Definition
A.Acute pancreatitis is defined as an inflammatory pancreatic condition characterized by local injury, systemic inflammatory response, and possibly organ failure. The most common causes of acute pancreatitis are gallstones and alcohol use.
B.Pancreatitis is subdivided into several categories based on the 2012 Atlanta Classification of acute pancreatitis including:
1.Mild acute pancreatitis:
a.No organ failure, local or systemic complications.
2.Moderately severe acute pancreatitis:
a.Organ failure that resolves within 48 hours, and/or
b.Local or systemic complications without persistent organ failure:
i.Local complications of acute pancreatitis include.
•Acute peripancreatic fluid collections.
•Pancreatic pseudocysts.
•Acute necrotic collections.
•Walled-off pancreatic necrosis.
3.Severe acute pancreatitis-persistent organ failure > 48 hours.
4.Interstitial edematous acute pancreatitis.
5.Necrotizing acute pancreatitis.
6.Organ failure and systemic complications of acute pancreatitis.
Incidence
A.Pancreatitis is the most common gastroenterological condition resulting in hospitalization.
B.In the United States, the incidence is 600 to 700 per 100,000 people with an approximate 2% mortality rate. The peak age of acute pancreatitis is in the 5th and 6th decades; however mortality increases with age.
C.The most common causes are alcohol use and gallstones. However, incidence is on the rise in part due to hypertriglyceridemia and metabolic syndrome.
Pathogenesis
A.Pancreatitis involves is localized destruction in the pancreas and systemic inflammatory response. There is also a genetic predisposition for pancreatitis.
B.The inciting event is the premature activation of trypsinogen to trypsin. Normal feedback mechanisms that prevent over accumulation or early release of digestive enzymes are impaired. Accumulation of digestive enzymes creates injury to the pancreas.
C.Impairment can occur at any point along the pathway of digestive enzymes from injury of the acinar cells that produce digestive enzymes, to early release of enzymes from their transport mechanism to problems involving the release along the brush border of the duodenum.
D.Once injury occurs, the inflammatory response ensues and causes increased vascular permeability of pancreas leading to hemorrhage and edema. Necrosis of the tissue can then occur.
E.Mediators of this event are released into the blood stream leading to bacteremia, acute respiratory distress syndrome, pleural effusion, gastrointestinal (GI) hemorrhage, and renal failure.
F.Immune mediated toxicity is thought to be the cause of amino salicylates and sulfonamides, direct toxicity with diuretics and accumulation of toxic metabolites with valproate and pentamidine.
G.Drug-induced; common drugs include azathioprine, erythromycin, simvastatin, itraconazole, lamivudine, olanzapine, and sulfasalazine.
Predisposing Factors
A.Alcohol use.
B.Gallstones.
C.The mnemonic IT HURTS BADLE can be used to identify other predisposing factors:
1.Infectious (bacterial, viral, and parasitic).
2.Tumor.
3.Hypercalcemia and hypertriglyceridemia.
4.Ulcer (penetrating).
5.Renal failure.
6.Trauma.
7.Stricture.
8.Biliary tract obstruction.
9.Alcohol or anatomic abnormality.
10.Drugs.
11.Lipids—hypertriglyceridemia.
12.Endoscopic retrograde cholangiopancreatography (ERCP; postprocedure).
Common Complaints
Cardinal symptoms: Characteristic abdominal pain: Located in the epigastrium or left upper quadrant (LUQ), acute onset and steadily progressive; described as steady, boring and dull; radiating into the back or flank occurring with nausea and anorexia.
Other Signs and Symptoms
A.Fever.
B.Dehydration.
C.Tachycardia/tachypnea.
D.Abdominal bloating and distention.
E.Diarrhea.
F.Fatigue.
G.Jaundice.
Subjective Data
A.Elicit information regarding onset, duration, location and character of pain, aggravating and alleviating symptoms, radiation of the pain, and severity of symptoms.
B.Obtain the patient’s past medical history with thorough review of systems.
C.Review the all of the patient’s prescription and over-the-counter (OTC) medications and herbals.
D.Inquire regarding the patient’s social habits:
1.Alcohol use (how much, how often, over what length of time).
2.Smoking (how much, how often, what length of time).
3.Assess hobbies and occupation to assess risk of toxin exposure.
4.Inquire regarding surgeries and recent procedures especially an ERCP.
E.Inquire about familial pancreatitis.
F.Review bowel habits and note changes: Constipation, diarrhea, anorexia, food intolerance, nausea, vomiting, or bloating.
Physical Examination
Evaluate for a surgical abdomen,
defined as a rapidly worsening prognosis in the absence of surgical intervention. Once a surgical abdomen has been excluded, the remainder of the evaluation will be guided by the cause, chronicity of symptoms along with the location of pain.
A.Check temperature, blood pressure (BP; hypotension in severe cases), pulse (tachycardia), respirations (tachypnea), height, and weight to calculate body mass index (BMI). Notice any weight loss.
B.Inspect:
1.Observe overall appearance: Facial expressions, demeanor with walking, refusal to
move/writhing, note grimace during exam.
