Pediatric Pancreatitis and Pancreatic Pseudocyst Workup
- Author: Andre Hebra, MD; Chief Editor: Carmen Cuffari, MD more...
Laboratory Studies
- If pancreatitis is suspected, amylase and lipase levels should be measured, as they may support a clinical diagnosis. However, these laboratory test findings alone are not reliable or cost effective as a screening tool, and the magnitude of enzyme elevation does not correlate with the severity of pancreatic injury.[7]
- Elevated serum or urine amylase levels aid in the diagnosis of pancreatitis and peak 48 hours after onset. Serum amylase levels are typically elevated for as long as 4 days. Amylase levels have been found to be within the reference range in 10-15% of patients with pancreatitis. Amylase levels can be elevated in patients with other abdominal conditions, but typically, they are not as high as levels found in patients with pancreatitis.
- Serum lipase is more specific than amylase for acute pancreatitis, and typically, lipase levels remain elevated 8-14 days longer than amylase levels. Serum lipase levels can also be elevated in patients with other diseases or conditions; therefore, all laboratory results should be evaluated in the context of the clinical presentation.
- Other laboratory abnormalities found in patients with pancreatitis may include coagulopathies, leukocytosis, hyperglycemia, glucosuria, hypocalcemia, hyperbilirubinemia, and elevated gamma glutamyl transpeptidase.
- Urinary levels of trypsin activator peptide (TAP) may help determine the severity of the pancreatitis.
Imaging Studies
- Ultrasonography and CT scanning are the preferred imaging modalities used to diagnose and follow the course of pancreatitis and pancreatic pseudocysts. Ultrasonography is the primary screening tool for evaluation of the pediatric pancreas, due to the absence of ionizing radiation and ability to image without sedation. CT scanning may be better suited for evaluation of chronic pancreatitis and its complications, pancreatic trauma, and neoplastic conditions and is often used to further evaluate abnormalities found on ultrasonography.
- Ultrasonography findings may include a focally or diffusely enlarged, hypoechoic, sonolucent, or edematous pancreas; dilated pancreatic ducts; a pancreatic mass; a fluid collection or peripancreatic fluid; an abscess; or a pseudocyst demonstrated as a well-defined, hypoechoic mass, which may be multilocular.
- CT scan findings include an enlarged gland with ill-defined margins; peripancreatic fluid; areas of decreased or enhanced density; or pseudocysts with a well-defined wall or capsule and central area of low attenuation. CT scanning is a better modality for evaluating presence and extent of pancreatic necrosis and inflammation of peripancreatic fat.
- Of note, findings on imaging studies initially appear normal in 20% of children with acute pancreatitis.
- MRI is another modality to diagnose pancreatitis and is used for the same indications as CT scanning.
- Endoscopic retrograde cholangiopancreatography (ERCP) is essential for evaluation of pancreatic and biliary anomalies. ERCP can aid in the diagnosis of various ductal abnormalities or obstructions and may serve as a therapeutic intervention (ie, sphincterotomy, stent placement).
- Magnetic resonance cholangiopancreatography (MRCP) is a noninvasive alternative to ERCP but lacks therapeutic capabilities.
- Roentgenography may demonstrate nonspecific findings ranging from a distended loop of small intestine (ie, sentinel loop), calcifications, radio-opaque gallstones, dilation of the transverse colon (ie, cutoff sign), ascites, peripancreatic extraluminal gas bubbles, ileus, left-sided basal pleural effusion, and blurring of the left psoas margin to pancreatic calcifications from chronic or recurrent pancreatitis.
Histologic Findings
- Acute pancreatitis is characterized by enzymatic necrosis and inflammation of the pancreas. Focal areas of fat necrosis are interspersed with areas of interstitial hemorrhage secondary to destruction of blood vessels. In severe cases, large blue-black hemorrhagic foci are interspersed with yellow-white chalky areas of fat necrosis.
- Chronic pancreatitis is characterized by irreversible destruction of the pancreatic parenchyma and subsequent replacement with fibrous tissue. Histologic features include intraglandular fibrosis, acinar cell destruction, lymphocytic infiltration, and pancreatic duct obstruction. The pancreatic ducts are dilated and obstructed with protein plugs in their lumens. Grossly, the gland is hard.
