Pediatric Care Pancreatitis in Children CHRIS KRAMER, RN, BSN, CCRN ALVIN JEFFERY, RN-BC, MSN, CCRN, FNP-BC Although the incidence of acute pancreatitis among children is less than that in adults, the physical and psychosocial impact on children and their families can be overwhelming. Pancreatitis is manifested as pain accompanied by a host of other complex issues. These issues are manifested more markedly when the patient has additional concomitant diagnoses. Pain management, liver function tests, amylase and lipase levels, endocrine and exocrine functionality, and recognition of systemic inflammation are especially important. Management after discharge from the hospital is often an ongoing stress for these patients and families, and multiple admissions to the intensive care unit may be necessary for feeding and pain complications. Presented in the context of an actual clinical case at a 500-bed tertiary care pediatric hospital, this patient’s scenario illustrates the importance of ensuring adequate nutrition, maintaining hydration, providing appropriate pain management, and preventing infection and thromboembolic events. (Critical Care Nurse. 2014;34:43-53) haracterized by localized edema and systemic inflammation, pancreatitis is a potentially life-threatening disease that has long-term consequences for many patients. Clinicians who primarily care for adults most likely see patients with pancreatitis far more often than do those who primarily care for children. Because of the lower incidence among children, little has been published on pancreatitis in this age group. In this article, we address the scarcity of available information by discussing pancreatitis in the context of a case review. We also illustrate key concepts and current trends in the management of pancreatitis in children. C CNE Continuing Nursing Education This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives: 1. Describe the common etiologies and diagnostic criteria for a child with pancreatitis 2. State common nursing and medical interventions for the child with pancreatitis 3. List complications experienced by the child with pancreatitis ©2014 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2014533 www.ccnonline.org CriticalCareNurse Vol 34, No. 4, AUGUST 2014 43 Table 1 Overview of cell types contained in the pancreasa Type of cell Type of gland Components secreted Acinar Exocrine Enzymes and fluids Promotes digestion Duct Exocrine Enzymes and fluids Promotes digestion Endocrine Insulin Decreases blood glucose levels by promoting glucose uptake into cells and conversion to glycogen Endocrine Glycogen Increases blood glucose levels by promoting glycogenolysis and gluconeogenesis Endocrine Somatostatin Helps regulate digestion and absorption of nutrients and regulates the secretion of other pancreatic hormones F Endocrine Pancreatic polypeptide Inhibits exocrine secretions of pancreas and contractions of gallbladder a Based Function on information from Stanfield.1 Overview of Pancreatic Function The pancreas is positioned in the middle of the abdomen near the stomach, left kidney, and parts of the small intestine. Rich in bicarbonate and several digestive enzymes, the pancreas is responsible for producing pancreatic amylase (which breaks down starch and glycogen) and pancreatic lipase (which breaks down fats). Relative to its weight, the pancreas secretes more protein than any other tissue in the body. The pancreas functions as both an endocrine and an exocrine gland with many different cell types1 (Table 1). Table 2 Category Gallstones, sludge in gallbladder Medications Valproic acid, prednisone, L-asparaginase Systemic diseases Sepsis, hemolytic uremic syndrome, systemic lupus erythematosus Trauma Transplants Alvin Jeffery is an education specialist in the Center for Professional Excellence/Education at Cincinnati Children’s Hospital Medical Center. Corresponding author: Chris Kramer, RN, BSN, CCRN, Pediatric Intensive Care Unit, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave, MLC 11017, Cincinnati, OH 45229 (e-mail: [email protected]). To purchase electronic or print reprints, contact the American Association of CriticalCare Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected] 44 CriticalCareNurse Vol 34, No. 4, AUGUST 2014 Solid organs, bone marrow Systemic infections Metabolic disorders Authors Chris Kramer is a registered nurse in the pediatric intensive care unit at Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio. Examples Biliary diseases Acute Pancreatitis in Children The annual incidence of acute pancreatitis is 3.6 to 13.2 per 100000 for children2,3 and 4 to 45 per 100000 for adults.4 The most common causes in children include biliary diseases, complications from medications, systemic diseases, systemic infections, trauma, and organ transplant (Table 2). Regardless of the cause, the pathophysiology of pancreatitis starts with injury to acinar cells and the release of proteases and other enzymes Causes of pancreatitis in childrena Diabetic ketoacidosis, hypertriglyceridemia, hypercalcemia Hereditary causes Idiopathic causes a Based on information from Bai et al5 and Srinath and Lowe.6 (eg, trypsin, elastase, lipase) that destroy cells and