Pancreatitis

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Chapter 343 Pancreatitis

343.1 Acute Pancreatitis

Acute pancreatitis, the most common pancreatic disorder in children, is increasing in incidence. At least 30-50 cases are now seen in major pediatric centers per year. In children, blunt abdominal injuries, multisystem disease, biliary stones or microlithiasis (sludging), and drug toxicity are the most common etiologies. Although many drugs and toxins can induce acute pancreatitis in susceptible persons, in children, valproic acid, L-asparaginase, 6-mercaptopurine, and azathioprine are the most common causes of drug-induced pancreatitis. Other cases follow organ transplantation or are due to infections, metabolic disorders, and mutations in susceptibility genes (Chapter 343.2). Less than 5% of cases are idiopathic (Table 343-1).

Table 343-1 ETIOLOGY OF ACUTE PANCREATITIS IN CHILDREN

DRUGS AND TOXINS

GENETIC

INFECTIOUS

OBSTRUCTIVE

SYSTEMIC DISEASE

TRAUMATIC

After an initial insult, such as ductal disruption or obstruction, there is premature activation of trypsinogen to trypsin within the acinar cell. Trypsin then activates other pancreatic proenzymes, leading to autodigestion, further enzyme activation, and release of active proteases. Lysosomal hydrolases co-localize with pancreatic proenzymes within the acinar cell. Pancreastasis (similar in concept to cholestasis) with continued synthesis of enzymes occurs. Lecithin is activated by phospholipase A2 into the toxic lysolecithin. Prophospholipase is unstable and can be activated by minute quantities of trypsin. After the insult, cytokines and other proinflammatory mediators are released.

The healthy pancreas is protected from autodigestion by pancreatic proteases that are synthesized as inactive proenzymes; digestive enzymes that are segregated into secretory granules at pH 6.2 by low calcium concentration, which minimizes trypsin activity; the presence of protease inhibitors both in the cytoplasm and zymogen granules; and enzymes that are secreted directly into the ducts.

Histopathologically, 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 can develop.

Clinical Manifestations

Mild Acute Pancreatitis

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