- Pancreatic pseudocysts are localized collections of pancreatic secretions walled off by granulation tissue that lack a true epithelial lining. The stomach, duodenum, small bowel, colon, or omentum may abut or form part of the pseudocyst capsule.
Benifla M, Weizman Z. Acute Pancreatitis in Childhood: Analysis of Literature Data. J Clin Gastroenterol. 2003;37(2):169-172. [Medline].
Burnweit C, Wesson D, Stringer D, Filler R. Percutaneous drainage of traumatic pancreatic pseudocysts in children. J Trauma. Oct 1990;30(10):1273-7. [Medline].
Graham KS, Ingram JD, Steinberg SE, Narkewicz MR. ERCP in the management of pediatric pancreatitis. Gastrointest Endosc. Jun 1998;47(6):492-5. [Medline].
Hsu RK, Draganov P, Leung JW, et al. Therapeutic ERCP in the management of pancreatitis in children. Gastrointest Endosc. Apr 2000;51(4 Pt 1):396-400. [Medline].
[Guideline] Adler DG, Baron TH, Davila RE, et al. ASGE guideline: the role of ERCP in diseases of the biliary tract and the pancreas. Gastrointest Endosc. Jul 2005;62(1):1-8. [Medline].
Bellin MD, Carlson AM, Kobayashi T, et al. Outcome after pancreatectomy and islet autotransplantation in a pediatric population. J Pediatr Gastroenterol Nutr. Jul 2008;47(1):37-44. [Medline].
Adamson WT, Hebra A, Thomas PB, et al. Serum amylase and lipase alone are not cost-effective screening methods for pediatric pancreatic trauma. J Pediatr Surg. Mar 2003;38(3):354-7; discussion 354-7. [Medline].
Ford EG, Hardin WD, Mahour GH, Woolley MM. Pseudocysts of the pancreas in children. Am Surg. Jun 1990;56(6):384-7. [Medline].
Behrman RE. Pancreatitis. In: Nelson Textbook of Pediatrics. Philadelphia, PA: WB Saunders Co; 2000.
Gates LK. Preventive strategies and therapeutic options for hereditary pancreatitis. Med Clin North Am. May 2000;84(3):589-95. [Medline].
Kimble RM, Cohen R, Williams S. Successful endoscopic drainage of a posttraumatic pancreatic pseudocyst in a child. J Pediatr Surg. Oct 1999;34(10):1518-20. [Medline].
Kisra M, Ettayebi F, Benhammou M. Pseudocysts of the pancreas in children in Morocco. J Pediatr Surg. Sep 1999;34(9):1327-9. [Medline].
Lerner A, Branski D, Lebenthal E. Pancreatic diseases in children. Pediatr Clin North Am. Feb 1996;43(1):125-56. [Medline].
Neblett WW 3rd, O'Neill JA Jr. Surgical management of recurrent pancreatitis in children with pancreas divisum. Ann Surg. Jun 2000;231(6):899-908. [Medline].
Nijs E, Callahan MJ, Taylor GA. Disorders of the pediatric pancreas: imaging features. Pediatr Radiol. 2005;35:358-73. [Medline].
Pietzak MM, Thomas DW. Pancreatitis in childhood. Pediatr Rev. Dec 2000;21(12):406-12. [Medline].
Pitchumoni CS, Agarwal N. Pancreatic pseudocysts. When and how should drainage be performed?. Gastroenterol Clin North Am. Sep 1999;28(3):615-39. [Medline].
Sinclair DB. Valproic acid-induced pancreatitis in childhood epilepsy: case series and review. Journal of Child Neurology. 2004;19:498-502. [Medline].
Stringer MD. Multidisciplinary management of surgical disorders of the pancreas in childhood. Journal of Pediatric Gastroenterology and Nutrition. 2005;40:363-7. [Medline].
Weber TR, Keller MS. Operative management of chronic pancreatitis in children. Arch Surg. May 2001;136(5):550-4. [Medline].
Weckman L, Kylanpaa ML, Puolakkainen P, Halttunen J. Endoscopic treatment of pancreatic pseudocysts. Surg Endosc. Apr 2006;20(4):603-7.
Werlin SL. Pancreatitis in children. Journal of Pediatric Gastroenterology and Nutrition. 2003;37:591-5. [Medline].