tissues.5 This process results in pancreatic edema and local inflammation. Inflammatory mediators and large amounts of trypsin are released, which can then lead to systemic inflammatory response syndrome (SIRS) and pancreatic necrosis5-7 (see Figure). The SIRS is the pathological reaction responsible for pulmonary complications and renal failure.8 In acute episodes of pancreatitis, damage to the pancreas itself is reversible.7 The median hospital length of stay for children with pancreatitis is 5 to 8 days.6 Treatment focuses on ensuring adequate nutrition, maintaining hydration, providing appropriate pain management, and preventing infection and thromboembolic events. www.ccnonline.org Injury Decreased oral intake Pain Dehydration Thrombosis Acinar cell releases... Systemic inflammatory response syndrome Pulmonary complications Renal failure Sepsis/shock Pancreatic edema Local inflammation C (tum ytoki ne Trypsin o plat r nec prod elet ros ucti acti is fa on vati ctor ng fact and or) Proteases Enzymes e tissu Cell/ ction u r dest Ileus of bowel loops Hematuria from left kidney Infection Figure Pathophysiology and sequelae of acute pancreatitis. Case Review: First Admission Initial Signs and Symptoms TN is a 13-year-old, 120-kg boy with allergies to fentanyl and clindamycin and a history of obesity, sleep apnea, and Angelman syndrome. Angelman syndrome is a neurogenic disorder that is often misdiagnosed as cerebral palsy or autism. The syndrome is characterized by developmental delay, seizures, aphasia, and gait instability.9 TN is developmentally similar to a 3-yearold child except that he is nonverbal. TN initially was brought to the emergency department because he had epigastric abdominal discomfort (as evidenced by his localization of pain to the affected area), constipation, dehydration, oral intake less than 240 mL (8 ounces), and urine output less than 0.5 mL/kg per hour in the preceding 12 hours. Vital signs at the time of admission indicated tachycardia, tachypnea, slight oxygen desaturation, hyperthermia, and slight hypotension (see First time vital signs in Table 3). While in the emergency department, TN received a total of 40 mL/kg of physiological saline for dehydration, two 5-mg doses of morphine sulfate for pain, and one 1200-mg dose of oral acetaminophen (Tylenol) for fever. The pancreas was not well visualized during abdominal sonography because of the patient’s inability to cooperate and gaseous distention. Consequently, contrast-enhanced computed tomography (CT) was performed and showed a mildly edematous pancreas with a small amount of peripancreatic fluid and inflammation reflecting pancreatitis. No evidence of necrosis www.ccnonline.org or abscess was detected. Transient oxygen desaturations to 86% to 89% were noted in the emergency department, and administration of supplemental oxygen was efficacious. While TN was still in the emergency department, blood samples were obtained for various laboratory studies, including complete blood cell count, renal and liver function tests, and venous blood gas analysis (Table 3). Serum levels of amylase (734 U/L) and lipase (9453 U/L) were the most abnormal values during the first admission to the emergency department (to convert amylase and lipase values to microkatals per liter, multiply by 0.0167). The clinical features, elevated levels of pancreatic enzymes, and CT results suggested acute pancreatitis, and TN was admitted to the gastrointestinal unit for further management of dehydration, pain, and diet. Maintenance intravenous fluids consisting of 5% dextrose and physiological saline were started at 1.5 times greater than basal need. Oral oxycodone for the epigastric pain and intravenous piperacillin-tazobactam (Zosyn) for prophylactic antibiotic coverage were ordered. After 4 days, a repeat CT showed an edematous pancreas with no fluid collection and no evidence of necrosis or abscess. The lipase level had also decreased to 198 U/L. TN was showing marked clinical improvement, with decreased pain, minimal oxygen requirement (0.5 L/min by nasal cannula), and vital signs within the reference range. A lowfat diet for pancreatic rest was started, and although oral intake was returning to baseline values, low urine output (<1 mL/kg per hour) and constipation continued to be CriticalCareNurse Vol 34, No. 4, AUGUST 2014 45 Table 3 Relevant clinical findingsa Visit to emergency department Clinical finding First time Second time Admission to intensive care unit Body temperature, °C (normal value: 36-38) 38.7 (High) 39.5 (High) 39.8 (High) Heart rate, beats per minute (normal value: 70-110) 142 (High) 150 (High) 145 (High) Respiratory rate, breaths per minute (normal value: 12-20) 22 (High) 25 (High) 30 (High) 100/60 (Low) 98/56 (Low) 85/44 (Low) Mean arterial pressure, mm Hg (normal value: 80-95) 78 (Low) 69 (Low) 55 (Low) Oxygen saturation as measured by pulse oximetry, % (normal value: >93) 89 (Low) 90 (Low) 85 (Low) Amylase, serum, U/L (normal value: 50-150) 734 (High) 908 (High) Lipase, serum, U/L (normal value: 10-140) 9453 (High) >15 000 (High) Blood pressure, mm Hg (normal value: 110-120/70-80) Aspartate aminotransferase, serum level, U/L (normal value: 15-45) 30 52 (High) Alanine