2.Assess for signs of dehydration include: confusion, muscle weakness, fever, dizziness, poor skin turgor, dry mucous membranes, hypotension, and tachycardia.
3.Observe for jaundice and skin changes:
a.Sclera icterus.
b.Skin:
i.Ecchymosis due to hemorrhage:
•Grey-Turner sign-Back/flank.
•Cullen’s sign-abdominal/periumbilical.
ii.Xanthomas—hypertriglyceridemia.
C.Auscultate:
1.Heart.
2.Lungs:
a.Rales may be present if patient has atelectasis due to shallow respirations or pneumonia.
b.Decreased breath sounds due to pleural effusions.
3.Abdomen—Assess for bowel sounds in all four quadrants. Diminished bowel sounds; possibly tinkling bowel sounds due to distention.
D.Palpation:
1.Neck—Parotid mass if pancreatitis is secondary to mumps infection.
2.Abdomen examination:
a.Classical: Tenderness in the epigastrium.
b.Palpate for hepatomegaly and splenomegaly, rebound tenderness, and peritoneal signs.
c.Elderly patients may lack classical peritoneal signs of rebound and guarding.
E.Percuss abdomen for hepatomegaly or splenomegaly. Tympany may be present with a distended abdomen.
F.Neurological exam—Assess for mental status changes which could be indicative of encephalopathy, impending coma or shock.
Diagnostic Tests
A.Laboratory:
1.Serum amylase and lipase—In all patients suspected of acute pancreatitis. A three-fold elevation of serum lipase or amylase is identified by the American College of Gastroenterology as one of the three clinical features necessary for diagnosis, along with classic pain consistent with acute pancreatitis and abdominal imaging consistent with acute pancreatitis (ultrasound, CT, or MRI):
a.Lipase has a higher diagnostic accuracy compared to amylase as the serum lipase levels are elevated for a longer period of time.
b.Amylase for patients with hypertriglyceridemia may be falsely low.
2.C-reactive protein (CRP) on admission and daily for the first 72 hours after admission.
3.Complete blood count (CBC).
4.Comprehensive metabolic profile (CMP).
5.Liver function tests: Alanine transaminase (ALT), AST, lactate dehydrogenase (LDH), triglycerides.
6.Blood urea nitrogen (BUN). and creatinine:
7.Arterial blood gases.
B.ECG—Assess for acute coronary syndrome.
C.Imaging:
1.X-ray:
a.Chest—For pneumonia or pleural effusion.
b.Abdominal plain films—To assess for free air.
2.Ultrasound—Should be performed in all patients at baseline to assess the biliary tract to determine if there is the presence of gallstones and/or a stone in the CBD.
3.CT abdomen with contrast:
a.Selective use when there is a broad differential diagnosis that include acute pancreatitis or suspected local complications suggested on ultrasound.
b.Assessment of local complications 48- to 72 hours after the onset of symptoms.
c.Contraindications to CT with contrast include renal dysfunction and allergy to the contrast medium.
4.Magnetic resonance cholangiopancreatography (MRCP)—Reserved for severe cases with an elevation of liver enzymes and CBD is not visualized adequately or is found to be normal on ultrasound.
5.ERCP—Within 24–72 hours in patients with acute gallstone pancreatitis associated with bile duct obstruction or cholangitis.
Differential Diagnoses
A.Pancreatitis.
B.Causes of acute abdomen:
1.Cholecystitis.
2.Appendicitis.
3.Ectopic pregnancy.
4.Ischemic bowel.
5.Small or large bowel obstruction.
6.Perforated viscus.
C.Infectious origin:
1.Abscess.
2.Pyelonephritis.
3.Viral—HIV, cytomegalovirus (CMV), Epstein-Barr, mumps, Cocksackie.
4.Bacterial—Campylobacter jejuni, Legionella, Mycobacterium tuberculosis, Mycoplasma, Shigella.
5.Parasitic—Ascaris lumbricoides, Cryptosporidium, Microsporidia.
D.Gastrointestinal pathology:
1.Esophagitis.
2.Esophageal rupture.
3.Peptic ulcer disease (PUD).
4.Bowel perforation.
5.Bowel obstruction.
E.Cardiovascular pathology:
1.Acute coronary syndrome.
2.Aortic dissection.
F.Hepatic pathology—Hepatitis (all types).
G.Renal pathology—Nephrolithiasis.
H.Pancreatic cancer (increases at age 40 years or older).
Plan
A.Acute pancreatitis management is dependent not only on the etiology of the illness but more importantly on the severity. Acute pancreatitis can range from mild and self-limited to life-threatening.
B.Patients diagnosed with acute pancreatitis are managed in-patient. For severe cases, defined by organ failure, ICU admission is necessary.
C.Once the diagnosis is confirmed, rapid assessment of hydration status is warranted. Fluid resuscitation is critical within the first 24 hours to prevent complications.
D.Risk assessment should be performed to determine the severity of pancreatitis; results guide further management. There are several risk assessment tools available: