| disease | Acute Pancreatitis in Children |
| alias | Acute Pancreatitis |
Acute pancreatitis in children is relatively rare, and its onset is related to the overflow of pancreatic juice into the pancreatic interstitium and surrounding tissues. It is now widely believed to be associated with viral infections, medications, obstruction of pancreatic ducts, certain systemic diseases, or overeating. At least half of the cases are caused by mumps virus or blunt trauma to the upper abdomen, while the cause remains unknown in 30% of cases. Relevant studies suggest that acute pancreatitis involves a pathophysiological process of acute microcirculatory disturbances.
bubble_chart Etiology
The etiology of acute pancreatitis in children is complex, and sometimes the disease can occur suddenly, making it difficult to determine the cause.
Currently, the following factors are considered to potentially cause acute pancreatitis in children.
1. Secondary to bacterial or viral infections in other parts of the body: such as acute epidemic parotitis, pneumonia, bacillary dysentery, tonsillitis, etc.
2. Upper digestive tract diseases or malformations at the junction of the bile and pancreas, causing bile reflux into the pancreas and leading to pancreatitis.
3. Drug-induced: the use of large amounts of adrenal hormones, immunosuppressants, morphine, as well as L-asparaginase in the treatment of acute lymphoblastic leukemia can all cause acute pancreatitis.
4. It may complicate systemic lupus erythematosus, allergic purpura, and hyperparathyroidism.
However, in about half of the cases, no definite causative factors can be identified.
bubble_chart Pathological Changes
1. Edematous pancreatitis accounts for about 80-90%, with the entire or partial pancreas showing edema and congestion, leading to an increase in size and obstruction of pancreatic fluid drainage, thereby elevating amylase levels in the blood and urine.
2. Hemorrhagic necrotizing pancreatitis accounts for about 10-20%, characterized by rapid progression. Due to ischemia, hemorrhage, or necrosis, the pancreas appears dark red or purplish-black. A large amount of exudate, including pancreatic fluid, flows into the abdominal cavity, causing diffuse peritonitis, which may lead to shock or even death. At this stage, the highly digestive pancreatic fluid acts on fat-rich tissues such as the greater omentum and mesentery, causing widespread fat necrosis and breaking down fat into glycerol and fatty acids. The latter then absorbs calcium from the blood to form calcified lesions. Blood calcium levels may drop significantly, resulting in hand and foot convulsions.
When the pancreatic parenchyma is inflamed, the islet cells are also damaged, affecting glucose metabolism, which can lead to complications such as diabetes.bubble_chart Clinical Manifestations
The main symptom is epigastric pain, which is often persistent and frequently accompanied by nausea and vomiting. The vomitus consists of food and gastric or duodenal secretions. In severe cases, apart from an acutely ill appearance, dehydration and early signs of shock may occur, along with abdominal distension and fullness due to intestinal paralysis. Jaundice may appear due to compression of the distal end of the common bile duct by edema of the pancreatic head, though this is rare in children.
In grade I edematous cases, there may be epigastric tenderness (in the epigastrium or slightly to the left), which could be the only abdominal sign. In severe cases, in addition to abdominal distension and fullness, there is tenderness and muscle rigidity, most pronounced in the epigastrium. In some children, the skin around the umbilicus or waist may appear bluish-purple, caused by capillary hemorrhage due to subcutaneous fat breakdown from leaked pancreatic fluid.
bubble_chart Auxiliary Examination
1. Amylase Measurement: This is the primary diagnostic criterion, measured using the Somogyi colorimetric method. Normal values in children are below 64U, while in acute pancreatitis, the levels can exceed 500U. Serum amylase levels begin to rise within 3 hours of onset and gradually increase, peaking at 24–48 hours before declining. Urinary amylase follows a similar pattern, though normal levels are also below 64U. However, urinary amylase rises more slowly and declines later than serum amylase, and its accuracy is affected by renal function and urine concentration, making it less reliable than serum amylase. Other acute abdominal conditions, such as intestinal perforation, obstruction, or necrosis, may also elevate amylase levels, but these rarely exceed 300–500U.
2. Serum Lipase Measurement: Levels begin to rise 24 hours after onset and remain elevated for a longer duration, making it useful for diagnosing advanced-stage patients. The normal range is 0.5–1U (Comfort).
3. Abdominal Paracentesis: In severe cases with peritonitis, distinguishing pancreatitis from other causes of peritonitis can be challenging, especially if pancreatic damage is severe but serum amylase levels do not rise. In such cases, abdominal paracentesis may be performed. The nature of the peritoneal fluid (e.g., bloody or containing fat necrosis) and elevated amylase levels can aid in diagnosis.