aminotransferase, serum level, U/L (normal value: 10-45) 32 120 (High) 14 100 (High) 15 400 (High) 15.3 15.9 White blood cells, blood level, /μL (normal value: 4500-13 500) Hemoglobin, blood level, g/dL (normal value: 13-16) Hematocrit, blood level, % (normal value: 37-49) 43 45.5 222 000 297 000 Sodium, serum level, mmol/L (normal value: 136-145) 143 144 Potassium, serum level, mmol/L (normal value: 3.6-5.0) 4.9 3.8 118 (High) 134 (High) Platelets, blood level, /μL (normal value: 135 000-466 000) Glucose, serum level, mg/dL (normal value: 75-110) pH, venous blood gas analysis (normal value: 7.35-7.45) 7.18 (Low) Pco2, venous blood gas analysis, mm Hg (normal value: 37-47) 72 (High) Base excess, venous blood gas analysis (normal value: -2 to +2) -8 (High) a Blank cells indicate that value was not measured. SI conversion factors: to convert amylase, lipase, alanine aminotransferase, and aspartate aminotransferase to μkat/L, multiply by 0.0167; to convert glucose to mmol/L, multiply by 0.0555. problems. TN was discharged after 11 days in the hospital. Discharge planning focused on adequate hydration, pain management, maintenance of a strict low-fat diet, improvement of defecation with milk of magnesia, and oxygen at night to maintain oxygen saturations greater than 91%. Discussion A diagnosis of acute pancreatitis can be made once 2 of the following 3 criteria are present: abdominal pain, serum level of amylase or lipase or both at least 3 times the upper value of the reference range, and imaging results consistent with pancreatitis.10 TN met all 3 of these criteria. Although diagnosis of acute pancreatitis could have been made simply on the basis of pain and altered serum levels of pancreatic 46 CriticalCareNurse Vol 34, No. 4, AUGUST 2014 enzymes, sonography is often used to rule out obstructive causes such as cysts or tumors, trauma, or stones.10 Acute pancreatitis in children most commonly is manifested as abdominal pain or irritability (either occurs in as many as 91% of cases), epigastric tenderness (86% of cases), and nausea or vomiting (74% of cases).6,11 For patients who are nonverbal because of developmental age (such as TN), irritability is more common.7 Causes of pain associated with pancreatitis may be more complex than previously thought but most likely are due to a combination of inflammation (increased pressure), inflammatory mediators, cell death, and genetic expression.5,12 In TN’s case, most likely severe pain resulted in decreased oral intake, which eventually led to constipation and dehydration. www.ccnonline.org Serum levels of amylase and lipase are commonly determined when pancreatitis is suspected. Although lipase is a more sensitive indicator (ie, more likely to be elevated in pancreatitis) than is amylase,10,11 some investigators6 have found elevations in serum levels of amylase without concomitant increases in lipase. As in this case, transabdominal sonography is routinely the first imaging study used in children with suspected pancreatitis.10 Transabdominal or endoscopic sonography, contrast-enhanced CT, and magnetic resonance imaging or magnetic resonance cholangiopancreatography are all acceptable forms of diagnostic imaging.10 Findings suggestive of acute pancreatitis include pancreatic or peripancreatic edema, necrosis, inflammation, hemorrhage, abscess, and fluid collections.10 Based primarily on guidelines for adults, treatment for children with pancreatitis focuses on correcting dehydration, managing abdominal pain, ensuring nutritional intake, and preventing adverse events (ie, thromboembolism and infection). Alleviating the cause of pancreatitis, if known, is also a priority. Correcting Dehydration Although initial management in the emergency department of children with dehydration includes rehydration with intravenous fluids,13 the presence of a profound inflammatory response makes such rehydration particularly important in patients with acute pancreatitis.6 The optimal type, rate, and volume of fluid have not been determined for children or adults,6 but maintenance fluids should be administered at a sufficient volume to result in urine output of at least 0.5 to 1 mL/kg per hour.13 Frequently assessing urine output and ensuring adequate vascular access are key nursing interventions that will affect patients’ outcomes. Because TN had no renal or cardiac disease, a liberal amount of intravenous fluids (40 mL/kg bolus followed by 1.5 times the continuous basal rate) was administered. Managing Pain Because of the intense pain associated with acute pancreatitis, analgesia is best achieved with opiates.7 TN was given morphine because of his allergy to fentanyl; however, morphine is typically avoided because it might cause spasms of the sphincter of Oddi14 (even though occurrence of this complication has yet to be proven in studies in humans).14,15 Meperidine should be avoided in children because of its potential neurotoxic effects, such as seizures.16 When a patient has allergies to medications, finding an appropriate pharmacological www.ccnonline.org intervention for pain relief may be difficult. Nurses should promptly report the presence of pain to the patient’s prescribing provider. Ensuring Nutritional Intake Because of a