS1 gene, cystic fibrosis) ^[2]
• Cholesterol embolism

I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion venom, Hypercalcemia and hypertriglyceridemia, ERCP, and Drugs are causes of acute pancreatitis.

Sequence of events

1. Intrapancreatic activation of pancreatic enzymes: secondary to pancreatic ductal outflow obstruction (e.g., gallstones, cystic fibrosis) or direct injury to pancreatic acinar cells (e.g., alcohol, drugs)
2. Increased proteolytic and lipolytic enzyme activity → destruction of pancreatic parenchyma
3. Attraction of inflammatory cells (neutrophils, macrophages) → release of inflammatory cytokines → pancreatic inflammation (pancreatitis)

Sequelae of pancreatitis

• Capillary leakage: release of inflammatory cytokines and vascular injury by pancreatic enzymes → vasodilation and increased vascular permeability → shift of fluid from the intravascular space into the interstitial space (third-space fluid loss) → hypotension, tachycardia, warm and flushed skin → distributive shock
  • In severe cases, the third spacing of fluid from this inflammatory response can lead to hypovolemic shock.
• Pancreatic necrosis: uncorrected hypotension and third-spacing → decreased end-organ perfusion → multiorgan dysfunction (mainly renal) and pancreatic necrosis
• Hypocalcemia: lipase breaks down peripancreatic and mesenteric fat; → release of free fatty acids that bind calcium → hypocalcemia (fatty saponification) ^[3]

Symptoms

• Constant, severe epigastric pain
  • Classically radiating towards the back
  • Worse after meals and when supine
  • Improves on leaning forwards
• Nausea, vomiting
• Fever
• If pulmonary complications are present: chest pain, dyspnea

Examination findings

• General
  • Signs of shock: tachycardia, hypotension, oliguria/anuria
  • Possibly jaundice in patients with biliary pancreatitis
• Abdominal examination
  • Abdominal tenderness, distention, guarding
  • Ileus with reduced bowel sounds and tympany on percussion
  • Ascites
  • Skin changes (rare)
    • Cullen sign: periumbilical ecchymosis and discoloration (bluish-red)
    • Grey Turner sign: flank ecchymosis with discoloration
    • Fox sign: ecchymosis over the inguinal ligament
• Pulmonary examination: signs of pleural effusion and/or ARDS may be present

Diagnostic criteria for acute pancreatitis ^[4][5][6]

Two of the three following criteria should be met for a diagnosis of acute pancreatitis to be made.

• Characteristic abdominal pain
• ↑ Serum pancreatic enzymes: lipase or amylase ≥ 3× ULN
• Characteristic findings of acute pancreatitis on cross-sectional imaging (e.g., abdominal ultrasound, contrast-enhanced CT abdomen)

Approach ^[7][8][9]

• All patients
  • Perform laboratory studies to:
    • Establish the diagnosis: serum lipase and/or amylase levels
    • Determine severity: CBC, BMP, ABG, LDH, inflammatory markers, serum calcium
    • Evaluate for the underlying etiology: liver chemistries, serum or plasma triglyceride levels
  • Obtain ultrasound abdomen.
• Diagnostic uncertainty: Perform contrast-enhanced CT (CECT) abdomen.
• Confirmed diagnosis
  • Perform further diagnostics as needed to determine the etiology (e.g., MRCP for suspected biliary pancreatitis).
  • Calculate severity scores of acute pancreatitis to estimate severity and prognosis.
  • In patients with severe pancreatitis, consider CECT abdomen 5–7 days after the onset of symptoms to assess for necrotizing pancreatitis.

Simultaneously conduct tests to establish the diagnosis, assess severity, and rule out differential diagnoses of acute abdominal pain.

Acute pancreatitis is a medical emergency; begin fluid resuscitation as soon as it is suspected.

Laboratory studies

The degree of lipase and/or amylase elevation does not necessarily correlate with the severity of or prognosis for acute pancreatitis. ^[23]

Measure serum triglycerides promptly after symptom onset, as levels decrease rapidly with fasting. ^[24]

Determining calcium values is very important: Hypercalcemia may cause pancreatitis, which may then, in turn, cause hypocalcemia!

