Patients suffering from acute or chronic pancreatitis may commonly present with the following symptomatology:

• Upper abdominal pain is associated with the retroperitoneal irritation caused by the pancreas inflammation.
• Referred pain at the back, spinal and dermatomal nerves of the back are subsequently irritated by any inflammation at the retroperitoneal spaces.
• Post prandial abdominal pain because the obstructed ampulla or sphincter of Oddi may cause pain after a fatty or heavy meal. 
• Nausea and vomiting, the digestive dysfunctions associated with pancreatitis can cause these common symptomatology.
• Severe prostration, pancreatic juices may spill out from the inflamed pancreas and irritate other areas of the peritoneum and retroperitoneum.
• Weight loss is a sign of a defective digestive process.
• Steatorrhea, obstructed pancreatic juices may retard the normal digestion of fats in the intestine; thus, it is disposed in the same unmetabolized form.

The following diagnostic modalities and tests are being used to work up patients with pancreatitis:

• Alkaline phosphatase: A positive blood test of an elevated pancreatic enzyme alkaline phosphatase is very suggestive of a pancreatitis.
• Stool analysis of fats: Patients with chronic pancreatitis are usually analyzed with degree of fats in the stools which is indicative of a defective lipid metabolism and absorption.
• Abdominal and endoscopic Ultrasound is used to determine degree of obstruction in the bile duct system and the presence of obstructive bile stones.
• Computerized tomography (CT scan) will identify the size and location of gallstones, and the extent of pancreatic inflammation [8].
• Magnetic resonance imaging (MRI) will elucidate a more detailed view of the pancreas and the biliary tree.

Patients initially diagnosed with pancreatitis are usually hospitalized for stabilization and treatment. Initially, patients are asked to fast (NPO) until the pancreatic inflammation subsides. When the pancreatic inflammation is controlled, patients may be started on clear liquids and low fat diets [9]. Patients are placed in intravenous resuscitation to address dehydration and institute Intravenous analgesics to control pain symptoms. Non-medical approach to pancreatitis include biliary repair of obstruction using ERCP, cholecystectomy if bile stones are formed from the gallbladder [10], and pancreatic drainage of fluids and necrotic debris.

A great majority of pancreatitis cases is self-limiting without the need for surgery and medical interventions. Although, severe cases may lead to significant morbidity and mortality in 10 to 15% of cases. Patients with primary biliary problems are more associated with a worse prognosis compared to the alcohol induced form which has a lower morbidity rating. The advances in the medical health care delivery and supportive management have significantly reduced the morbidity and mortality ratings of pancreatitis in general. However, in patients seen in the emergency room presenting with organ failure, the mortality rate will rise to 30% in these cases [6].

The following systemic manifestations are among the serious systemic manifestations of pancreatitis: Acute renal failure, acute respiratory distress syndrome (ARDS), cardiac insufficiency, hypovolemic shock, and hemorrhage. An increase in the neutrophil lymphocytic ratio (NLR) observed within the first 48 hours of pancreatitis is associated with a severe form of pancreatitis and a poor prognosis [7].

Pancreatitis is commonly caused by obstructive biliary stones and chronic alcoholic intake [1]. An estimated 10-30% of pancreatitis cases have an unknown or idiopathic etiology. Some diagnostic modalities like the endoscopic retrograde cholangio-pancreatography (ERCP) can cause pancreatitis among patients after the procedure. The pathology in this complication is the eminent dysfunction of the sphincter of Oddi during and after the procedure. Blunt abdominal trauma and penetrating injuries to the abdomen can cause direct damage to the pancreatic gland and cause pancreatitis, this is seen in approximately 1.5% of cases. Less common causes of pancreatitis like viral infection has been documented especially with mumps, coxsackie, cytomegalovirus, Epstein-Barr, varicella, rubella and hepatitis virus infections. Accounting for 2% of cases of pancreatitis are drug-induced, the following drugs are proven to cause pancreatitis among susceptible patients:

• Azathioprine
• Chlorthiazide and Hydrochlorthiazide
• Metronidazole
• Methyldopa
• Piroxicam
• Cimetidine
• Corticosteroids
• Nitrofurantoin
• Estrogens
• Sulfonamides 

In the United States, there is an estimated 40 cases of pancreatitis per 100,000 adults per year [2]. In 1998 alone, an estimated 183,000 cases of acute pancreatitis have been admitted in the hospitals, and the trend has continually increased in the following decades [3]. The worldwide incidence of pancreatitis is between 5 to 80 cases per 100,000 population, with the highest incidence noted in the United States and Finland [4]. In the United States, the majority of cases of pancreatitis is alcohol induced while European countries and Hong Kong has a predominance of microlithiasis induced type of pancreatitis.