presumed need for pancreatic rest,6 adults with pancreatitis were previously expected to take nothing by mouth for at least 5 to 7 days.17 Current evidence in adults, however, suggests that during an episode of acute pancreatitis, early initiation of enteral nutrition (especially through a nasojejunal tube) is beneficial. This early initiation has resulted in a reduction in both infections and hospital Current guidelines on sepsis recommend length of prophylaxis for deep vein thrombosis in stay.18 Oral children with acute pancreatitis who are feeding can be resumed past puberty. once the pain begins to subside.7 No conclusive studies on the use of early enteral nutrition in children with pancreatitis have been done.6,7 In addition, a survey10 indicated that pediatricians are not likely to order enteral tube feedings in children with acute pancreatitis, most likely because of the hypothetical need for pancreatic rest. In patients receiving enteral nutrition, resumed pancreatic activity may cause the return of pain, and nurses should assess patients for pain associated with these changes in diet. Preventing Adverse Events If a patient has pancreatic infection and/or necrosis, other measures, including antibiotic prophylaxis, are needed.7,19 Additionally, current guidelines20 on sepsis recommend prophylaxis for deep vein thrombosis in children with acute pancreatitis who are past puberty. The similar systemic inflammatory effects of sepsis and pancreatitis provide sufficient rationale for many clinicians to start chemical prophylaxis, such as administration of enoxaparin (Lovenox). Potential Complications Additional sequelae of acute pancreatitis may include recurrence of acute pancreatitis (known as acute recurrent pancreatitis), formation of pseudocysts, and necrotizing pancreatitis. Acute recurrent pancreatitis is defined by the diagnostic criteria previously listed for acute pancreatitis plus either an interval of at least 1 pain-free month between diagnoses of acute pancreatitis or completely normal serum levels of amylase and lipase with no pain, CriticalCareNurse Vol 34, No. 4, AUGUST 2014 47 regardless of time between episodes.10 Although previous studies21 supported this nomenclature, more current recommendations refer to this recurrence as a complication of acute pancreatitis rather than as acute recurrent pancreatitis itself.10 Acute recurrent pancreatitis can occur in up to 15% to 36% of children who have acute pancreatitis.22,23 A pseudocyst, one of the more common complications of acute pancreatitis and acute recurrent pancreatitis, is defined as “a collection of amylase-rich pancreatic fluid that lacks an epithelial lining”19(p417) and includes nonnecrotic tissue. A more heterogeneous collection of fluid with necrotic tissue present is identified as postnecrotic collection or necrotizing pancreatitis.19 Differentiating between a pseudocyst and a postnecrotic collection is important for guiding further treatment. A more conservative (watch and wait) approach may be taken in a patient with a pseudocyst, or antibiotic therapy and surgical intervention may be necessary when necrotic tissue is the source of infection.19 Surgical options vary widely and depend on the resources available at the institution. Case Review: Second Admission Approximately 7 months after his first admission, TN was again brought to the emergency department. At the time of admission and according to his family, he had diaphoresis, abdominal and lower back pain, 3 incidents of loose stools, and 8 episodes of vomiting. Vital signs A more conservative (watch and wait) approach were even may be taken in a patient with a pseudocyst, more or antibiotic therapy and surgical intervention abnormal may be necessary when necrotic tissue is the than those source of infection. at the first admission. TN had tachycardia, tachypnea, oxygen desaturations, increased hyperthermia, and hypotension (Table 3). While in the emergency department, TN received a 1-L bolus of physiological saline, 20 mg of intravenous promethazine (Phenergan) for the nausea and vomiting, and one 2-mg dose of hydromorphone (Dilaudid) for pain. Once again, abdominal sonography could not be done because of TN’s recent oral intake. A CT scan showed a prominently edematous pancreas with possible necrotizing pancreatitis. Additionally, an area of localized fluid 7.4 6.1 10.7 cm in size was noted at the lesser sac near the pancreatic body, suggestive of a 48 CriticalCareNurse Vol 34, No. 4, AUGUST 2014 pancreatic pseudocyst. TN’s serum levels of amylase (908 U/L) and lipase (>15000 U/L) were markedly elevated (Table 3). TN’s clinical features, CT results, and elevated enzyme levels led to a diagnosis of acute pancreatitis complicated by a pseudocyst. Because of treatments received in the emergency department and the clinical signs and symptoms, physicians decided to admit TN to the pediatric intensive care unit (PICU). Admission to the unit was warranted because of respiratory distress related to fluid overload during correction of dehydration and the increasing need for sedation. TN’s escalating aggression and agitation most likely were due to confusion (a result of his neurological disorder) and pain. Table 3 highlights