Imaging

Ultrasound abdomen ^[9][25]

• Indications: first-line imaging modality for all patients
• Supportive findings
  • Features of acute pancreatitis (visible in 20% of cases) ^[9]
    • Enlarged hypoechoic pancreas (pancreatic edema)
    • Peripancreatic fluid and/or ascites
  • Features of biliary pancreatitis
    • Cholelithiasis and/or gallbladder sludge ^[9]
    • Dilated biliary tree
  • Evidence of complications: pancreatic pseudocysts, walled-off necrosis (typically > 4 weeks from symptom onset) ^[15]

Abdominal ultrasound for suspected acute pancreatitis is primarily used to identify gallstones as features of acute pancreatitis are only visible in approximately 20% of cases. ^[9]

CT abdomen and pelvis with IV contrast ^[4][9][15]

• Indications
  • Diagnostic uncertainty (e.g., typical clinical features in a patient with moderately elevated pancreatic enzymes)
  • Acute deterioration or lack of improvement within 48–72 hours of admission
  • Severe pancreatitis : optimally performed > 5–7 days after symptom onset ^[9]
  • To evaluate for underlying etiology if routine diagnostic studies are negative ^[7]
• Findings
  • Features of acute pancreatitis
    • Enlargement of the pancreatic parenchyma with edema
    • Indistinct pancreatic margins with surrounding fat stranding
    • Peripancreatic free fluid
  • Evidence of complications
    • Necrotizing pancreatitis: nonenhancing areas of pancreatic parenchyma
    • Acute necrotic collections: ill-defined, heterogeneous appearance with varying densities
    • Walled-off necrosis: an encapsulated collection of necrotic material, usually occurring > 4 weeks after the onset of necrotizing pancreatitis
    • Infection: air within the pancreatic or peripancreatic tissue or fluid collections

CT abdomen is not routinely required to establish a diagnosis of acute pancreatitis. If performed to evaluate for necrotic pancreatitis, the optimal timing to perform a CT abdomen is at least 5–7 days after symptom onset. ^[9]

Suspect pancreatic tumor as the underlying cause for idiopathic acute pancreatitis in patients aged > 40 years; see “Pancreatic cancer.” ^[4]

X-ray chest and abdomen ^[9][26][27]

• Indications: not routinely indicated; may be performed as part of the initial workup of undifferentiated abdominal pain ^[28]
• Supportive findings
  • On abdominal x-ray
    • Sentinel loop sign: dilatation of a loop of small intestine in the left upper abdomen (duodenum or jejunum) ^[29]
    • Colon cut off sign: gaseous distention of the ascending and transverse colon that abruptly terminates at the splenic flexure. ^[29]
    • Calcified gallstones or pancreatic stones
  • On chest x-ray: pleural effusion, pulmonary edema suggesting ARDS

MRI abdomen ^[7][9]

• Indications
  • In combination with MRCP in cases of suspected choledocholithiasis
  • An alternative to CT
• Supportive findings
  • Enlarged, edematous pancreas
  • Pancreatic necrosis
  • Complications (e.g., walled-off necrosis, pseudocysts)

Magnetic resonance cholangiopancreatography ^[5][7][9]

• Indications: prior to therapeutic ERCP in suspected biliary pancreatitis
• Findings
  • Evidence of choledocholithiasis ; see “MRCP” in “Choledocholithiasis” for details
  • Can also identify pancreatic ductal anomalies that may trigger acute pancreatitis

Endoscopic retrograde cholangiopancreatography

• Indications
  • Suspected choledocholithiasis (if MRCP or MRI are not feasible) ^[9]
  • To evaluate for sphincter of Oddi dysfunction in patients with recurrent pancreatitis and normal or inconclusive EUS and MRCP ^[30]

Endoscopic ultrasound ^[31]

• Indication: evaluation of the underlying cause if routine initial workup fails to establish the etiology
• Findings: occult microlithiasis, pancreatic neoplasms, chronic pancreatitis, other pancreatic parenchymal, ductal, and ampullary disorders may be identified

There are several scores used to assess the severity and prognosis of acute pancreatitis. The most commonly used and validated scores are described here.

Revised Atlanta grades of severity ^[6]

The revised Atlanta grades of severity classify pancreatitis as mild, moderately severe, or severe, depending on the presence of organ failure. Organ failure can be determined using the modified Marshall scoring system for organ dysfunction.

