Alcohol-induced pancreatitis occurs in the setting of prolonged, chronic alcohol use and its clinical features are similar to those of acute and chronic pancreatitis. Symptoms include nausea or vomiting and constant epigastric pain, which may also radiate to the mid-back or flanks. On examination, the abdomen may be normal or distended. In severe cases, alcohol-induced pancreatitis may be classically associated with periumbilical or flank ecchymosis, also known as Cullen’s or Grey Turner’s signs, respectively,  and represent significant peritoneal or retroperitoneal hemorrhage. Of note, pain may be less abrupt and poorly localized in alcoholic pancreatitis versus gallstone induced AP.  Severe presentations of AP may include peritonitis, sepsis, acute respiratory distress syndrome (ARDS), and/or shock. Chronic pancreatitis may display the additional features of pancreatic insufficiency, including steatorrhea secondary to fat malabsorption, and pancreatic diabetes secondary to endocrine cell destruction.

The diagnosis of acute pancreatitis requires that at least two of the following three criteria are met, based on the Revised Atlanta Classification system:

• Characteristic clinical features
• Laboratory evidence
• Imaging suggestive of pancreatitis

Clinical features include constant upper abdominal pain, with or without radiation to the back, and tenderness of the abdomen with palpation. Laboratory criteria include a serum lipase of at least three times the upper limit of normal.  Lipase peaks more rapidly, remains elevated for a more extended period, and has a higher sensitivity and specificity than amylase. Testing for both enzymes does not improve sensitivity or specificity.  A hepatic panel, calcium level, and triglyceride level may help differentiate alcoholic from other causes of AP. Finally, CT with IV contrast is the imaging modality of choice and findings may include pancreatic enlargement, loss of pancreatic borders, surrounding fluid, and/or fat stranding. Areas of no enhancement indicate pancreatic necrosis. Imaging is normal in 15-30% of cases of mild pancreatitis and is not routinely indicated or needed for diagnosis. An exception to this rule is in cases where the patient does not respond to treatment after 48 hours, and further imaging can rule out other abdominal pathology or complications. Endoscopic retrograde cholangiopancreatography (ERCP) is not beneficial in alcohol-induced pancreatitis unless there are signs of comorbid biliary etiology.[9]

Treatment and management of alcohol-induced pancreatitis follow the same principles as that for other causes of pancreatitis with the addition of alcohol cessation intervention during or after admission. Namely, these principles include accurate diagnosis, high-quality supportive care, recognizing and avoiding complications, and prevention of recurrence.  To accomplish this, clinicians employ goal-directed fluid therapy with either normal saline or lactated Ringers, give timely analgesics and antiemetics, and replete electrolyte as needed. The current recommendations are also to initiate feeding trials within 24 hours of disease onset instead of keeping the patient NPO. There are no clear indications for the type of diet, but typically small low-fat, soft or solid meals correlate with shorter hospital stays than starting a clear liquid diet with slow advancement to solid meals. Enteral feeds via a feeding tube is preferred to total parenteral nutrition in patients unable to tolerate PO. The AGA currently recommends against the use of prophylactic antibiotics in predicted severe AP and necrotizing pancreatitis. Additionally, providing brief alcohol intervention during admission or repeated counseling regularly at a primary care or gastrointestinal clinic appointments has been shown to decrease alcohol use, hospital admissions for recurrent attacks, and development of chronic pancreatitis.

Chronic pancreatitis pain can be managed with analgesics (avoiding high-potency opioids) and/or pancreatic enzyme replacement therapy. Antioxidants may be helpful in cases where other pharmaceutical options fail.  Endoscopic therapy or surgery are other options when pain is refractory to medical management.[10][11][12][8][5]

The differential diagnoses include, but are not limited to:

• Pancreatitis secondary to other causes
• Gastritis or gastroenteritis
• Biliary disease secondary to obstructive or infectious pathology
• Bowel perforation or obstruction
• Nephrolithiasis
• Ectopic pregnancy
• Ischemic heart disease
• Pneumonia
• Aortic pathology

There is a broad differential diagnosis for this condition, as conditions affecting the gallbladder, stomach, or upper GI tract may present with a similar pain pattern. A history of frequent alcohol use, in combination with the characteristic abdominal pain patterns, elevated lipase, and imaging findings can help narrow down the differential.

Also, sickle cell crisis or diabetic ketoacidosis should also merit consideration in patients with a corresponding past medical history.