significant clinical findings present on admission to the PICU. TN’s clinical features in the PICU included further hemodynamic instability, respiratory distress, persistent hyperthermia, and a combined respiratory-metabolic acidosis. The pseudocyst was the assumed culprit for all of the complications; however, TN’s condition needed to be stabilized before the pseudocyst could be addressed. A chest radiograph showed atelectasis and pulmonary edema. The radiographic findings, results of blood gas analysis, and the clinical signs and symptoms were enough for elective intubation to provide better airway management. TN was treated with adultdosage intravenous infusions of midazolam (Versed), hydromorphone (Dilaudid), and dexmedetomidine (Precedex) for sedation and airway management. He remained consistently febrile and was treated with cooling blankets and scheduled doses of acetaminophen (Tylenol) to achieve a temperature goal of less than 38ºC. TN had blood glucose levels from 100 to 350 mg/dL (to convert to millimoles per liter, multiply by 0.0555), so a continuous infusion of insulin was started and glucose levels were assessed hourly. In the PICU, 2 nontunneled central venous catheters were placed, 1 in the intrajugular vein and 1 in the left femoral vein. Central venous access was needed for continuous sedation, antibiotic therapy, parenteral nutrition, and sporadic use of inotropes. Because of TN’s weight (>40 kg) and prolonged bed rest, sequential compression devices were applied to prevent thromboembolic events. However, after the femoral venous catheter was removed, TN’s left lower extremity began to swell. Sonography revealed a nonocclusive thrombus that was managed www.ccnonline.org Table 4 Outline of patient’s progress after insertion of external drain Extubated 4 days after drain insertion Urinary catheter removed 6 days after drain insertion No central catheters except double-lumen peripherally inserted central catheter Glucose levels persistently <250 mg/dL Table 5 Discharge instructions Remain on insulin regimen of Lantus (insulin glargine) 20 units every night at bedtime Use Novolog (insulin aspart) correction factor to 1:35>120 mg/dL Remain on continuous feedings of Vivonex (enteral feeding formula) 60% at 150 mL/h for 20 hours Transferred to gastrointestinal unit 13 days after drain insertion Check blood glucose levels every 4 hours while receiving continuous feedings SI conversion factor: to convert glucose to mmol/L, multiply by 0.0555. Check blood glucose level 30 minutes after feedings have stopped No insulin correction 30 minutes before discontinuation of feedings with administration of enoxaparin. Urinary elimination continued to be a problem because an anatomical false passage had been created when an indwelling urinary catheter was initially placed during TN’s first admission to the emergency department. A urinary catheter that was correctly placed while the patient was in the PICU helped with urination and healing of the anatomic false passage. Hypotension associated with the continuous need for sedation and the SIRS was managed by using norepinephrine. TN was unable to tolerate oral feedings, necessitating placement of a postpyloric nasal tube and continuous, low-rate (5-10 mL/h) feedings. A nasogastric tube was also placed for continuous gastric decompression. After 15 days of the aforementioned treatments, TN’s condition finally became stable. Care providers from the institution’s interventional radiology, gastroenterology, and critical care medicine were consulted about the pseudocyst. Because severe pancreatitis and its complications are not often problems at pediatric institutions, the gastroenterology team at a neighboring hospital for adults was also consulted. After much debate, the teams agreed to use interventional radiology to place an external drain in the pseudocyst/ pancreas. After placement of the drain, TN’s persistent fevers, abdominal distention, pain and agitation, and hyperglycemia markedly decreased (Table 4). After 28 days in the PICU, TN was transferred to the gastrointestinal unit, and a transcutaneous gastrojejunal tube was placed for the continuation of a low-fat diet. TN was discharged to home after 71 days of inpatient treatment for acute pancreatitis complicated by pseudocyst formation. He still had the external pancreatic drain, the gastrojejunal tube, and a peripherally inserted central catheter in place. Discharge teaching focused on pain management, drain monitoring, maintaining a strict feeding regimen, and hydration (Table 5). www.ccnonline.org SI conversion factor: to convert glucose to mmol/L, multiply by 0.0555. Additional Complications of Pancreatitis in Children The rationale for many of the interventions used for TN during his stay in the PICU are described in the Discussion section following the description of his first admission to the emergency department. Additional anomalies that may further complicate acute pancreatitis in children are endocrine dysfunction, effects of SIRS, and long-term considerations. Endocrine Dysfunction TN did have some endocrine dysfunction, as indicated by hyperglycemia. Although intuitively hyperglycemia is due to dysfunction of cells in pancreatic islets