Acute pancreatitis

Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by gallstones and alcohol use. 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., 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)
  • 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]

I GET SMASHED: Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune, Scorpion poison, Hypercalcemia and hypertriglyceridemia, ERCP, and Drugs are the most common 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

Acute pancreatitis should be managed as a medical emergency as it is a potentially fatal condition. Initiate fluid resuscitation as soon as this diagnosis is suspected (see “Treatment of acute pancreatitis”). Simultaneously conduct diagnostics to establish the diagnosis, assess severity, and rule out potential differential diagnoses of acute abdominal pain.

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

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., contrast-enhanced CT abdomen)

Approach ^[6][7][8]

• 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.

Laboratory studies

The degree of lipase and/or amylase elevation does not necessarily correlate with the severity of or prognosis for acute pancreatitis. ^[22]

Measure serum triglycerides promptly after symptom onset, as levels decrease rapidly with fasting. ^[23]

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

Imaging

Ultrasound abdomen ^[8][24]

• Indications: first-line imaging modality for all patients
• Supportive findings
  • Features of acute pancreatitis (visible in 20% of cases) ^[8]
    • Enlarged hypoechoic pancreas (pancreatic edema)
    • Peripancreatic fluid and/or ascites
  • Features of biliary pancreatitis
    • Cholelithiasis and/or gallbladder sludge ^[8]
    • Dilated biliary tree
  • Evidence of complications: pancreatic pseudocysts, walled-off necrosis (typically > 4 weeks from symptom onset) ^[14]

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. ^[8]

CT abdomen and pelvis with IV contrast ^[6][8][14]

• Indications
  • Diagnostic uncertainty (e.g., typical clinical features in a patient with moderately elevated pancreatic enzymes)
  • Severe pancreatitis : optimally performed > 5–7 days after symptom onset ^[8]
  • Lack of improvement (after > 7 days) or sudden acute deterioration
  • To evaluate for underlying etiology if routine diagnostic studies are negative ^[6]
• 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 pancreatis 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 fuid 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. ^[8]

Suspect pancreatic tumor as the underlying cause for idiopathic acute pancreatitis in patients aged > 40 years; see “Pancreatic cancer.” ^[25]

X-ray chest and abdomen ^[8][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 ^[6][8]

• 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 ^[4][6][8]

• 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) ^[8]
  • 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 ^[5]

The revised Atlanta grades of severity classify pancreatitis as mild, moderate, 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
• Moderate 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. ^[5]

CT severity index ^[7][23][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 ^[7][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) ^[7]

• Mainly used in the ICU setting to determine the severity of acute pancreatitis
• Scores ≥ 8 indicate severe pancreatitis with a guarded prognosis. ^[7][10]

Bedside index of severity of acute pancreatitis (BISAP) ^[10]

• 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. ^{[4][6][10][25]}

Acute stabilization ^{[4][6][10][25]}

• 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 ^{[4][6][10][25]}

• Fluids and infusion rate
  • Crystalloids such as normal saline (NS) or lactated Ringer's solution (LR) are preferred. ^[4][10]
  • Hemodynamically stable patients ^[6][25]
    • 5–10 mL/kg/hour or 250–500 mL/hour
    • Exercise caution in patients with renal or cardiovascular disease.
  • Hemodynamically unstable patients
    • Administer rapid fluid bolus (e.g., for adults NS or LR 500–1000 mL IV bolus over 10–30 minutes).
    • Repeat as needed based on response.
  • See also “Fluid resuscitation” for further detail.
• Monitoring ^[7][11]
  • Monitor vitals, oxygen saturation, and urine output every 1–2 hours during the initial period of fluid resuscitation.
  • 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 ^[6]
  • 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% ^[36]
  • Hct 35–44%
• Replete electrolytes as needed.

Intravenous fluid resuscitation in the first 12–24 hours has the greatest impact on the clinical outcome of patients with acute pancreatitis. ^[25]

Supportive therapy

• Analgesics
  • NSAIDS (e.g., ketorolac , diclofenac , ibuprofen ) ^[37][38]
  • Opioids; (e.g., meperidine , hydromorphone , morphine ) ^[39][40][41]
  • Consider patient-controlled analgesia for management of severe pain. ^[10][38]
• Antiemetics as needed (e.g., ondansetron , metoclopramide )

In concurrent acute kidney injury, avoid NSAIDs and use opioids with caution because of the risk of accumulation. ^[10]

Prophylactic antibiotics are not recommended, and should only be used in patients with evidence of infected necrosis. ^[10]

Consults

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

Disposition ^[6][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. ^[6]

Nutrition

• Early oral feeding: Begin as soon as tolerated (i.e., not causing pain, nausea, or vomiting), ideally within 24 hours. ^[4][15][42]
• Enteral tube (nasogastric or nasojejunal): preferred over parenteral nutrition if patients cannot tolerate oral intake ^[4][43]
• Parenteral nutrition (total or partial): only in patients who cannot tolerate enteral feeds (e.g., those with persistent paralytic ileus) ^[44]

