Chapter 30
Acute Pancreatitis
John B. Kortbeek
Chapter Overview
Acute pancreatitis is a common and life threatening condition. It is estimated that there are over a quarter of a million admissions in the USA per annum alone. Understanding of the pathophysiology and natural progression of acute pancreatitis has improved dramatically over the past century. Classification of acute pancreatitis has evolved and is now a useful guide to management. Early acute pancreatitis management focuses on resuscitation while late disease management focuses on complications. Improvements in resuscitation along with a staged approach in applying drainage and surgical intervention have improved the morbidity and mortality associated with acute pancreatitis.
This chapter discusses factors relevant to understanding of acute pancreatitis. Practical principles of management are introduced to guide assessment, monitoring, and therapeutic approaches in the ICU patient with acute pancreatitis.
Significance and History
Pancreatitis is a common disorder with significant morbidity and mortality. Pancreas is derived from its Greek origins pan kreas, meaning all flesh. Classical scholars felt its role was to protect the great vessels and stomach. Vesalius (Italy) and Wirsung (Germany) (15th century) outlined the anatomy and the drainage of the ducts into the duodenum. Understanding of the nature and pathophysiology has progressed significantly over the last two centuries. Reginald Fitz, an American 19th century pathologist described the clinical presentation of pancreatitis as well as proposed important subtypes (hemorrhagic, gangrenous, and suppurative) based on his observations. Chiari (Germany) soon after described the concept of autodigestion. Bernard (France) identified the ability of pancreatic secretions to digest fat, carbohydrate, and protein. Pavlov (Russia) received the Nobel Prize in 1904 for demonstrating that both physical (food) and psychic (neural) stimuli were responsible for the release of gastric and pancreatic enzymes.1
In the 20th century, Banting, Best, Collip, and McLeod (Canada) isolated insulin. Starling (UK) introduced the world to Hormones and began the field of endocrinology. By mid century, Comfort had described chronic pancreatitis. The advent of nutritional and organ support resulted in patients surviving with severe pancreatitis and led to classification and prognostic systems (e.g., Ranson’s criteria) as well as evolving strategies to manage the complications associated with pancreatitis. Genetic models and advances in the sciences of immunology and inflammation have further advanced our knowledge of pancreatitis.2
Anatomy, Etiology, and Pathophysiology
The pancreas is located in the retroperitoneum and abuts the posterior abdominal wall, kidneys, and diaphragm as well as the stomach, the duodenum, and spleen. It is supplied by the pancreatico-duodenal and splenic arteries. Venous drainage is via the inferior and superior mesenteric and splenic veins. The confluence of the latter two forms the portal vein. The uncinate process encircles the superior mesenteric vessels (artery and vein). There is typically an accessory venous and arterial arcade lying along the posterior-inferior border and running parallel to the main splenic artery and vein.
The main pancreatic duct of Wirsung and a smaller accessory duct of Santorini open separately into the duodenum approximately 60% of the time. In 30%, the accessory duct ends blindly before reaching the duodenum. In 10%, the accessory duct drains most of the pancreas (pancreas divisum).3
The bulk of the pancreas is comprised of exocrine cells in clusters called acini and their related ducts. Embedded within these are numerous Islets of Langerhans, which are responsible for the production of endocrine hormones (primarily insulin and glucagon).
Autodigestion of the pancreas and surrounding tissues by excessive production or leakage of proteases may be precipitated in several ways. Hereditary pancreatitis appears to stem from alterations in genes resulting in increased production of proteases or decreased production of their inhibitors.4
Scorpion bites result in excessive acetylcholine and stimulation of exocrine cellular receptors. Exposure to certain insecticides containing acetylcholinesterase inhibitors can also result in excessive stimulation.
Caerulin is a peptide similar to cholecystokinin which when administered can result in secretagogue induced pancreatitis in animal models.
Gallstones are commonly associated with pancreatitis. The primary mechanism appears to be transient pancreatic duct obstruction. Pancreatic duct obstruction results in activation of lysosomal proteases (such as cathepsin) and subsequent release of intracellular calcium and induction of the cytokine inflammatory cascade with acinar and ductal cell wall disruption. The role of bile acid reflux in pancreatitis is less clear in recent studies. Alteration of ductal pH may also affect duct wall tight junctions and permeability. This may be important following endoscopic retrograde cholangiopancreatography (ERCP).5
Excessive alcohol consumption is also commonly associated with pancreatitis. These patients may have excessive lipopolysaccharide (LPS) production. LPS is a potent inducer of cytokines and inflammation.
Certain viral infections (coxsachie, mumps) may also induce pancreatitis. The virus is cleared from the pancreas though native immune response. Alcohol feeding and immunosuppressive therapy both potentiate pancreatitis in animal models.
This wide variety of pathologic mechanisms ultimately leads to inflammation of the pancreas and surrounding tissues, compounded by release of proteases and necrosis and the development of systemic inflammatory response syndrome (SIRS). If unchecked multiple organ dysfunction, failure, and death may ensue.
The two leading causes of pancreatitis are gallstones and alcohol. The relative incidence of these conditions will depend on the local prevalence of alcohol consumption. Less commonly hypertriglyceridemia, hypercalcemia, autoimmune, and drug induced acute pancreatitis may occur. Rarely arachnid bites that induce increased acetylcholine stimulation may be identified.
Diagnosis and Classification
The diagnosis of pancreatitis should be suspected in any patient presenting with generalized, central, or epigastric abdominal pain. A history of excessive or binge alcohol use or known cholelithiasis are suggestive. It should also be excluded in patients presenting with clinical SIRS.
SIRS can be diagnosed when two or more of the following criteria are present:
Tachycardia greater than 90 beats per minute.
Tachypnea greater than 20 breaths per minute of PaCO2 < 32.
Fever greater than 38°C (100.4°F) or less than 36°C (96.8°F).
Leukocytosis greater than 12 × 109 cells/L or less than 4 × 109 cells/L.
Bandemia (immature neutrophils) greater than 3%.
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