and decreases in insulin levels, pancreatic cells are also affected, and gluconeogenesis may be impaired.1 When determining the frequency of serum glucose assessments, nurses should consider the possibility of unexpected and counterintuitive changes in glucose levels in children with acute pancreatitis. Regardless, hyperglycemia associated with acute pancreatitis can be treated with oral antihyperglycemic agents; although, up to 30% of adults with this complication require insulin therapy.19 Effects of SIRS TN’s persistent fevers most likely were due to a severe form of SIRS (due to trypsin release with subsequent cytokine production). Inflammatory states are associated with temperature dysregulation,24 and a wide variety of nursing and medical interventions may be used to bring a patient’s temperatures to equilibrium. Another effect of SIRS is pulmonary edema, which TN experienced. The mixed respiratory-metabolic acidosis most likely CriticalCareNurse Vol 34, No. 4, AUGUST 2014 49 was due to this combination of SIRS, dehydration, atelectasis, and pulmonary edema. Long-Term Considerations Although many health care providers use the term chronic pancreatitis when a patient has recurrent episodes of pancreatitis over a prolonged period, some experts disagree. Some define chronic pancreatitis as a state of irreversible changes in the pancreas that can occur without a previous episode of acute pancreatitis. They recommend that Nurses must maintain an active role in ensuring the diagthat the families of children with pancreatitis nosis of obtain the resources needed. chronic pancreatitis not be made until imaging studies show chronic changes to the pancreas, such as ductal and parenchymal changes.10 Because of the high incidence of pancreatitis in patients with cystic fibrosis25 (and other genetic disorders), additional testing may include a genetic workup and stool fat assessments to detect fat malabsorption.7 Case Review: Subsequent Admissions During the next 3 months, TN required 3 more admissions to the PICU. Each admission lasted between 6 and 14 days. The main clinical problems in each readmission were pain, increased output from the external pancreatic drain, agitation, insulin maintenance, and diet management. Difficulty in diet management (feeding through a gastrojejunal tube) was a marked problem mainly because of TN’s developmental level; he could not comprehend why he could no longer consume food by mouth. He constantly wanted the oral satisfaction of eating food. His family managed the problem by keeping TN on a strict feeding regimen via the gastrojejunal tube while allowing minimal oral intake. The pseudocyst continued to produce output for 3 months after insertion of the drain. The drain was subsequently removed via interventional radiology during the second readmission; it had been in the pseudocyst for 56 days. TN’s last CT scan was performed 5 days after removal of the pseudocyst external drain. The size of the pseudocyst had decreased; it now measured 8 13 mm compared with 8 20 mm previously. The scan also showed minor atrophy of the pancreatic tail. Surrounding mesenteric edema and inflammatory changes were revealed, including a poorly defined fluid collection inferior to the pseudocyst, which was similar in size 50 CriticalCareNurse Vol 34, No. 4, AUGUST 2014 but more well-defined, suggestive of continuing but unremarkable pancreatic edema. After the third readmission, TN’s family was able to manage his home hydration, pain management, and low-fat diet regimen adequately. To date, TN continues to be fed through the gastrojejunal tube and is receiving oral antihyperglycemics daily for control of the diabetes associated with chronic pancreatitis and pseudocyst formation. However, TN’s hospital admissions have decreased in frequency, suggesting that the disease process is being successfully managed at home. Additional Considerations Consultation with a gastrointestinal service is appropriate in managing children with pancreatitis, not only because of the limited evidence available on the management of this condition in children but also because of the common occurrence of comorbid conditions (eg, cystic fibrosis), especially in infants and younger children.11 Critical care nurses will play a key role in coordinating these services and ensure that patients and patients’ family members are involved in care decisions. Nurses are instrumental in ensuring that a holistic approach is used every time a child with pancreatitis is treated. The multifaceted and interdisciplinary approach to the wide array of problems associated with pancreatitis can potentially leave these children and their families feeling overwhelmed. Therefore, nurses must maintain an active role in ensuring that the families obtain the resources needed. Normality and consistency are essential for continued success in the home setting; hence, accurate care plans allow for appropriate streamlined care for these patients (see Table 6 for a sample nursing care plan for TN). Families and patients need to feel comfortable with their chosen health care institutions, and as pancreatitis becomes more prevalent in children, education becomes more important. CCN Financial Disclosures