• Mild acute pancreatitis: no organ failure and no local or systemic complications
• Moderately severe acute pancreatitis: transient organ failure (< 48 hours) and/or local or systemic complications
• Severe acute pancreatitis: persistent organ failure (> 48 hours)

Patients with organ failure at presentation or within the first 24 hours of admission should be classified as having severe pancreatitis. If organ failure resolves within 48 hours, patients can be reclassified as having moderately severe acute pancreatitis. ^[6]

CT severity index ^[8][24][32]

The CT severity index for acute pancreatitis (CTSI) and modified CT severity index (MCTSI) can be used to estimate the severity, mortality, and morbidity of acute pancreatitis based on the extent of pancreatic inflammation and necrosis on a CT abdomen performed ideally > 5–7 days (or at least 72 hours) after symptom onset.

Ranson criteria ^[8][28]

The Ranson criteria is one of the oldest predictive models used to estimate severity and prognosis of biliary and nonbiliary pancreatitis; , but full assessment is only possible after 48 hours, and sensitivity for predicting severity and outcome can be as low as 70%.

Acute physiology and chronic health evaluation II (APACHE II score) ^[8]

• Mainly used in the ICU setting to determine the severity of acute pancreatitis
• Scores ≥ 8 indicate severe pancreatitis with a guarded prognosis. ^[8][11]

Bedside index of severity of acute pancreatitis (BISAP) ^[11]

• Used to estimate in-hospital mortality due to pancreatitis
• Each criterion is worth one point.
  • BUN > 8.9 mmol/L
  • Altered mental status
  • Presence of SIRS
  • Age > 60 years
  • Pleural effusion on chest x-ray
• BISAP ≥ 2 indicates severe pancreatitis.

The initial management is identical for all etiologies of acute pancreatitis and should be administered without delay. For management in pregnant individuals and children, see “Special patient groups.”

Acute stabilization ^{[4][5][7][11]}

• ABCDE survey
• Hemodynamic and respiratory support
• Maintain NPO status until potential causes of acute abdomen that require emergency surgery have been ruled out.

Goal-directed IV fluid therapy for acute pancreatitis ^{[4][5][7][11]}

Fluids and infusion rate ^[4][5][11]

• Crystalloids such as lactated Ringer's solution (LR) are preferred. ^[4]
• Hemodynamically stable patients ^[4]
  • Moderately aggressive IV fluid therapy in the first 24–48 hours
    • Normovolemic patients: LR 1.5 mL/kg/hour ^[4][36]
    • Hypovolemic patients: LR 10 mL/kg bolus ^[4][36]
  • Exercise caution in patients with renal or cardiovascular disease.
• Hemodynamically unstable patients ^[37]
  • Administer rapid fluid bolus (e.g., LR 500–1000 mL IV bolus over 10–30 minutes).
  • Repeat as needed based on response.
  • See also “Fluid resuscitation” for further detail.

Monitoring ^[8][12]

• Monitor vitals, oxygen saturation, and urine output every 1–2 hours during the initial period of IV fluid therapy.
• Obtain laboratory studies (CBC, BMP, HCT) every 6–12 hours to monitor adequacy of fluid resuscitation and tissue perfusion.
• Perform serial physical examination every 4–6 hours to assess for abdominal compartment syndrome.

Fluid therapy goals in acute pancreatitis ^[7]

• Heart rate < 120 bpm, MAP 65–85 mm Hg
• Urine output > 0.5–1 mL/kg/hour
• Central venous pressure 8–12 mm Hg, central venous oxygen saturation ≥ 70% ^[38]
• Hct 35–44%
• Reduction in BUN ^[4]

Intravenous fluid resuscitation in the first 12–24 hours has the greatest impact on the clinical outcome of patients with acute pancreatitis. ^[4]

Supportive therapy

• Analgesics: based on the WHO analgesic ladder ^[39]
  • NSAIDS (e.g., ketorolac , diclofenac , ibuprofen ) ^[40][41]
  • Opioids; (e.g., hydromorphone , morphine ) ^[42]
  • Consider patient-controlled analgesia for management of severe pain. ^[11][41]
• Antiemetics (e.g., ondansetron , metoclopramide )
• Electrolyte repletion

In concurrent acute kidney injury, avoid NSAIDs and use opioids with caution because of the risk of accumulation. ^[11]

Prophylactic antibiotics are not recommended, and should only be used in patients with evidence of infected necrosis. ^[4]

Consults

• Multidisciplinary care is ideal.
• Urgent gastroenterology, surgery, and/or interventional radiology for cholangitis, choledocholithiasis, or localized complications

Disposition ^[7][28]

