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Basic Information ⬇

AUTHOR: David J. Lucier Jr, MD, MBA, MPH

Definition

  • Acute pancreatitis is an inflammatory process of the pancreas with intrapancreatic activation of enzymes that may also involve peripancreatic tissue and/or remote organ systems. The diagnosis of acute pancreatitis requires at least two of the following criteria: Serum amylase or lipase ≥3 times normal, abdominal pain consistent with pancreatitis, and radiographic findings (CT or MRI) of acute pancreatitis.
  • The Ranson scoring system for acute pancreatitis is described in Boxes 1 and 2.
  • The Revised Atlanta Criteria (Box 3) uses early prognostic signs, organ failure, and local complications to define disease severity:
    1. Mild pancreatitis: No organ failure, no local or systemic complications, pancreatitis typically resolves in first week
    2. Moderate pancreatitis: Transient organ failure (≤48 h) or local complications (e.g., pancreatic necrosis, peripancreatic fluid collections, peripancreatic necrosis) or exacerbation of comorbid disease
    3. Severe pancreatitis: Persistent organ failure (>48 h)
  • The BALI Score evaluates only four variables:
    1. BUN ≥25 mg/dl
    2. Age ≥65 yr
    3. LDH ≥300 U/L
    4. Interleukin-6 level ≥300 pg/ml
  • These measurements are taken at admission and at 48 h. Mortality is >25% for a score of 3 and exceeds 50% with a score of 4.
  • Severe acute pancreatitis (SAP) is diagnosed by the presence of any of the following four criteria:
    1. Organ failure with one or more of the following: Shock (systolic blood pressure <90 mm Hg), pulmonary insufficiency (PaO2≤60 mm Hg), renal failure (serum creatinine >2 mg/dl after rehydration), and gastrointestinal bleeding (>500 ml/24 h)
    2. Local complications such as necrosis, pseudocyst, or abscess
    3. At least three of the Ranson criteria (see Boxes 1 and 2) or
    4. At least eight of the Acute Physiology and Chronic Health Evaluation II (APACHE II) criteria

Box 3 Atlanta Criteria for Acute Pancreatitis

Organ Failure, as Defined by

Shock (systolic blood pressure <90 mm Hg)

Pulmonary insufficiency (PaO2 <60 mm Hg)

  • Renal failure (creatinine level >2 mg/dl after fluid resuscitation)
  • Gastrointestinal bleeding (>500 ml/24 h)
  • Systemic Complications

Disseminated intravascular coagulation (platelet count ≤100,000)

  • Fibrinogen <1 g/L
  • Fibrin split products >80 μg/dl
  • Metabolic disturbance (calcium level ≤7.5 mg/dl)
Local Complications

  • Necrosis
  • Abscess
  • Pseudocyst
  • Severe pancreatitis is defined by the presence of any evidence of organ failure or a local complication.

From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.

Box 1 Ranson Prognostic Criteria for Nongallstone Pancreatitis

  • At presentation
    1. Age >55 yr
    2. Blood glucose level >200 mg/dl
    3. White blood cell count >16,000 cells/mm3
    4. Lactate dehydrogenase level >350 IU/L
    5. Aspartate aminotransferase level >250 IU/L
  • After 48 h of admission
    1. Hematocrit∗: Decrease >10%
    2. Serum calcium level <8 mg/dl
    3. Base deficit >4 mEq/L
    4. Blood urea nitrogen level: Increase >5 mg/dl
    5. Fluid requirement >6 L
    6. PaO2 <60 mm Hg
  • Ranson score ≥3 defines severe pancreatitis.

From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.

Box 2 Ranson Prognostic Criteria for Gallstone Pancreatitis

  1. At presentation
    • Age >70 yr
    • Blood glucose level >220 mg/dl
    • White blood cell count >18,000 cells/mm3
    • Lactate dehydrogenase level >400 IU/L
    • Aspartate aminotransferase level >250 IU/L
  2. After 48 h of admission
    • Hematocrit∗: Decrease >10%
    • Serum calcium level <8 mg/dl
    • Base deficit >5 mEq/L
    • Blood urea nitrogen level: Increase >2 mg/dl
    • Fluid requirement >4 L
    • PaO2: Not available
  3. Ranson score ≥3 defines severe pancreatitis.

