Gastrointestinal Supportive Care in Pediatric Oncology irantextbook.ir 93df

upper GI bleed Abdulrahman et al. 2004 . Less is known about the utility of gastric lavage in pediatric oncology patients. In children with bright red blood or evidence of brisk bleeding during gastric lavage, management includes prompt endoscopic ligation or sclerotherapy. If the patient has esophageal varices, systemic infu- sion of vasopressin for 24 h may decrease portal circulation enough to halt bleeding without endoscopic intervention. Although endoscopy potentially increases the risk of infection in neutropenic patients, it is the standard method to identify and control both upper and lower GI hemorrhage. If endoscopy fails to identify the origin of the bleed, angiogra- phy or radionuclide scans may help localize the source, assuming that the rate of bleeding exceeds 1 or 0.5 mLmin for these different diagnostic methodologies, respectively. If hemorrhage per- sists or recurs, management includes reevalua- tion and treatment of anemia, thrombocytopenia, and coagulopathies followed by repeat endos- copy or surgical intervention Arul and Spicer 2008 . Surgical intervention should precede endoscopic hemostasis if bleeding is associated with tumor. Figure 7.1 outlines the algorithmic approach to the management of acute GI bleed- ing in pediatric oncology patients.

7.4 Pancreatitis

Pancreatitis represents a rare but well-known complication of multiple chemotherapeutic agents, most notably asparaginase, steroids, mer- captopurine and cytarabine Haut 2005 ; Trivedi and Pichumoni 2005 ; Garg et al. 2010 . L-asparaginase and PEG-asparaginase derived from E. coli are well described for inducing acute pancreatitis of all degrees of severity with a reported incidence of 2–18 Knoderer et al. 2007 ; Kearney et al. 2009 . Although suggested in some studies, it is not clear that PEG- asparaginase leads to an increased risk of pancre- atitis as compared to L-asparaginase Silverman et al. 2001 ; Knoderer et al. 2007 . Older patients i.e. 9 years have been noted to have a signifi cantly increased risk of pancreatitis with pancreatitis occurring early after asparagi- nase introduction and typically days after L-asparaginase and weeks after PEG- asparaginase secondary to differences in drug half-life Silverman et al. 2001 ; Knoderer et al. 2007 ; Kearney et al. 2009 . No difference in pan- creatits incidence has been noted with intramus- cular versus intravenous PEG-asparaginase to date Silverman et al. 2010 . In their retrospec - tive review, Knoderer et al. 2007 note that asparaginase-associated pancreatitis was signifi - cantly correlated with concomitant prednisone and daunomycin and signifi cantly less likely with dexamethasone. Reintroduction of aspara- ginase after pancreatitis is controversial. In their review, Kearney et al. 2009 did not show a sig- nifi cant difference in outcome in those patients with and without pancreatitis although their gen- eral practice was to rechallenge patients. Knoderer et al. 2007 reported a 7.7 incidence of pancreatitis with rechallenge as compared to Kearney et al. 2009 who reported a 63 recurrence rate. Clinical diagnosis of asparagi- nase-associated pancreatitis is relatively straight- forward; Kearney et al. 2009 note that all patients presented with abdominal or back pain and the majority had nausea or emesis. Severity of pancreatitis was not noted to correlate with degree of elevation of amylase and lipase Kearney et al. 2009 . Laboratory workup merely supports the clini- cal suspicion of acute pancreatitis. Initial labora- tory tests should include: 1 electrolytes to evaluate for hypocalcemia secondary to its pre- cipitation; 2 renal and liver function tests to monitor for multiorgan failure secondary to cyto- kine release from the infl amed or necrotic pan- creas; 3 triglycerides, inciting agents that when hydrolyzed to free fatty acids lead to free radical damage; and 4 the exocrine enzymes amylase and lipase, which when elevated suggest pancre- atic autodigestion and are the hallmark of diagno- sis Tsuang et al. 2009 . Of note, amylase and lipase may not be signifi cantly elevated. Excessive cytokine release can lead to respiratory distress and therefore arterial blood gas and chest radiog- raphy may be clinically indicated for proper man- agement Arul and Spicer 2008 . 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