None reported. Now that you’ve read the article, create or contribute to an online discussion about this topic using eLetters. Just visit www.ccnonline.org and select the article you want to comment on. In the full-text or PDF view of the article, click “Responses” in the middle column and then “Submit a response.” To learn more about pediatric care, read “The KIDS SAFE Checklist for Pediatric Intensive Care Units” by Ullman et al in the American Journal of Critical Care, January 2013;22:61-69. Available at www.ajcconline.org. www.ccnonline.org Table 6 Treatment focus, related to Sample nursing care plan Subjective/objective data Nutrition assurance Interventions Nursing diagnosis: imbalanced nutrition (less than body requirements) Inability to ingest food (because of pain) Inability to digest food (because of pancreatic exocrine dysfunction) Increased metabolic needs (because of acute illness and fever) Dehydration correction Presence of pain Constipation Hypoactive bowel sounds Hyperthermia Assess pain (refer to acute pain diagnosis) Assess temperature (refer to hyperthermia diagnosis) Assess bowel sounds Maintain parenteral and/or enteral nutrition If enteral tube present, assess and maintain patency Encourage oral intake once diet is resumed Assess tolerance of oral intake Nursing diagnosis: fluid volume, deficient Decreased fluid intake (because of pain) Increased insensible fluid loss (because of acute illness and fever) Pain management Tachycardia Hypotension Decreased urine output Monitor vital signs and urine output Assess and maintain patency of intravenous catheters Administer intravenous fluids, including boluses Report abnormal serum concentrations of sodium, creatinine, and pH Encourage oral intake once diet is resumed Nursing diagnosis: acute pain Pancreatic edema, inflammation, and irritation Pain scales (verbal and/or nonverbal cues) Assess pain routinely, after interventions for pain relief, and after changes in oral intake Administer routine and as-needed analgesics, as prescribed Notify prescribing provider of unmanageable pain Provide nonpharmacological pain interventions (eg, play and/or distraction) Nursing diagnosis: risk for ineffective family therapeutic regimen management Coordination of care Complexity of care regimen Excessive demands on patient’s family members Multiple prescribed medications Patient’s unique diet regimen Frequent clinic visits Assess knowledge of medication use and administration, teaching when appropriate Assess knowledge of and skill at enteral tube feeding, teaching when appropriate Assess financial and transportation resources of patient’s family (if assistance needed, explore available social programs) Combine multiple clinic visits into the same day Interventions for adverse events and other complications Nursing diagnosis Intervention Hyperthermia (associated with systemic inflammatory response syndrome) Assess body temperature Maintain cool environment through use of fans, cooling blankets, ice packs, etc Administer antipyretics, as ordered Risk for ineffective breathing pattern (related to hyperventilation associated with pulmonary edema) Assess respiratory rate, breath sounds, and ease of respiration Monitor pulse oximetry Administer oxygen, as ordered Risk for ineffective tissue perfusion (related to venous thromboembolism) Assess pulses and capillary refill in all extremities Assess respiratory rate, breath sounds, and ease of respiration Encourage and assist with ambulation and range-of-motion activities Administer antithrombotic medications, as ordered Risk for infection (related to pancreatic inflammation) Assess body temperature Report abnormal serum white blood cell counts Administer antibiotics, as ordered References 1. Stanfield C. Endocrine system. In: Principles of Human Physiology. 5th ed. Boston, MA: Pearson; 2013:504-530. 2. Nydegger A, Heine RG, Ranuh R, Gegati-Levy R, Crameri J, Oliver MR. www.ccnonline.org Changing incidence of acute pancreatitis: 10-year experience at the Royal Children’s Hospital, Melbourne. J Gastroenterol Hepatol. 2007;22(8): 1313-1316. 3. Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute CriticalCareNurse Vol 34, No. 4, AUGUST 2014 51 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 52 pancreatitis at an American pediatric tertiary care center: is greater awareness among physicians responsible? Pancreas. 2010;39(1):5-8. Yadav D, Lowenfels AB. Trends in the epidemiology of the first attack of acute pancreatitis: a systematic review. Pancreas. 2006;33(4):323-330. Bhatia M, Wong FL, Cao Y, et al. Pathophysiology of acute pancreatitis. Pancreatology. 2005;5(2-3):132-144. Bai HX, Lowe ME, Husain SZ. What have we learned about acute pancreatitis in children? J Pediatr Gastroenterol Nutr. 2011;52(3):262-270. Srinath AI, Lowe ME. Pediatric pancreatitis. Pediatr Rev. 2013;34(2):79-90. Meyer A, Coffey MJ, Oliver MR, Ooi CY. Contrasts and comparisons between childhood and adult onset acute pancreatitis. Pancreatology. 