• Hospital admission is usually required.
• Consider ICU admission in the following cases:
  • Organ dysfunction or failure
  • Ongoing SIRS or fluid resuscitation requirements
  • Significant electrolyte imbalances
  • Older age or high-risk comorbidities
  • Severe pancreatitis on severity scores
• Refer to a specialist center if the need for surgical or interventional procedures is anticipated. ^[7]

Nutrition

• Early oral feeding: : low-fat, solid diet as soon as tolerated, ideally within 24 hours ^[4][5][43]
• Enteral tube (nasogastric or nasojejunal): preferred over parenteral nutrition if patients cannot tolerate oral intake ^[5][44]
• Parenteral nutrition (total or partial): only in patients who cannot tolerate enteral feeds (e.g., those with persistent paralytic ileus) ^[45]

Bowel rest is no longer routinely recommended. Enteral nutrition, via oral route or enteral tube, should be initiated as early as tolerated. ^[5]

Management of the underlying cause

Biliary pancreatitis

• Therapeutic ERCP ^[5][7][38]
  • Indication: biliary pancreatitis associated with cholangitis or persistent CBD obstruction
  • Timing: Urgent therapeutic ERCP (within < 24 hours) is indicated if there is concurrent cholangitis.
  • Procedure: sphincterotomy and stone removal; see “Treatment of choledocholithiasis”
  • Complications: aggravation of pancreatitis, perforation, hemorrhage ^[9]
• Cholecystectomy ^[5][7][46]
  • Indications
    • All patients with biliary pancreatitis to prevent recurrence
    • Consider in patients with a recurrent episode of acute pancreatitis of unclear etiology ^[4]
  • Timing: recommended during the initial admission for patients with mild biliary pancreatitis

Urgent ERCP is not indicated in acute biliary pancreatitis unless acute cholangitis is present. ^[5]

Hypertriglyceridemia-induced pancreatitis ^[24]

• Initiate measures to rapidly decrease triglyceride levels alongside fluid resuscitation and analgesia.
  • Insulin therapy ; monitor blood glucose levels.
  • Plasmapheresis and hemofiltration
• Evaluate for secondary causes of hypertriglyceridemia ; consider screening for familial hypertriglyceridemia if none are present.
• Long-term management
  • Initiate long-term lipid-lowering therapy e.g., with fibrates, as soon as tolerated to prevent recurrences.
  • Dietary and lifestyle modifications
• See “Treatment of hypertriglyceridemia in adults” for details.

Hypercalcemia-induced pancreatitis ^[18]

• Initial treatment: See “Treatment of hypercalcemia.”
• Definitive management: Investigate for primary hyperparathyroidism; if this is the underlying cause, perform parathyroidectomy.

Alcohol-induced pancreatitis

• Check magnesium and phosphorus levels and replete as needed. ^[8][47]
• Vitamin supplementation (thiamine, pyridoxine)
• See “Treatment of alcohol use disorder” for details.
• Provide counseling on alcohol use disorder before discharge. ^[5]

"PANCREAS": Perfusion (fluid replacement), Analgesia, Nutrition, Clinical (observation), Radiology (imaging), ERCP, Antibiotics (if indicated), Surgery (surgical intervention, if necessary)

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Acute pancreatitis (adult)

Assessment: This is a @AGE@-year-old @SEX@ with a [**]-day history of constant, severe epigastric pain radiating to the back, lipase [**amylase] ≥ 3x ULN, and features of acute pancreatitis on ultrasound [**CT].

Most likely diagnosis: acute pancreatitis

Severity

-Mild [**no organ failure and no local or systemic complications]

-Moderate to severe [**organ failure and/or local or systemic complications]

Differential diagnoses: peptic ulcer disease, gastritis, acute peritonitis, acute cholecystitis, acute cholangitis, biliary colic, myocardial infarction

Plan

Disposition

-ICU admission is appropriate because the patient has [**organ dysfunction or failure, ongoing SIRS or fluid resuscitation requirements, significant electrolyte imbalances, older age or high-risk comorbidities, severe pancreatitis based on severity scores].

-OR Inpatient admission is appropriate because the patient does not have severe pancreatitis, organ dysfunction or failure, SIRS or sepsis, require ongoing hemodynamic support, have significant electrolyte disturbances, high-risk comorbidities.

