In general, the preferred abdominal imaging modality to identify the extent of pancreatic
edema, hemorrhage, necrosis, and other abnormal- ities is CT with IV contrast although Kearney et al.
2009 note signifi cant correlation between US
and CT when utilizing US as the primary imaging modality in patients with asparaginase-associated
pancreatitis. Plain fi lm is usually unremarkable although abdominal radiography i.e., kidney, ure-
ter, bladder; KUB may show a sentinel loop in the left upper abdomen representing a localized ileus
as a result of peripancreatic infl ammation.
Treatment of acute pancreatitis has histori- cally included nasogastric decompression, gut
rest, hydration with electrolyte replacement or parenteral nutrition for prolonged gut rest, anal-
gesia that usually includes opioids, and antiemet- ics. Whether nasogastric decompression is
necessary is unclear; Kearney et al.
2009 reported that only 29 of pediatric patients with
asparaginase-associated pancreatitis were treated with nasogastric decompression with no differ-
ence in outcome. Additional pediatric data are lacking. Similarly, the need for gut rest has
recently come into question. In adult patients with severe acute pancreatitis, Kumar et al.
2006 showed that enteral nutrition via both
nasogastric and nasojejunal routes was well
Clinically significant GI bleeding Shock
↓↓ Hemoglobin Aggressive fluid resuscitation
Correction of thrombocytopenia i.e., 75 x 10
9
L Correction of coagulopathy
Transfuse PRBCs as necessary Consultation with gastroenterology, surgery and critical care
Treat underlying causes e.g., GVHD, infection Other potential adjunctive treatments i.e., rFVIIa, octreotide, vasopressin
Identify upper versus lower GI bleed Hematemesis
Melena EGD
Bleeding stops tRBC scan
Meckel’s scan CT angiogram
Capsule endoscopy Diagnostic laparoscopy
Laparotomy Bleeding stops
Bleeding restarts
Bleeding restarts
Source found and controlled
Source found and controlled
Unclear source Unable to control bleeding
Rigid sigmoidoscopy Flexible sigmoidoscopy
Colonoscopy Hematochezia
Fig. 7.1 Algorithm for management of clinically signifi -
cant gastrointestinal bleeding in pediatric oncology patients. GI gastrointestinal, PRBC packed red blood cell,
GVHD graft-versus-host disease,
rFVIIa recombinant
factor VIIa, EGD
esophagogastroduodenoscopy, tRBC
technetium- 99m-tagged red blood cell, CT
computed tomography
tolerated, while in a meta-analysis Petrov et al. 2007
reported that oral refeeding in adults was signifi cantly associated with pain relapse. In a
review by Kumar and Gariepy 2013
they con- clude that early introduction of enteral feeding
should be strongly considered in pediatric patients no matter the severity of the pancreatitis
while early oral refeeding can be considered in those with mild disease although pediatric data
are lacking. Despite its theoretical association with reduced sphincter of Oddi spasms, no clini-
cal studies support meperidine over other narcot- ics Thompson
2001 . Potential complications
include development of an abscess, pseudocyst, necrosis or hemorrhage. Most cases of pancreati-
tis resolve spontaneously and complications are rare; incidence of asparaginase-induced hemor-
rhagic pancreatitis in pediatric oncology is 0.5 Top et al.
2005 . Unlike uncomplicated
acute pancreatitis, hemorrhagic pancreatitis is a medical emergency with mortality rates
approaching 100 if untreated Top et al. 2005
. Hypovolemic shock is common and initial man-
agement parallels that of any GI bleed. Pediatric oncology patients are generally
placed on an empiric antibiotic regimen as uti- lized in neutropenic enterocolitis at the time of
pancreatitis diagnosis. Procurement of cultures to guide antibiotic therapy can be accomplished via
CT-guided fi ne-needle aspiration Tenner et al.
2013 . Duration of antimicrobial coverage is gen-
erally 10–14 days, depending on the patient’s clinical status. Surgical debridement becomes
necessary only when clinical deterioration per- sists despite adequate antibiotic coverage; percu-
taneous catheter drainage to irrigate the necrosis can be considered prior to surgical debridement
Top et al.
2005 . The synthetic somatostatin
octreotide, which inhibits exocrine pancreatic enzyme production, represents a promising
experimental option in pediatrics but is still investigational Wu et al.
2008 .
7.5 Bowel Obstruction
Bowel obstruction results from luminal obstruc- tion, lesions within the bowel wall, extrinsic
bowel compression, dysfunctional motility, and radiation-induced enteritis Arul and Spicer
2008 ;
Yip and Goddard 2010
. Primary tumors that invade through the GI mucosa and contribute to luminal or
intrinsic obstruction include non- Hodgkin lym-
phoma especially Burkitt lymphoma, rhabdo- myosarcoma and teratoma. In patients with primary
abdominal Burkitt lymphoma, almost a fi fth of patients present with small bowel intussusception at
the time of diagnosis Gupta et al.
2007 . Tumors
that contribute to extrinsic compression include neuroblastoma and peritoneal metastases of Wilms
tumor. Postoperative complications after tumor resection may also contribute to GI luminal obstruc-
tion; these include stricture formation, intussuscep- tion, and, less frequently, hernia. Although
postoperative adhesions are the most common cause of extrinsic bowel compression, these gener-
ally present as obstruction months to years later. In contrast, postoperative small bowel intussusception
usually occurs within 2 weeks of surgery. Functional motility obstruction commonly follows administra-
tion of vinca alkaloids and opiates as well as after any abdominal surgical procedure. Of note, fecal
impaction is a common cause of obstruction in both immunocompetent and immunocompromised
pediatric patients. The risk of radiation-
induced bowel obstruction increases with prior abdominal
surgery, treatment with concomitant radiation- sensitizing chemotherapy, radiation doses 45 Gy
to the bowel and young age at time of therapy Silliman et al.