From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis, 2022, Elsevier.

ICD-10CM CODES
K85.0Idiopathic acute pancreatitis
K85.1Biliary acute pancreatitis
K85.2Alcohol-induced acute pancreatitis
K 85.3Drug-induced pancreatitis
K85.6Other acute pancreatitis
K85.9Acute pancreatitis, unspecified
Epidemiology & Demographics

  • The incidence of pancreatitis is increasing in the U.S. Admissions for acute pancreatitis have increased dramatically, and acute pancreatitis was the number-one GI-related cause for admission across U.S. hospitals in 2012. There are >270,000 cases of acute pancreatitis reported annually in the U.S., with 40%+ resulting from gallstone disease (most common cause) and 30% caused by alcohol consumption.
  • Incidence in urban areas is twice that of rural areas (20/100,000 persons in urban areas).
  • 20% of patients have necrotizing pancreatitis; the remainder have interstitial, or edematous, pancreatitis.
  • Drugs are responsible for less than 5% of all cases of acute pancreatitis.
Physical Findings & Clinical Presentation

  • Epigastric tenderness and guarding, often radiating to the back; pain usually developing suddenly, reaching peak intensity within 10 to 30 min, severe and lasting several hours without relief. Rarely, some patients can have painless severe pancreatitis
  • Nausea and vomiting (up to 90% of cases)
  • Hypoactive bowel sounds (from ileus)
  • Tachycardia, shock (from decreased intravascular volume)
  • Confusion (from metabolic disturbances)
  • Fever (SIRS response or infection when pancreatic necrosis is present)
  • Decreased breath sounds (pleural effusions) or rales (atelectasis, acute respiratory distress syndrome [ARDS])
  • Jaundice (from obstruction or compression of biliary tract)
  • Ascites (from tear in pancreatic duct, leaking pseudocyst)
  • Palpable abdominal mass (pseudocyst, phlegmon, abscess, carcinoma)
  • Evidence of hypocalcemia (Chvostek sign, Trousseau sign)
  • Evidence of retroperitoneal bleeding (hemorrhagic pancreatitis):
    1. Ecchymosis around the umbilicus (Cullen sign)
    2. Ecchymosis involving the flanks (Grey Turner sign)
  • Tender subcutaneous nodules (caused by subcutaneous fat necrosis)
Etiology

  • The most common causes of acute pancreatitis are gallstones (40% of cases) and excessive alcohol consumption (30% of cases). Alcohol-related pancreatitis is most common after long term (>10 yr of heavy drinking). The pathophysiology of severe acute pancreatitis is illustrated in Fig. 1
  • Hypertriglyceridemia (usually >1000 mg/dl) from any cause
  • Drugs (e.g., thiazides, furosemide, corticosteroids, tetracycline, estrogens, valproic acid, metronidazole, azathioprine, methyldopa, pentamidine, ethacrynic acid, procainamide, amiodarone, sulindac, nitrofurantoin, ACE inhibitors, danazol, cimetidine, piroxicam, gold, ranitidine, sulfasalazine, isoniazid, acetaminophen, cisplatin, didanosine, opiates, erythromycin, metformin, GLP-1 receptor agonists, incretin mimetics)
  • Abdominal trauma
  • Surgery
  • Endoscopic retrograde cholangiopancreatography (ERCP), especially with manipulation of the pancreatic duct
  • Infections (predominantly viral)
  • Peptic ulcer (penetrating duodenal ulcer)
  • Pancreas divisum (congenital failure to fuse of dorsal or ventral pancreas)
  • Idiopathic
  • Pregnancy
  • Vascular (vasculitis, ischemic)
  • Hypercalcemia
  • Pancreatic carcinoma (primary or metastatic)
  • Renal failure
  • Hereditary pancreatitis, such as in patients with cystic fibrosis
  • Immunoglobulin G subclass 4 (IgG4) disease
  • Occupational exposure to chemicals: Methanol, cobalt, zinc, mercuric chloride, creosol, lead, organophosphates, chlorinated naphthalenes
  • Others: Scorpion venom, obstruction at ampulla region (neoplasm, duodenal diverticula, Crohn disease, rarely celiac disease), hypotensive shock, autoimmune pancreatitis
  • Causes of acute pancreatitis in pediatric patients are summarized in Table E1