The relative median age of onset for pancreatitis is dependent on its etiology [5]. For example alcoholic pancreatitis which peaks at 39 years old, biliary pathology which are more prone by 69 years old, and drug induced types of pancreatitis that occurs at a mean age of 42. There is a male predominance over its female counterpart for pancreatitis. A racial predilection among the black population is notably observed over the light skinned races.

During the process of normal digestion, the inactivated enzymes from the exocrine pancreas traverse to the intestinal lumen where they are activated to digest the food contents of the small intestine. In the actual pancreatitis, these enzymes are activated within the gland causing cellular autodigestion, irritation, and inflammations. Acute inflammation will convey the usual signs and symptoms of acute pancreatitis. When recurrent bouts of acute pancreatic inflammation occurs in a long standing period, this is now referred to as chronic pancreatitis. The post inflammatory scarring of the pancreatic tissues will cause a subsequent loss of function of the gland causing digestion problems and diabetes consequently.

One of the corner stone in the control of pancreatitis is the eventual control of alcohol dependence. Smoking can also impair digestion and advertently cause pancreatitis; thus, abstinence from this vice can prevent the inflammation. The dietary modifications of a low fat diet can reduce the incidence of pancreatitis, and reduce its digestive menace. Adequate hydration can help keep the pancreas hydrated and safe.

Pancreatitis is a clinical disease characterized by the inflammation of the exocrine pancreas which may lead to autodigestion of the gland itself. Pancreatitis is generally classified as acute which presents suddenly and resolves in days, and chronic which presents in the course of many years. In most mild cases of pancreatitis, the inflammation subsides spontaneously even without treatment but in some occasion pancreatitis can be very severe that it can cause life threatening complications.

Definition

Pancreatitis is a clinical disease characterized by the inflammation of the exocrine pancreas which may lead to auto digestion of the gland. 

Cause

Pancreatitis is primarily caused by alcohol binge drinking and biliary microlithiasis obstructions. Less common causes include: Viral infection, abdominal trauma, hereditary, and diagnostic procedures like ERCP.

Symptoms

Upper abdominal pain is a very common presenting sign of pancreatitis. Other signs includes nausea and vomiting, prostration, steatorrhea and weight loss.

Diagnosis

Blood test with alkaline phosphatase, ERCP, Ultrasound, CT scan and MRI.

Treatment and follow-up

Patients are asked to fast with intravenous fluid support. Pain management and surgical correction of underlying pathology. Patients are advised to refrain from alcohol intake to prevent recurrence.

1. Whitcomb DC, Yadav D, Adam S, et al. Multicenter approach to recurrent acute and chronic pancreatitis in the United States: the North American Pancreatitis Study 2 (NAPS2). Pancreatology. 2008; 8(4-5):520-31.
2. Granger J, Remick D. Acute pancreatitis: models, markers, and mediators. Shock. Dec 2005; 24 Suppl 1:45-51.
3. Singla A, Csikesz NG, Simons JP, Li YF, Ng SC, Tseng JF, et al. National hospital volume in acute pancreatitis: analysis of the Nationwide Inpatient Sample 1998-2006. HPB (Oxford). Aug 2009; 11(5):391-7.
4. Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest Endosc. Dec 2002; 56(6 Suppl):S226-30.
5. Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute pancreatitis at an American pediatric tertiary care center: is greater awareness among physicians responsible? Pancreas. Jan 2010; 39(1):5-8.
6. Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. May 18 2006; 354(20):2142-50.
7. Suppiah A, Malde D, Arab T, Hamed M, Allgar V, Smith AM, et al. The Prognostic Value of the Neutrophil-Lymphocyte Ratio (NLR) in Acute Pancreatitis: Identification of an Optimal NLR. J Gastrointest Surg. Feb 1 2013.
8. Balthazar EJ, Ranson JH, Naidich DP, Megibow AJ, Caccavale R, Cooper MM. Acute pancreatitis: prognostic value of CT. Radiology. Sep 1985; 156(3):767-72.
9. Jacobson BC, Vander Vliet MB, Hughes MD, Maurer R, McManus K, Banks PA. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. Aug 2007; 5(8):946-51.
10. Aboulian A, Chan T, Yaghoubian A, Kaji AH, Putnam B, Neville A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. Apr 2010; 251(4):615-9.