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Pancreatitis
Acute Pancreatitis
Keywords
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Acute pancreatitis
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acute pancreatitis etiology
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acute pancreatitis diagnosis
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drug-induced pancreatitis
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(serum) amylase
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(serum) lipase
Acute pancreatitis (AP), the most common pancreatic disorder in children, is increasing in incidence, and 50 or more cases are usually seen in major pediatric centers per year. In children, blunt abdominal injuries, multisystem disease such as the hemolytic uremic syndrome and inflammatory bowel disease, biliary stones or microlithiasis (sludging), and drug toxicity are the most common etiologies. Although many drugs and toxins can induce AP in susceptible persons, in children, valproic acid, l -asparaginase, 6-mercaptopurine, and azathioprine are the most common causes of drug-induced pancreatitis. Alcohol should be considered in adolescents. Other cases follow organ transplantation or are caused by infections, metabolic disorders, or mutations in susceptibility genes (see Chapter 378.1 ). Only 10–20% of cases are idiopathic ( Table 378.1 ).
Table 378.1
Etiology of Acute and Recurrent Pancreatitis in Children
| DRUGS AND TOXINS |
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| GENETIC |
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| INFECTIOUS |
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| OBSTRUCTIVE |
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| SYSTEMIC DISEASE |
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| 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 colocalize with pancreatic proenzymes within the acinar cell. Pancreastasis (similar in concept to cholestasis) with continued synthesis of enzymes occurs. Lecithin is activated by phospholipase A 2 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.
The diagnosis of pancreatitis in children is made when 2 of 3 of the following are present: abdominal pain; serum amylase and/or lipase activity at least 3 times greater than the upper limit of normal; and imaging findings characteristic of, or compatible with, AP.
Clinical Manifestations
The severity of AP in children has been defined by a consensus committee.
Mild Acute Pancreatitis: AP that is not associated with organ failure, local or systemic complications, and usually resolves within the 1st wk after presentation. This is the most common form of pediatric AP.
The patient with mild AP has moderate to severe abdominal pain, persistent vomiting, and possibly fever. The pain is epigastric or in either upper quadrant, steady, often resulting in the child's assuming an antalgic position with hips and knees flexed, sitting upright, or lying on the side. The child is uncomfortable, irritable, and appears acutely ill. The abdomen may be distended and tender and a mass may be palpable. The pain can increase in intensity for 24-48 hr, during which time vomiting may increase and the patient can require hospitalization for fluid and electrolyte therapy and analgesia. There is no organ failure, and imaging does not demonstrate peri- or pancreatic necrosis. The prognosis for complete recovery in the acute uncomplicated case after 4-7 days is excellent.
Moderately Severe Acute Pancreatitis : AP with either transient organ failure/dysfunction (lasting <48 hr) or development of local or systemic complications, such as exacerbation of previously diagnosed comorbid disease (such as lung or kidney disease). Imaging may reveal sterile (peri-) pancreatic necrosis. The prognosis for these patients is also excellent but recovery may be prolonged.
Severe Acute Pancreatitis : AP with development of organ dysfunction that persists longer than 48 hr. Persistent organ failure may be single or multiple. Severe AP is uncommon in children. In this life-threatening condition, the patient is acutely ill with severe nausea, vomiting, and abdominal pain. Shock, high fever, jaundice, ascites, hypocalcemia, and pleural effusions can occur. A bluish discoloration may be seen around the umbilicus (Cullen sign) or in the flanks (Grey Turner sign). The pancreas is necrotic and can be transformed into an inflammatory hemorrhagic mass. The mortality rate, which is approximately 20%, is related to the systemic inflammatory response syndrome with multiple organ dysfunction, shock, renal failure, acute respiratory distress syndrome, disseminated intravascular coagulation, gastrointestinal bleeding, and systemic or intra-abdominal infection. The percentage of necrosis seen on CT and failure of pancreatic tissue to enhance on CT (suggesting necrosis) predicts the severity of the disease.
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