Figure 1 Pathophysiology of severe acute pancreatitis.

The local injury induces the release of tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1). Both cytokines produce further pancreatic injury and amplify the inflammatory response by inducing the release of other inflammatory mediators, which cause distant organ injury. This abnormal inflammatory response is responsible for the mortality seen during the early phase of acute pancreatitis. ERCP, Endoscopic retrograde cholangiopancreatography; PAF, platelet-activating factor.

From Townsend CM et al: Sabiston textbook of surgery, ed 21, St Louis 2022, Elsevier.

TABLE E1 Causes of Acute Pancreatitis in Children

Obstructive
Cholelithiasis and biliary sludge
Choledochal cyst
Pancreas divisum
Anomalous junction of biliary and pancreatic ducts
Annular pancreas
Ampullary obstruction (mass, inflammation from Crohn disease)
Ascaris infection
Medications and Toxins
l-asparaginase
Valproic acid
Azathioprine and 6-mercaptopurine
Didanosine
Pentamidine
Tetracycline
Opiates
Mesalamine
Sulfasalazine
Alcohol
Cannabis
Systemic Diseases
Inflammatory bowel disease
Hemolytic uremic syndrome
Diabetic ketoacidosis
Collagen vascular disease
Kawasaki disease
Shock
Sickle cell disease
Infectious
Sepsis
Mumps
Coxsackievirus
Cytomegalovirus
Varicella-zoster
Herpes simplex
Mycoplasma
Ascaris
Genetic
Cystic fibrosis-CFTR mutations
Hereditary pancreatitis-SPINK, PRSS1, and CTRC mutations
Other
Trauma
Hyperlipidemia
Hypercalcemia
Autoimmune

From Marcdante KJ et al: Nelson essentials of pediatrics, ed 9, Philadelphia, 2023, Elsevier.

∗Compared with admission value.

∗Compared with admission value.

Diagnosis ⬆ ⬇

Differential Diagnosis

  • PUD
  • Acute cholangitis, biliary colic
  • High intestinal obstruction
  • Early acute appendicitis
  • Diabetic ketoacidosis
  • Pneumonia (basilar)
  • Myocardial infarction (inferior wall)
  • Renal colic
  • Ruptured or dissecting aortic aneurysm
  • Mesenteric ischemia
Laboratory Tests

Pancreatic enzymes:

  • Amylase is increased, usually elevated in the initial 3 to 5 days of acute pancreatitis. Isoamylase determinations (separation of pancreatic cell isoenzyme components of amylase) are useful in excluding occasional cases of salivary hyperamylasemia. The use of isoamylase rather than total serum amylase reduces the risk of erroneously diagnosing pancreatitis and is preferred by some as initial biochemical test in patients suspected of having acute pancreatitis.
  • Urinary amylase determinations are useful to diagnose acute pancreatitis in patients with lipemic serum, to rule out elevated serum amylase caused by macroamylasemia, and to diagnose acute pancreatitis in patients whose serum amylase is normal.
  • Serum lipase levels are elevated in acute pancreatitis; the elevation is less transient than serum amylase and more sensitive in patients with alcoholic pancreatitis. Concomitant evaluation of serum amylase and lipase does not improve diagnostic accuracy of acute pancreatitis. Serial measurements have limited usefulness because levels are not predictors of severity. Elevated serum trypsin levels are diagnostic of pancreatitis (in absence of renal failure).
  • Serum C-reactive protein is an excellent laboratory marker of severity; a level >150 mg/dl at 48 h is associated with severe pancreatitis.
  • Rapid measurement of urinary trypsinogen-2 (if available) is useful in the emergency department as a screening test for acute pancreatitis in patients with abdominal pain; a negative dipstick test for urinary trypsinogen-2 rules out acute pancreatitis with a high degree of probability, whereas a positive test indicates need for further evaluation.
  • Interleukin-6 level: Worse prognosis with level ≥300 pg/ml.
Additional Tests