1994 ; Kaste et al.
1999 . Radiation-
induced bowel injury leading to obstruction occurs within 6–24 months after completion of radiother-
apy Kaste et al. 1999
. Although the etiologies differ, the symptoms,
signs, laboratory results and imaging suggestive of mechanical obstruction in pediatric oncology
patients mimic any patient with an abdominal mechanical obstruction. Patients may have inter-
mittent abdominal pain, intractable nausea or bil- ious emesis, constipation, hematochezia, or
abdominal distension. Physical exam consistent with obstruction includes hyperactive or high-
pitched bowel sounds, peritoneal signs and a pal- pable mass. In contrast, absent bowel sounds
suggest an ileus or functional obstruction. Due to emesis and decreased oral intake, patients often
present dehydrated on exam and laboratory assess- ment; patients may have a relative increase from
baseline white blood count with evidence of hemoconcentration as well as hypochloremic met-
abolic alkalosis. Imaging studies begin with supine, upright and decubitus abdominal radio-
graphs. Although not pathognomonic, air-
fl uid levels in dilated bowel loops and pneumatosis
intestinalis on KUB are strongly supportive of obstruction. Dilated and contracted bowel loops
may be appreciated proximal and distal to the obstruction, respectively. Abdominal CT with oral
contrast will best localize the obstruction and identify the etiology Silliman et al.
1994 ; Yip and
Goddard 2010
. Patients with neutropenia or necrotic bowel are at high risk of infection and
perforation of the thinned intestinal mucosa and should not undergo small bowel follow-through
exam using barium.
Management of obstruction includes bowel rest, decompression via nasogastric tube, and intrave-
nous fl uids to resolve electrolyte derangements and treat dehydration. Additional supportive care mea-
sures include antiemetics, anticholinergics and analgesics. As bowel cleansing preparations are
contraindicated in gastrointestinal obstruction, ene- mas and suppositories are suggested to resolve
fecal impaction and can be used with caution in immunocompromised patients Arul and Spicer
2008 ; Yip and Goddard
2010 . Indications for sur-
gical intervention include: 1 persistent bleeding in the absence of neutropenia, thrombocytopenia or
coagulopathy; 2 intraperitoneal perforation; 3 clinical deterioration of unknown etiology, espe-
cially if requiring blood pressure support with either colloids or vasopressors; and 4 any abdom-
inal process that would require surgery in an immu- nocompetent host such as a mass lesion Silliman
et al.
1994 . In contrast to non-oncologic episodes
of intussusception, children with intussusception caused by tumor require surgical reduction rather
than air- contrast or barium enema Fisher and
Rheingold 2011
.
7.6 Tumor Rupture and Organ
Perforation
Tumor rupture and organ perforation are surgical emergencies. Etiologies include the malignancy
itself, treatment sequelae, iatrogenic intervention and unresolved obstruction. The most common
cause of GI perforation is iatrogenic intervention, specifi cally endoscopy Gagneja and Sinicrope
2002 . Tumors at risk for spontaneous rupture
include Wilms tumor, hepatoblastoma, neuro- blastoma and B-cell lymphoma Arul and Spicer
2008 . Tumor rupture in patients with Burkitt
lymphoma may occur at presentation, during sur- gical intervention or steroid therapy, or with
tumor necrosis Fisher and Rheingold 2011
. If lymphoma erodes the intestinal wall, it can cause
GI perforation at the site of transmural invasion. Tumor rupture and organ perforation are not lim-
ited to solid tumors or bowel; leukemic patients with splenomegaly have a small risk for splenic
rupture, either spontaneously or with trivial trauma Gagneja and Sinicrope
2002 . In addi-
tion, therapy with prolonged corticosteroids, bev- acizumab or radiation disrupts the GI mucosal
epithelium. As previously mentioned, bevaci- zumab potentially increases the risk of gastric
perforation Demshar et al.
2011 . Sequelae like
peptic ulcer disease and adhesions, acting as lead points for mesenteric twisting, represent condi-
tions that further weaken the intestinal wall. Frequent endoscopic procedures, unresolved
obstruction or infection, or medically refractory conditions such as gastritis and ulcers predispose
to perforation Yip and Goddard
2010 ; Fisher
and Rheingold 2011
. Although shock and peritoneal signs strongly
suggest perforation, presentation varies consider- ably in immunocompromised pediatric oncology
patients. Exam may reveal the classic acute abdo- men with the patient rigid in a fl exed position and
exhibiting rebound tenderness or, in contrast, dis- play only mild evidence of discomfort, tender-
ness, or distension. Intestinal distension usually results from the patient swallowing excessive
amounts of air or from excessive gas production from bacterial overgrowth. Cecal diameters
13 cm dramatically increase the risk of perfora- tion. Occasionally subcutaneous emphysema
may be appreciated. Bowel sounds range from absent to hyperactive. Gastric perforation com-
monly presents with acute onset of severe abdom- inal pain that is often associated with nausea and
vomiting, including hematemesis. Patients may complain of shoulder pain, which is referred pain