IV fluid therapy

-[**Normovolemic] LR 1.5 mL/kg/hour for 24–48 hours

-[**Hypovolemic] LR 10 mL/kg bolus, then 1.5 mL/kg/hour for 24–48 hours

Monitoring

-Vital signs, O2 sat, and UOP every 1–2 hours during initial fluid resuscitation

-CBC, BMP every 6–12 hours to monitor fluid resuscitation and tissue perfusion

-Abdominal exam every 4–6 hours to assess for abdominal compartment syndrome

Pain management

NSAIDs

-Ketorolac 15–30 mg IV/IM every 6 hours PRN

-OR [Diclofenac 37.5 mg IV every 6 hours PRN]

-OR [Ibuprofen 400–800 mg IV every 6–8 hours PRN]

Opioids (for NSAID contraindication or severe pain)

-Hydromorphone hydrochloride (immediate release) 2–4 mg PO every 4–6 hours PRN

-OR [Hydromorphone hydrochloride 0.2–1 mg IV every 2–3 hours PRN]

-OR [Morphine sulfate 0.1–0.2 mg/kg IV every 4 hours PRN]

-OR [Morphine sulfate 10 mg IM every 4 hours PRN]

-OR [Patient-controlled analgesia for severe pain]

Antiemetics

-[Ondansetron 4–8 mg PO/IV every 8 hours PRN]

-OR [Metoclopramide 10 mg IV/IM/PO every 4–8 hours PRN]

F/E/N

-Replete electrolytes.

-Low-fat, solid diet as soon as tolerated OR [Enteral tube feeding for patients who cannot tolerate oral intake] OR [Parenteral nutrition for patients who cannot tolerate enteral intake]

Consults: [**GI/surgery/IR] for ERCP for biliary pancreatitis with cholangitis or CBD obstruction

Acute pancreatitis during pregnancy ^[48]

Epidemiology

• Incidence is 1:1000–1:10,000 pregnancies
• More commonly affects multiparous individuals (75%)
• The majority of cases occur in the third trimester (50%), followed by the early postpartum period (38%), and the first and second trimester (12%)

Etiology

• Most commonly gallstones, heavy alcohol use, and familial hypertriglyceridemia
• Physiologic changes during pregnancy such as altered progesterone and estrogen levels increase the risk of choledocholithiasis.
• ↑ Progesterone → ↑ pressure on the sphincter of Oddi → bile stasis
• Estrogen alters the composition of bile, making it more lithogenic.

Clinical features

Similar to clinical features of acute pancreatitis in nonpregnant individuals

Diagnostics

• CBC
  • May show physiologic alterations due to pregnancy (e.g., leukocytosis, increased serum amylase and lipase)
  • If amylase and/or lipase are > 3 times greater than normal, acute pancreatitis is likely ^[48]
• Imaging: abdominal ultrasound or MRI are preferred (e.g., to identify choledocholithiasis or complications of acute pancreatitis such as hemorrhage, edema, or pseudocysts)

Treatment

• Identical to that for nonpregnant individuals (see “Treatment of acute pancreatitis.”)
• See “Overview of analgesics to avoid during pregnancy” for further details.

Complications

• See “Complications of acute pancreatitis.”
• Pregnancy-related complications: increased risk of preterm labor, premature birth, and/or fetal death

Acute pancreatitis in children ^[49][50][51]

Epidemiology

Incidence is 3–13 cases per 100,000 people per year. ^[51]

Etiology ^[51]

• Biliary pancreatitis (most common cause)
• Medications (e.g., valproic acid, mesalamine, glucocorticoids)
• Systemic disease (e.g., metabolic disorders, hemolytic uremic syndrome, Kawasaki disease)
• Underlying genetic conditions (e.g., cystic fibrosis)
• Anatomical anomalies of the pancreas (e.g., pancreas divisum, annular pancreas)
• Trauma and/or child maltreatment
• Infection (e.g., mumps, influenza, herpes viruses, hepatitis)
• Critical illness (e.g., sepsis)
• Autoimmune pancreatitis

Approximately 20% of children have > 1 underlying cause. ^[51]

Clinical features ^[51]

• Similar to clinical features of acute pancreatitis in adults
• Symptoms common in infants and young children include:
  • Generalized abdominal pain
  • Irritability

Diagnostics

• Similar to diagnostics for acute pancreatitis in adults ^[49][50]
• Use adult diagnostic criteria for acute pancreatitis.
  • Serum lipase is more reliable than amylase in infants. ^[51]
  • Abdominal ultrasound is the preferred initial imaging modality. ^[49]
• Studies considered by a specialist (e.g., gastroenterology) may include:
  • Genetic studies ^[50]
  • Diagnostics for cystic fibrosis
  • Stool studies

Management of pediatric pancreatitis ^[49][50]