  • CBC: Reveals leukocytosis; hematocrit (Hct) may be initially increased as a result of hemoconcentration; decreased Hct may indicate hemorrhage or hemolysis.
  • Blood urea nitrogen (BUN) is increased because of dehydration. Serial BUN measurements are the most valuable lab test for predicting mortality during the initial 48 h.
  • Elevation of serum glucose in a previously normal patient correlates with the degree of pancreatic malfunction and may be related to increased release of glycogen, catecholamines, and glucocorticoid release and decreased insulin release.
  • Liver profile: Aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) are increased as a result of tissue necrosis; bilirubin and alkaline phosphatase may be increased from common bile duct obstruction. A threefold or greater rise in serum alanine aminotransferase concentrations is an excellent indicator (95% probability) of biliary pancreatitis.
  • Serum calcium is decreased because of saponification, precipitation, and decreased parathyroid hormone response.
  • Arterial blood gases: PaO2 may be decreased as a result of ARDS, pleural effusion(s); pH may be decreased as a result of lactic acidosis, respiratory acidosis, and renal insufficiency.
  • Serum electrolytes: Potassium may be increased from acidosis or renal insufficiency; sodium may be increased from dehydration.
Imaging Studies

  • Abdominal plain films are useful initially to distinguish other conditions that may mimic pancreatitis (perforated viscus). They may reveal localized ileus (sentinel loop), pancreatic calcifications (chronic pancreatitis), blurring of left psoas shadow, dilation of transverse colon, calcified gallstones.
  • Chest x-ray may reveal elevation of one or both diaphragms, pleural effusions, basilar infiltrates, or platelike atelectasis.
  • Abdominal ultrasonography is useful in detecting gallstones (sensitivity of 60% to 70% for detecting stones associated with pancreatitis). Its availability and noninvasive nature make it the initial imaging study of choice; its major limitation is the presence of distended bowel loops overlying the pancreas.
  • CT scan (Fig. 2) is less sensitive than ultrasound in identifying gallstones and exposes the patient to risk of contrast-induced nephropathy. It is, however, superior to ultrasonography in identifying pancreatitis and defining its extent, and it also plays a role in diagnosing pseudocysts (they appear as a well-defined area surrounded by a high-density capsule); gastrointestinal fistulization or infection of a pseudocyst can also be identified by the presence of gas within the pseudocyst. Sequential contrast-enhanced CT is useful for detection of pancreatic necrosis. The severity of pancreatitis can also be graded by CT scan (Table 2). (A = normal pancreas, B = enlarged pancreas [1 point], C = pancreatic and/or peripancreatic inflammation [2 points], D = single peripancreatic collection [3 points], E = at least two peripancreatic collections and/or retroperitoneal air [4 points]. Percentage of pancreatic necrosis <30% [2 points], 30% to 50% [4 points], >50% [6 points]. The CT severity index is calculated by adding grade points to points assigned for percentage of necrosis.)
  • Magnetic resonance cholangiopancreatography (MRCP) has >90% sensitivity for cho-ledocholithiasis and can identify other anatomic abnormalities.
  • Endoscopic ultrasonography (EUS) is a minimally invasive test that provides high-resolution imaging of the pancreas. It is useful to identify anatomic abnormalities of the pancreas and has good sensitivity and specificity for small gallstones (≤5 mm).
  • ERCP indications: Useful to perform biliary sphincterotomy and stone removal in the presence of a retained bile duct stone seen on imaging. The role and timing of ERCP in patients with acute biliary pancreatitis has been controversial. Guidelines from the American College of Gastroenterology suggest that urgent ERCP (within 24 h of admission) is indicated in patients with biliary pancreatitis who have concurrent acute cholangitis, but it is not needed in most patients who do not have evidence of ongoing biliary obstruction.
Figure 2 Gallstone Pancreatitis and Normal Pancreas for Comparison, Axial Computed Tomography Without Contrast

