Sandbox:Abdul qudoos

For training Associate Editor(s)-in-Chief: Abdul Qudoos Iqbal, MBBS[1]

Acute Pancreatitis

Overview

Acute pancreatitis is an inflammatory condition of the pancreas characterized by abdominal pain and elevated levels of pancreatic enzymes in the blood. Several conditions are associated with acute pancreatitis. Depending on its severity, it can have severe complications and high mortality despite treatment.

Historical Perspective

Nicholas Tulp, a Dutch anatomist presented a clinical description of acute pancreatitis in the year 1652. In the late 19th and early 20th century, Reginald Fitz, Nicholas Senn, Eugene Opie, and others made seminal contributions that continue to influence our present understanding of acute pancreatitis. In 1901 Eugene Opie postulated that impairment of the pancreatic outflow due to obstruction of the pancreatic duct causes pancreatitis. This initial ’duct obstruction hypothesis’ was somewhat forgotten when Opie published his second ‘common channel’ hypothesis during the same year. This later hypothesis predicted that an impacted gallstone at the papilla of Vater creates a communication between the pancreatic and the bile duct (the so-called ‘common channel’) through which bile flows into the pancreatic duct and thus causes pancreatitis. 1963, the first Marseilles Symposium favored a clinic pathologic classification of pancreatitis. In 1984 the second Marseilles Symposium revised that classification. Finally, in 1992, the Atlanta Symposium established a clinically based classification system for acute pancreatitis.

Classification

Acute pancreatitis is divided into the following:

• Mild acute pancreatitis, which is characterized by the absence of organ failure and local or systemic complications.
• Moderately severe acute pancreatitis, which is characterized by transient organ failure (resolves within 48 hours) and/or local or systemic complications without persistent organ failure (>48 hours).
• Severe acute pancreatitis, which is characterized by persistent organ failure that may involve one or multiple organs.

Pathophysiology

The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by activation of pancreatic enzymes. Once the disease has been initiated, the appearance of interstitial edema and inflammatory infiltration are the basic features of acute pancreatitis. The accumulation of polymorphonuclear granulocytes in pancreatic and extrapancreatic tissue and the release of leukocyte enzymes play an essential role in the further progression of the disease and in the development of systemic complications.

Causes

There are many causes of acute pancreatitis. Few of them are outlined below for better understanding:

1. Gallstones: Gallstones are the most common cause of acute pancreatitis accounting for 40 to 70 percent of cases.
2. Alcohol: Alcohol is responsible for approximately 25 to 35 percent of cases of acute pancreatitis in the United States.
3. Hypertriglyceridemia: Serum triglyceride concentrations above 1000 mg/dL (11 mmol/L) can precipitate attacks of acute pancreatitis, although lower levels may also contribute to severity. Hypertriglyceridemia may account for 1 to 14 percent of cases of acute pancreatitis.
4. Post ERCP: Acute pancreatitis occurs in about 3 percent of patients undergoing diagnostic ERCP, 5 percent undergoing therapeutic ERCP, and up to 25 percent undergoing sphincter of Oddi manometric studies.
5. Genetic: Patients with genetic risk for pancreatitis may present as recurrent acute pancreatitis, or childhood pancreatitis without a known cause and eventually progress to chronic pancreatitis.
6. Medications: Pancreatitis due to medications is rare. The prognosis of drug-induced pancreatitis is generally excellent and mortality is low.
7. Infections and toxins: Pancreatitis has been associated with the following infections:
   • Viruses – Mumps, coxsackievirus, hepatitis B, cytomegalovirus, varicella-zoster, herpes simplex, human immunodeficiency virus (HIV)
   • Bacteria – Mycoplasma, Legionella, Leptospira, Salmonella
   • Fungi – Aspergillus
   • Parasites – Toxoplasma, Cryptosporidium, Ascaris
8. Other Rare causes: Biliary sludge and microlithiasis, Biliary obstruction, Hypercalcemia.

Differentiating Acute Pancreatitis from Other Diseases

The differential diagnosis of acute pancreatitis includes other causes of epigastric abdominal pain. Acute pancreatitis can be distinguished from these causes based on clinical features and laboratory studies. Few of the differentials to be considered are:

• Peptic ulcer disease: Patients may have a history of longstanding epigastric pain that is usually intermittent. The pain does not radiate to the back.
• Choledocholithiasis or cholangitis: Patients with choledocholithiasis and cholangitis may have a history of gallstones or biliary manipulation such as ERCP.
• Cholecystitis: Patients with acute cholecystitis typically complain of abdominal pain, most commonly in the right upper quadrant or epigastrium that may radiate to the right shoulder or back.
• Perforated viscus: Patients with a perforated viscus present with sudden onset abdominal pain and have peritoneal signs with guarding, rigidity and rebound tenderness that are not associated with acute pancreatitis.
• Intestinal obstruction: Patients with intestinal obstruction have abdominal pain with anorexia, emesis, obstipation, or constipation and elevation in serum amylase and lipase.