Acute pancreatitis typically resolves with non-surgical therapy within 3–7 days, with symptoms gradually disappearing. However, hemorrhagic necrotizing pancreatitis is more severe, has a prolonged course, and may lead to death due to complications like shock. It can also result in localized abscess formation or the development of pancreatic pseudocysts.
1. Clinical Symptoms Mostly occur in children over 4 years old, mainly manifested as upper abdominal pain, nausea, vomiting, and abdominal tenderness.
2. Amylase Test Often serves as the primary diagnostic basis. If measured using the Somogyi colorimetric method, normal children typically have values below 64 units, while children with acute pancreatitis may exhibit levels as high as 500 units. Serum amylase levels begin to rise 3 hours after onset and gradually increase, peaking at 24–28 hours before declining. Urinary amylase follows a similar pattern but rises more slowly after onset and declines later than serum amylase, influenced by renal function and urine concentration, making it less accurate than serum amylase. Other acute abdominal conditions, such as intestinal perforation, obstruction, or necrosis, may also elevate amylase levels, though rarely exceeding 300–500 units.
3. Serum Lipase Test Begins to rise 24 hours after onset and remains elevated for an extended period, serving as a diagnostic method for advanced-stage patients. The normal range is 0.5–1U (Comfort).
4. Abdominal Paracentesis In severe cases with peritonitis, differentiation from peritonitis caused by other factors can be challenging. If the pancreas is severely damaged, serum amylase may not rise, further complicating diagnosis. In such cases, if there is significant peritoneal effusion, abdominal paracentesis may be performed. The nature of the effusion (bloody, mixed with fat necrosis) and amylase testing can aid in diagnosis.
5. B-mode Ultrasound Valuable for confirming edema-type pancreatitis and late-stage (third-stage) complications such as pancreatic cysts. The former shows significant pancreatic enlargement, while the latter reveals cystic masses connected to the pancreas.
1. Non-surgical treatment is the primary therapeutic measure. For mild cases, sedatives, analgesics (avoid morphine), and antispasmodics such as atropine, 654-2, probanthine, meperidine, and wintermin are used. Acupuncture therapy can also be employed for pain relief, and Chinese medicine can be used to clear and drain damp-heat, regulate qi, and relieve pain. For severe cases, measures include gastric decompression, intravenous fluid therapy (to maintain water and electrolyte balance), blood transfusion, and continuous intravenous nutrition to sustain caloric intake. Large doses of vitamins B and C, as well as antibiotics, are administered. Since the causative bacteria are difficult to identify, broad-spectrum antibiotics such as chloramphenicol, which achieve high concentrations in pancreatic secretions, should be selected. For patients with low blood calcium, 10% calcium gluconate should be administered, especially in cases of hemorrhagic pancreatitis. If the child has elevated blood glucose, an appropriate amount of insulin and potassium chloride should be added to the glucose infusion. Gastrointestinal motility usually gradually recovers within 3–4 days. When the child’s abdominal distension subsides, they begin passing gas rectally, and their appetite returns, small amounts of food can be introduced, primarily carbohydrates supplemented with protein, while fat intake should be restricted for an extended period.
In recent years, anti-enzyme therapy has been widely used. Typically, aprotinin (trasylol) is administered via slow intravenous drip in the early stages, at a dosage of 10,000–50,000 units daily for 7–9 days, which can alleviate shock and prevent deterioration. After urinary amylase levels return to normal, treatment should continue for an additional 2–3 days, but caution is required to prevent allergic reactions.
2. Surgical treatment is considered only under the following circumstances: ① When non-surgical treatment fails, with persistent high fever, poor mental state, abdominal distension and fullness, abdominal muscle rigidity, and unrelieved tenderness, surgical exploration and peritoneal drainage are necessary. ② If the diagnosis is unclear and other surgical acute abdominal conditions cannot be ruled out, surgery should be performed as soon as possible. ③ For complications such as localized abscesses or large pancreatic pseudocysts, incision and drainage or internal drainage into the digestive tract are required.
In general, acute pancreatitis can be treated non-surgically, with symptoms typically resolving within 3 to 7 days, leading to gradual recovery. However, hemorrhagic and necrotizing pancreatitis are more severe, with a prolonged course. They may result in death from shock, the formation of localized abscesses, or the development of post-inflammatory pseudocysts.
Early complications include water and electrolyte imbalances, hypocalcemia, and hand-foot convulsions. Late stage [third stage] complications may involve abscess formation, pseudocyst development, or progression to chronic pancreatitis.