A, Gallstone pancreatitis CT. A dilated gallbladder is visible with a hyperdense dependent lesion consistent with a gallstone. The region of the pancreas shows significant inflammatory stranding. In this patient the pancreas lies just anterior to the left renal vein, which can be seen crossing anterior to the aorta and entering the inferior vena cava. B, A normal pancreas is visible. This pancreas is surrounded by uninflamed fat, which is dark (nearly black). Compare this normal fat with normal subcutaneous fat.

From Broder JS: Diagnostic imaging for the emergency physician, Philadelphia, 2011, Saunders.

TABLE 2 Computed Tomography (CT) Severity Index Score for Pancreatitis∗

Grade†CT FindingsScore
ANormal pancreas0
BFocal or diffuse enlargement of the pancreas, contour irregularities, heterogeneous attenuation, no peripancreatic inflammation1
CGrade B plus peripancreatic inflammation2
DGrade C plus a single fluid collection3
EGrade C plus multiple fluid collections or gas4
Percent Necrosis Present on CT
0
<33
33-50
>50

∗Severity Index Score = Grade score + Percent necrosis score. Maximum score = 10; severe disease = 6 or higher.

† Severity of the acute inflammatory process.

From Adams JG et al: Emergency medicine: clinical essentials, ed 2, Philadelphia, 2013, Elsevier.

Treatment ⬆ ⬇

Nonpharmacologic Therapy

  • Bowel rest with avoidance of liquids or solids during the acute illness. Limited data suggest that early feeding in patients with acute pancreatitis does not seem to increase adverse events and, for patients with mild to moderate pancreatitis, may reduce length of hospital stay.
  • Avoidance of alcohol and any drugs associated with pancreatitis.
Acute General Rx
General Measures

  • Assess severity of pancreatitis.
  • An algorithm for the management of acute pancreatitis is described in Fig. 3.
  • Maintain adequate intravascular volume with IV hydration. The ideal quantity of fluid resuscitation has been controversial. Traditionally aggressive fluid resuscitation (250 to 500 ml/h) with isotonic crystalloids was regarded as critical in managing acute pancreatitis, unless cardiac or renal disease precluded it. Recent trials have show that moderate fluid resuscitation results in similar clinical outcomes as did aggressive resuscitation with less fluid overload.1
  • Patient should remain NPO until clinically improved, stable, and hungry. Enteral feedings are preferred over total parenteral nutrition if supplemental nutrition is necessary. Enteral nutrition reduces mortality, multiple organ failure, systemic infections, and operative interventions more than total parenteral nutrition does in patients with acute pancreatitis. Parenteral nutrition may be necessary in patients who do not tolerate enteral feeding or in whom an adequate infusion rate cannot be reached within 2 to 4 days. The American Gastroenterological Association recommends that oral feedings be started within 24 h of admission in patients with mild to moderate pancreatitis. A recent trial revealed that patients started on a low-fat diet on admission were discharged about 5 days earlier than patients in whom feeding was delayed.
  • Nasogastric suction is useful only in severe pancreatitis to decompress the abdomen in patients with ileus.
  • Control pain: IV hydromorphone or fentanyl. Meperidine and morphine are also commonly used narcotics for pain control, although morphine has been shown to increase sphincter of Oddi pressure and has delayed metabolite clearance in patients with concomitant renal failure.
  • Correct metabolic abnormalities (e.g., replace calcium and magnesium as necessary).
  • Prophylactic antibiotics are not recommended, regardless of the severity or presence of pancreatic necrosis.
  • An algorithm for the management of acute pancreatitis at various stages is described in Fig. 3.
Figure 3 Algorithm for the Management of Acute Pancreatitis at Various Stages in its Course

NJ, Nasojejunal.