Bowel rest is no longer routinely recommended. Enteral nutrition, via oral route or enteral tube, should be initiated as early as tolerated. ^[4]

Management of the underlying cause

Biliary pancreatitis

• Therapeutic ERCP ^[4][6][36]
  • 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 ^[8]
• Cholecystectomy ^[4][6][45]
  • Indication: all patients with biliary pancreatitis to prevent recurrence
  • 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. ^[4]

Hypertriglyceridemia-induced pancreatitis ^[23]

• 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 ^[17]

• 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. ^[7][46]
• Vitamin supplementation (thiamine, pyridoxine)
• See “Treatment of alcohol use disorder” for details.
• Provide counseling on alcohol use disorder before discharge. ^[4]

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

• Start oxygen therapy if hypoxic.
• Establish IV access with two large-bore cannulas.
  • Send laboratory studies.
  • Perform ABG.
• Commence goal-directed IV fluid resuscitation.
• Replete electrolytes as needed.
• Administer supportive therapy: analgesics (e.g., NSAIDs), antiemetics
• Obtain ultrasound abdomen for all patients and CT abdomen in cases of diagnostic uncertainty.
• Establish the diagnosis based on the diagnostic criteria for acute pancreatitis.
• Assess severity, e.g., revised Atlanta grades of severity, BISAP , APACHE II
• Urgent consults as needed, e.g.,
  • Gastroenterology consult for urgent therapeutic ERCP in patients with biliary pancreatitis and concomitant cholangitis
  • Early general surgery consult for suspected severe or necrotizing pancreatitis
• Admit to hospital; consider ICU admission if any of the following are present:
  • Organ dysfunction or failure
  • Ongoing SIRS
  • Significant fluid resuscitation requirements or electrolyte imbalances
  • Older age or high-risk comorbidity
• Monitor vitals, urine output, laboratory studies, and perform serial abdominal examinations (see “Fluid therapy goals for acute pancreatitis”).
• Initiate enteral nutrition (either PO or via nasogastric or nasojejunal tube) as early as tolerated.
• Identify and treat the underlying cause.

Acute pancreatitis during pregnancy ^[47]

• Epidemiology
  • Incidence is 1:1000–10,000 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: See “Clinical features” above.
• 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 ^[47]
  • 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” above)
  • See “Overview of analgesics to avoid during pregnancy” for further details.
• Complications
  • See “Complications” above.
  • Pregnancy-related complications: increased risk of preterm labor, premature birth, and/or fetal death

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

Reference:^[7]

The differential diagnoses listed here are not exhaustive.

Necrotizing pancreatitis ^[14]

• 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 ^[8]
• Treatment ^[14]
  • Sterile necrotizing pancreatitis can usually be managed conservatively. ^[6]
  • Encourage enteral nutrition if feasible.
  • Provide supplemental nutritional support as needed.

Infected necrotizing pancreatitis ^[14]

• 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 ^[14]
  • CECT abdomen: gas within the pancreas and/or peripancreatic tissue or fluid collections ^[5]
  • Fine-needle aspiration of necrotic areas: not routinely recommended ^[6][10]
• Treatment ^[14]
  • Supportive care: fluid therapy, analgesics, nutritional support
  • Broad-spectrum empiric antibiotics with good tissue penetration (e.g., carbapenems ) for 4 weeks ^[14]
  • 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. ^[14]
    • 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%) ^[14]

Walled-off necrosis

• Definition
  • An encapsulated collection of sterile necrotic material, usually occurring > 4 weeks after the onset of necrotizing pancreatitis ^[5]
  • Previously known as pancreatic abscess
• Diagnostics: CT abdomen with IV contrast showing an encapsulated heterogenous collection containing fluid and debris ^[8]
• Treatment (of symptomatic walled-off necrosis): percutaneous drainage or transmural endoscopic necrosectomy ^[14]

Other localized complications ^[49][50]

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

Systemic complications ^[51]

• Shock, SIRS, sepsis, DIC
• Pneumonia, respiratory failure, ARDS ^[51]
• 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
• Important predictors of severity
  • Age > 55
  • Gastrointestinal bleeding
  • Fall in Hct within 48 hours s
  • Hypocalcemia and/or hyperglycemia
  • Inflammatory markers: ↑↑ CRP, ↑ IL-6, ↑ IL-8
  • Evidence of shock and/or organ failure
    • ↑ AST, ↑ ALT
    • ↑ BUN, creatinine
    • ↑ LDH
    • ABG: pO₂ < 60 mm Hg, metabolic acidosis with a base deficit > 4 mmol/L
  • CT findings: pancreatic edema, peripancreatic fluid collection, and/or necrosis of > 33% of the pancreas
  • See “Severity scores for acute pancreatitis” for details.

Amylase and lipase, which are used for the diagnosis of pancreatitis, cannot be used to predict the prognosis!

References:^[9][52][53]

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