Many staging systems exist for prognostication of acute pancreatitis. Today the Atlanta classification is used to differentiate between acute and severe cases of acute pancreatitis which includes the following:

• Presence of local complications- abscess, necrosis or pseudocyst
• Evidence of organ injury (SBP less than 90, Cr more than 2 or GI bleeding more than 500 ml)
• Ranson score of 3 or greater or APACHE score of 8 or higher

Various scoring systems have been created to predict the severity of acute pancreatitis based on clinical, laboratory, and radiology findings; however, they have largely demonstrated low specificity and low positive predictive values. These include Ranson’s criteria, the APACHE II score, BISAP, and the CT severity index, among others. Further, the American Pancreatic Association and the American College of Gastroenterology differ in their criteria for prognosticating a severe disease course. While the number of hospital admissions for acute pancreatitis is increasing and 15 to 25% of cases categorize as severe acute pancreatitis, the mortality rate has significantly decreased to 1 to 2% throughout the last ten years. A recent report showed that following an initial episode of acute alcoholic pancreatitis, there was a 24% chance for a recurrent AP episode and a 16% chance of developing chronic pancreatitis.[13]

Complications from this disease can have both localized and systemic effects including:

• Acute peri-pancreatic fluid collection, seen as a homogenous fluid collection adjacent to the pancreas on CT imaging, usually beginning <4 weeks after symptoms onset
• Pancreatic pseudocyst, seen as a walled-off fluid collection, usually arising >4 weeks from symptom onset
• Necrotizing pancreatitis (5-10%), seen as an intra/extra-pancreatic heterogenous fluid collection and necrosis
• Walled-off necrosis, seen as a heterogeneous collection of fluid and necrosis with a well-defined wall, usually occurring >4 weeks from symptom onset

Systemic complications include sepsis, bacteremia from the migration of intestinal flora, pleural effusions, ARDS, and shock.

Chronic pancreatitis patients are also at increased risk of developing pancreatic cancer, pancreatic diabetes, bile duct obstruction, and splenic vein thrombosis.

Consultations from the following specialties may be necessary:

• Gastroenterology
• General Surgery
• Radiology
• Intensive Care Specialist
• Endocrinology
• Nutritionist
• Psychiatrist

As mentioned above, patients with acute pancreatitis or chronic pancreatitis secondary to alcohol use should receive brief alcohol intervention when admitted to the hospital or receive alcohol counseling during their primary care or gastroenterology outpatient visits.

Alcohol use syndrome is one of the most common causes of both acute and chronic pancreatitis, but likely requires other factors such as smoking and diet to manifest.

• Alcohol-induced pancreatitis likely results from alcohol causing increased, viscous secretions that block small pancreatic ducts and by premature activation of digestive and lysosomal enzymes within acinar cells
• Diagnosis of AP requires meeting at least two of the following three criteria: characteristic clinical features, lipase levels three times the upper limit of normal, and/or imaging suggestive of pancreatitis
• Treatment includes a combination of goal-directed fluid therapy, pain control, antiemetics, electrolyte replacement, early enteral nutrition, and alcohol cessation counseling

Alcohol counseling has shown benefits to patients as it decreases total hospital admissions for acute pancreatitis. One randomized controlled trial showed that repeated counseling during gastroenterology clinic visits by an interprofessional team of physicians, physician assistants, nurse practitioners, and nurses decreases the risk of hospitalization for recurrent pancreatitis attacks. The team should report back to the team leader concerns or lack of patient compliance. Alcohol intervention strategies employed by the clinicians and nurses have also been shown to reduce alcohol consumption in men significantly. Smoking cessation and dietary modifications are also recommendations, as these are risk factors when combined with alcohol. Reducing both alcohol and tobacco consumption was shown to reduce the risk of recurrent attacks, the progression to chronic pancreatitis, and the development of secondary pancreatic malignancy. [Level I]

Patients with alcohol-induced pancreatitis usually need attention from many specialists including pain specialists, dietitians, mental health nurse, and pharmacists. At each refill for medications, the pharmacist should educate the patient about the harms of alcohol and the importance of abstaining from this beverage. If the patient is non-compliant, the pharmacist should inform the clinician of concerns.

For patients with uncomplicated chronic pancreatitis, medical management remains the first line of therapy. Behavior modification counseling for the cessation of alcohol consumption and smoking is also in order; therefore, certified therapists play a large role in patient outcomes. [Level 2b]

Since extraneous factors such as diet may play a synergistic role in leading to initial and recurrent episodes of pancreatitis, consultation with a nutritionist would benefit such patients. Patients should adhere to a low-fat diet and eat frequent small meals to decrease the stress on the pancreas. Endoscopic, surgical, or radiology guided interventions may be required for cases of pancreatic pain refractory to medical therapy and conservative measures or used to treat the complications associated with acute pancreatitis such as pancreatic necrosis.[12][14][15][10]