!!flowchart!!

From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 10, Philadelphia, 2016, Elsevier.

Specific Measures

  • Pancreatic or peripancreatic infection develops in 30% of patients with pancreatic necrosis. The use of antibiotics is justified if the patient has evidence of septicemia, pancreatic abscess, or pancreatitis caused by biliary calculi with concomitant cholangitis. Their use should generally be limited to 5 to 7 days to prevent development of fungal superinfection. Appropriate empiric antibiotic therapy should penetrate pancreatic necrosis. Options include a carbapenem alone (due to anaerobic coverage) or a quinolone, ceftazidime, or cefepime, combined with an enteric anaerobic agent such as metronidazole. CT-guided fine-needle aspiration (FNA) can be performed to culture the infected necrosis and tailor antibiotic therapy. If sampling of infected necrosis occurs and is sterile, antibiotics should be discontinued
  • Surgical therapy has a limited role in acute pancreatitis; it is indicated in the following:
    1. Gallstone-induced pancreatitis: Cholecystectomy when acute pancreatitis subsides. However, randomized trials have shown that patients with mild gallstone pancreatitis can undergo cholecystectomy safely during the first 48 h of hospitalization
    2. Perforated peptic ulcer
    3. Necrotizing pancreatitis with infected necrotic tissue is associated with an elevated rate of complications and increased risk of death. Traditional treatment has been open necrosectomy; surgical necrosectomy induces a proinflammatory response and is associated with a high complication rate. Recent trials have shown that a step-up approach consisting of percutaneous drainage followed, if necessary, by minimally invasive retroperitoneal necrosectomy may have a lower rate of complications and death. A recent trial did not show superiority of immediate drainage over postponed drainage with regard to complications in infected necrotizing pancreatitis. Endoscopic transgastric necrosectomy, a form of natural orifice transluminal endoscopic surgery, has been shown in recent trials to be effective in reducing the proinflammatory response as well as reducing complications
  • Identification and treatment of complications:
    1. Pseudocyst: Round or spheroid collection of fluid, tissue, pancreatic enzymes, and blood
      1. Diagnosed by CT scan or sonography.
      2. Treatment: Pancreatic pseudocysts can be drained surgically or endoscopically. The endoscopic approach is preferable when the patient’s anatomy is suitable and an experienced endoscopist is available. CT scan or ultrasound-guided percutaneous drainage (with a pigtail catheter left in place for continuous drainage) can be used, but the recurrence rate is high; the conservative approach is to reevaluate the pseudocyst (with CT scan or sonography) after 6 to 7 wk and surgically drain it if the pseudocyst has not decreased in size.
      3. Generally, pseudocysts <5 cm in diameter are reabsorbed without intervention, whereas those >5 cm require surgical intervention after the wall has matured.
    2. Phlegmon: Represents pancreatic edema. It can be diagnosed by CT scan or sonography. Treatment is supportive as it usually resolves spontaneously
    3. Pancreatic abscess: Diagnosed by CT scan (presence of air in the retroperitoneum); Gram staining and cultures of fluid obtained from guided percutaneous aspiration usually identify bacterial organism. Therapy is surgical (or catheter) drainage and IV antibiotics (carbapenem is the drug of choice)
    4. Pancreatic ascites: Usually caused by leaking of pseudocyst or tear in pancreatic duct. Paracentesis reveals very high amylase and lipase levels in the pancreatic fluid; ERCP may demonstrate the lesion. Treatment is surgical correction if exudative ascites from severe pancreatitis does not resolve spontaneously
  • Abdominal compartment syndrome: Caused by intraabdominal leakage of fluids from volume resuscitation or ascites. Diagnosed with sustained intraabdominal pressure >20 mm Hg with new-onset organ failure
  • Gastrointestinal bleeding: Caused by alcoholic gastritis, bleeding varices, stress ulceration, or disseminated intravascular coagulation (DIC)
  • Renal failure: Caused by hypovolemia, resulting in oliguria or anuria, cortical or tubular necrosis (shock, DIC), or thrombosis of renal artery or vein
  • Hypoxia: Caused by ARDS, pleural effusion, or atelectasis
  • Vascular: Splenic, portal, or superior mesenteric vein thrombosis; pseudoaneurysm
Therapy Of Uncommon Forms Of Pancreatitis

