Steven L. Werlin


Acute pancreatitis is most common pancreatic disorder in children, second only to cystic fibrosis in prevalence. Blunt abdominal trauma, viral infections (especially mumps), and multisystem disease account for the majority of cases of known etiology. Other causes are much less common (Box 366.1). Child abuse is recognized as a major cause of traumatic pancreatitis in young children. More recently defined causes of pancreatitis include organic acidemias and protease inhibitors used in the treatment of acquired immunodeficiency syndrome (AIDS). Improved techniques have led to increased recognition of congenital abnormalities.

Acute pancreatitis is believed to occur after the activation of proteolytic pancreatic proenzymes, which follows colocalization with lysosomal hydrolases within the acinar cell. This process then leads to autodigestion and further activation and release of active proteases. In the lysosome, trypsinogen is activated to trypsin by lysosomal hydrolases. Then trypsin activates other proteases, elastase, and phospholipase A2. Lecithin is activated by phospholipase A2 into the toxic lysolecithin. These activated enzymes then spill into the cytoplasm and interstitium, initiating the inflammatory process. The healthy pancreas is protected by three factors: (a) pancreatic proteases synthesized as inactive proenzymes, (b) digestive enzymes segregated into secretory granules, and (c) the presence of protease inhibitors.

The histopathologic findings of acute pancreatitis are related to the release of activated proteolytic and lipolytic enzymes. Interstitial edema appears early. Later, as the episode of pancreatitis progresses, localized and confluent necrosis, blood vessel disruption leading to hemorrhage, and an inflammatory response in the peritoneum may develop.

The definition of acute pancreatitis and its differentiation from chronic pancreatitis have been the subject of much dispute. The definition accepted most widely holds that acute pancreatitis is an isolated episode, with complete morphologic and histologic resolution. Acute pancreatitis may recur but, unless structural damage occurs, it rarely becomes chronic.

Clinical Manifestations and Complications

Clinically, children with acute pancreatitis have continuous, midepigastric, and periumbilical abdominal pain often radiating to the back; vomiting; and frequently fever. They appear acutely ill and are both restless and uncomfortable. They may lie on their side. The pain increases in severity for 24 to 48 hours. During this interval, vomiting may increase, and affected patients may require hospitalization for fluid and electrolyte therapy. Usually, acute cases are self-limited, and the prognosis is excellent.

In more severe cases, jaundice, ascites, and pleural effusions may occur. Acute hemorrhagic pancreatitis, the most severe form of acute pancreatitis, is rare in children. In this life-threatening condition, affected children are severely ill with intractable nausea, vomiting, and abdominal pain. The pancreas may become necrotic and may be transformed into an infected, inflammatory, hemorrhagic mass or phlegmon. Mortality from shock, renal failure, infection, massive gastrointestinal bleeding, and other complications approaches 50%. A number of classification systems have been devised to predict
the outcome of a case of pancreatitis. None of these systems are relevant to pediatric patients.

Jul 24, 2016 | Posted by in ORTHOPEDIC | Comments Off on Pancreatitis

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