• Treatment of acute pancreatitis in children is similar to adults with the following changes:
  • Use pediatric parameters for fluid resuscitation (e.g., lactated Ringer's solution or normal saline). ^[49]
    • Bolus: 10–20 mL/kg once in hemodynamically unstable patients ^[49]
    • Maintenance rate: 1.5–2 times the typical weight-based maintenance rate for 24–48 hours ^[49]
  • Pain management according to the WHO analgesic ladder may include both of the following:
    • Nonopioid oral analgesia in children (e.g., acetaminophen, NSAIDs)
    • Opioids for acute pain
• Consult a specialist (e.g., gastroenterology, surgery) for:
  • Clinical deterioration
  • Suspected complications
  • Consideration of invasive procedure
  • Recurrent acute pancreatitis

Up to 40% of children with acute pancreatitis eventually progress to chronic pancreatitis. ^[51]

• Intestinal manifestations
  • Acute peritonitis
  • Appendicitis
  • Acute mesenteric ischemia
  • Acute cholecystitis
  • Acute cholangitis
  • Peptic ulcer disease
  • Biliary colic
  • Abdominal aortic aneurysm
• Extraintestinal manifestations
  • Myocardial infarction
  • Bacterial pneumonia
• See also “Differential diagnoses of acute abdomen.”

Reference:^[8]

The differential diagnoses listed here are not exhaustive.

Necrotizing pancreatitis ^[15]

• Definition: necrosis of pancreatic and peripancreatic tissue
• Clinical features: fever, persistent tachycardia, or insufficient symptomatic improvement over several days
• Diagnostics: nonenhancing areas of pancreatic parenchyma on CECT abdomen ^[9]
• Treatment ^[15]
  • Sterile necrotizing pancreatitis can usually be managed conservatively. ^[7]
  • Encourage enteral nutrition if feasible.
  • Provide supplemental nutritional support as needed.

Infected necrotizing pancreatitis ^[15]

• Definition: bacterial superinfection of necrotic pancreatic parenchyma
• Clinical features: similar to those of necrotizing pancreatitis
• Diagnostics
  • Laboratory studies: persistent or worsening leukocytosis, bacteremia, increasing inflammatory markers ^[15]
  • CECT abdomen: gas within the pancreas and/or peripancreatic tissue or fluid collections ^[6]
  • Fine-needle aspiration of necrotic areas: not routinely recommended ^[4][7][11]
• Treatment ^[15]
  • Supportive care: fluid therapy, analgesics, nutritional support
  • Broad-spectrum empiric antibiotics with good tissue penetration (e.g., carbapenems , quinolones, third- or higher-generation cephalosporins, metronidazole) for 2–4 weeks ^[4][15]
  • Drainage of infected material if there is clinical deterioration or persistence of symptoms despite antibiotic therapy
    • Operative pancreatic debridement (necrosectomy) should ideally be performed at least 2–4 weeks after initial presentation. ^[4][15]
    • Minimally invasive procedures (e.g., image-guided percutaneous drainage) can be performed in the first 2 weeks in seriously ill patients.
• Prognosis: high mortality rate (30%) ^[15]

Walled-off necrosis

• Definition
  • An encapsulated collection of sterile necrotic material, usually occurring > 4 weeks after the onset of necrotizing pancreatitis ^[6]
  • Previously known as pancreatic abscess
• Diagnostics: CT abdomen with IV contrast showing an encapsulated heterogeneous collection containing fluid and debris ^[9]
• Treatment: (of symptomatic walled-off necrosis): percutaneous drainage or transmural endoscopic necrosectomy ^[15]

Other localized complications ^[53][54]

• Pancreatic pseudocyst
• Abdominal compartment syndrome
• Pancreatic hemorrhage (blood vessel erosion with bleeding)

Systemic complications ^[55]

• Shock, SIRS, sepsis, DIC
• Pneumonia, respiratory failure, ARDS ^[55]
• Pleural effusion
• Prerenal failure due to volume depletion
• Hypocalcemia
• Paralytic ileus
• Pancreatic ascites

We list the most important complications. The selection is not exhaustive.

• Mortality
  • In patients without organ failure: < 1%
  • In patients with organ failure: ∼ 30%
  • Higher mortality in patients with biliary pancreatitis than in patients with alcohol-induced pancreatitis
• Risk factors for severe disease: See “Severity scores for acute pancreatitis.” ^[4][56]

References:^[10][57][58]