  • Autoimmune pancreatitis (AIP): Fibroinflammatory disease characterized by an IgG4 lymphoplasmacytic infiltrate. It is a variant of chronic pancreatitis and has been associated with other autoimmune disorders (e.g., primary sclerosing cholangitis, Sjögren syndrome). The inflammatory process is generally responsive to corticosteroid therapy. Older men aged 60 to 70 yr are primarily affected. Patients present with abdominal pain, weight loss, anorexia, and obstructive jaundice. IgG4 levels are elevated. Radiographically on CT, the pancreas is diffusely enlarged, with a characteristic smooth, capsulelike rim (“sausage pancreas”). Features of type 1 and type 2 autoimmune pancreatitis are summarized in Table 3. Type II autoimmune hepatitis (idiopathic duct-centric chronic pancreatitis) is associated with inflammatory bowel disease and not related to IgG4 cell deposition.
  • Hypertriglyceridemic pancreatitis (HTGP): IV insulin therapy is the cornerstone of immediate treatment, with supplemental IV glucose infusion if the serum glucose levels are not elevated. IV heparin was previously used as well, but its effectiveness has come into question. Antihyperlipidemic agents (fibrates) should be initiated as adjuvant therapy as soon as possible for long-term control. Beneficial results have been reported with early (within 48 h) initiation of apheresis with therapeutic plasma exchange when there is concomitant hypocalcemia, lactic acidosis, or other signs of organ dysfunction.

TABLE 3 Features of Type 1 and Type 2 Autoimmune Pancreatitis

FeatureType 1Type 2
HistologyLymphoplasmacytic infiltration
Dense periductal infiltrate without damage to ductal epithelium
Storiform fibrosis
Obliterative phlebitis
Abundant (>10 cells/HPF) IgG4-positive cells
Fibroinflammatory process may extend to peripancreatic region		Periductal lymphoplasmacytic and neutrophilic infiltration
Destruction of the duct epithelium by neutrophils (granulocytic epithelial lesion [GEL])
Obliterative phlebitis is rare
No IgG4-positive cells
Average age at presentation60-70 yr40-50, but may present in young adults and even children
Gender predominanceMaleEqual
Usual clinical presentationsObstructive jaundice (75%)
Acute pancreatitis (15%)		Obstructive jaundice (50%)
Acute pancreatitis (33%)
Pancreatic imagingDiffuse pancreatic enlargement (40%)
Focal pancreatic enlargement (60%)		Diffuse pancreatic enlargement (15%)
Focal pancreatic enlargement (85%)
IgG4Level elevated in serum (∼⅔ of patients)
Positive in staining of involved tissues		Not associated
Other organ involvementBiliary strictures
Pseudotumors
Kidney
Lung
Others
Retroperitoneal fibrosis
Sialoadenitis		Not associated
Associated diseasesSee above (other organ involvement)IBD
Long-term outcomeFrequent relapsesRare or no relapse

HPF, High power field; IBD, inflammatory bowel disease; IgG4, immunoglobulin G, subclass 4.

From Feldman M et al: Sleisenger and Fordtran’s gastrointestinal and liver disease, ed 10, Philadelphia, 2016, Elsevier.

Disposition

Prognosis varies with the severity of pancreatitis; overall mortality rate in acute pancreatitis is 5% to 10%. Prognostic criteria for acute pancreatitis are described in Table 4.

TABLE 4 Prognostic Criteria for Acute Pancreatitis

Ranson Criteria∗Simplified Glasgow Criteria†Computed Tomography Criteria‡
On admission: Age >55 yr
WBC >16,000/μL
AST >250 U/L LDH >350 U/L
Glucose >200 mg/dl
48 h after admission:
Hematocrit decrease by >10
BUN increase by >5 mg/dl
Ca2+ <8 mg/dl
Arterial PO2 <60 mm Hg
Base deficit >4 mEq/L
Fluid sequestration >6 L		Within 48 h of admission: Age >55 yr
WBC >15,000/μL
LDH >600 U/L
Glucose >180 mg/dl
Albumin <3.2 g/dl
Ca2+ <8 mg/dl
Arterial PO2 <60 mm Hg
BUN >45 mg/dl		Normal
Enlargement
Pancreatic inflammation
Single fluid collection
Multiple fluid collection

AST, Aspartate aminotransferase; BUN, blood urea nitrogen; LDH, lactate dehydrogenase; WBC, white blood cells.

∗Three or more Ranson criteria predict a complicated clinical course. Data from Ranson JH et al: Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis, Surg Gynecol Obstet 143:209-219, 1976.

† Data from Blamey SL et al: Prognostic factors in acute pancreatitis, Gut 25:1340, 1984.

‡ Grades A and B represent mild disease with no risk of infection or death. Grade C represents moderately severe disease with a minimal likelihood of infection and essentially no risk of mortality. Grades D and E represent severe pancreatitis with an infection rate of 30% to 50% and mortality rate of 15%. Data from Balthazar EJ et al: Acute pancreatitis value of CT in establishing prognosis, Radiology 174:331, 1990.

From Goldman L, Ausiello D (eds): Cecil textbook of medicine, ed 24, Philadelphia, 2012, Saunders.

Referral

  • Hospitalization is indicated in moderate to severe cases of pancreatitis.
  • Surgical consultation is needed in suspected gallstone pancreatitis, perforated peptic ulcer, or presence of necrotic or infected foci. Acute pancreatitis can generally be attributed to gallstones when patients have both abnormal liver enzymes and gallstones (or sludge) on imaging. Such patients should consider cholecystectomy before discharge to prevent recurrent pancreatitis.
  • Gastroenterology consultation in severe or recurrent pancreatitis, when ERCP is needed for gallstone pancreatitis, or when the cause of pancreatitis is unclear.
  • Consider intensive care unit transfer for patients who require aggressive fluid resuscitation and are at risk of volume overload from cardiac or renal causes. Similarly, consider transfer for patients with developing ARDS, patients with abdominal compartment syndrome (with surgical consultation), and those who require apheresis.

Pearls & Considerations ⬆ ⬇

Related Content

Acute Pancreatitis (Patient Information)

Suggested Readings ⬆ ⬇

  1. Bakker O.J. : Early versus on-demand nasogastric tube feeding in acute pancreatitisN Engl J Med. ;371:1983-1993, 2014.
  2. Banks P.A. : Acute Pancreatitis Classification Working Group: classification of acute pancreatitis-2012: revision of the Atlanta classification and definitions by international consensusGut. ;62(1):102-111, 2013.
  3. Fogel E.L., Sherman S. : ERCP for gallstone pancreatitisN Engl J Med. ;370:150-157, 2014.
  4. Forsmark C.E. : Acute pancreatitisN Engl J Med. ;375:1972-1981, 2016.
  5. Gardner B. : In the clinic: acute pancreatitisAnn Intern Med Feb 2021. :ITC18-ITC29, 2021.
  6. Quinlan J.D. : Acute pancreatitisAm Fam Physician. ;90(9):632-639, 2014.
  7. Tess A. : How would you treat this patient with gallstone pancreatitis?Ann Int Med. ;170:178-181, 2019.
  8. Vaughn V.M. : Early versus delayed feeding in patients with acute pancreatitis, a systematic reviewAnn Intern Med. ;66:883-892, 2017.

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    1. de-Madaria E. : Aggressive or moderate fluid resuscitation in acute pancreatitisN Engl J Med. ;387(11):989-1000, 2022.