2013;13(4):429-435. Angelman Syndrome Foundation. Medical information. http://www .angelman.org/understanding-as/medical-info/. Published 2012. Accessed April 25, 2014. Morinville VD, Husain SZ, Bai H, et al; INSPPIRE Group. Definitions of pediatric pancreatitis and survey of present clinical practices. J Pediatr Gastroenterol Nutr. 2012;55(3):261-265. Park AJ, Latif SU, Ahmad MU, et al. A comparison of presentation and management trends in acute pancreatitis between infants/toddlers and older children. J Pediatr Gastroenterol Nutr. 2010;51(2):167-170. di Sebastiano P, di Mola FF, Bockman DE, Friess H, Büchler MW. Chronic pancreatitis: the perspective of pain generation by neuroimmune interaction. Gut. 2003;52(6):907-911. Carcillo J, Tasker R. Fluid resuscitation of hypovolemic shock: acute medicine’s great triumph for children. Intensive Care Med. 2006;32(7): 958-961. Helm JF, Venu RP, Geenen JE, et al. Effects of morphine on the human sphincter of Oddi. Gut. 1988;29(10):1402-1407. Wu B, Conwell D. Acute pancreatitis, I: approach to early management. Clin Gastroenterol Hepatol. 2010;8(5):410-416. Benner KW, Durham SH. Meperidine restriction in a pediatric hospital. J Pediatr Pharmacol Ther. 2011;16(3):185-190. Martindale RG, McClave SA, Vanek VW, et al; American College of Critical Care Medicine; A.S.P.E.N. Board of Directors. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: executive summary. Crit Care Med. 2009;37(5):1757-1761. Al-Omran M, Albalawi Z, Tashkandi M, Al-Ansary L. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev. 2010;(1):CD002837. doi:10.1002/14651858.CD002837.pub2. Wu B, Conwell D. Acute pancreatitis, II: approach to follow-up. Clin Gastroenterol Hepatol. 2010;8(5):417-422. Dellinger RP, Levy MM, Rhodes A. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580-637. Jackson W. Pancreatitis: etiology, diagnosis, and management. Curr Opin Pediatr. 2011;13:447-451. Park A, Latif SU, Shah AU, et al. Changing referral trends of acute pancreatitis in children: a 12-year single-center analysis. J Pediatr Gastroenterol Nutr. 2009;49(3):316-322. Stringer MD, Davison SM, McClean P, et al. Multidisciplinary management of surgical disorders of the pancreas in childhood. J Pediatr Gastroenterol Nutr. 2005;40(3):363-367. Romanovsky AA, Almeida MC, Aronoff DM, et al. Fever and hypothermia in systemic inflammation: recent discoveries and revisions. Front Biosci. 2005;10:2193-2216. Bronstein MN, Sokol RJ, Abman SH, et al. Pancreatic insufficiency, growth, and nutrition in infants identified by newborn screening as having cystic fibrosis. J Pediatr. 1992;120(4, pt 1):533-540. CriticalCareNurse Vol 34, No. 4, AUGUST 2014 www.ccnonline.org CNE Test Test ID C1442: Pancreatitis in Children Learning objectives: 1. Describe the common etiologies and diagnostic criteria for a child with pancreatitis 2. State common nursing and medical interventions for the child with pancreatitis 3. List complications experienced by the child with pancreatitis 1. Which of the following laboratory tests best reflect pancreatic function? a. Trypsin and elastase b. Amylase and lipase c. Total bilirubin and lipase d. Direct bilirubin and lipase 8. At the time of the second admission for TN, CT findings were suggestive of what complication? a. Transaminitis c. Hydronephrosis b. Hypersplenism d. Pancreatic pseudocyst 9. Which laboratory value illustrates endocrine dysfunction experienced by TN? a. Blood glucose level of 300 mg/dL b. Sodium level of 140 mmol/L c. Lipase level of 10 U/L d. Aspartate aminotransferase level of 30 U/L 2. Which medication is associated with causing pancreatitis? a. Clindamycin c. Regular insulin b. Lasix d. Valproic acid 3. The diagnosis of pancreatitis could be made for which patient? a. 8 year old reporting abdominal pain b. 14 year old with jaundiced sclera and elevated lipase level c. 6 year old with an elevated amylase level, abdominal pain, and pancreatic edema on computed tomography (CT) scan d. 17 year old with abdominal pain and elevated white blood cell count 10. What was the most likely cause of TN’s persistent fevers? a. Urinary tract infection b. Systemic inflammatory response syndrome c. Lack of trypsin release d. Pancreatic-cell function 4. The most common symptom of pancreatitis in children is what manifestation? a. Vomiting c. Fever b. Jaundice d. Pain or irritability 11. The authors contend that the multiple readmissions were most likely attributable to which of the following? a. Inadequate discharge planning b. Insulin resistance c. Poor oral intake d. Developmental level 5. Pain management would be best achieved with what medication? a. Fentanyl c. Demerol b. Morphine d. Tylenol 12. What nursing intervention would be part of the nursing care plan for TN? a. Pain assessment and management b. Intracranial pressure assessment and management c. Wound assessment and management d. Assessment and management of external drain 6. Clear liquids have been prescribed for a child with pancreatitis; as the nurse caring for the child, you would report what symptom of concern? a. Normal blood glucose level, as would expect hypoglycemia b. Abdominal pain, as this can recur from pancreatic stimulation c. Normoactive bowel sounds, as you would expect hypoactive bowel sounds d. Normal lipase level, as would expect it to be elevated 13. Assessment findings indicating that TN has a fluid volume deficit would include which of the following? a. Urine output of 2 mL/kg per hour and hypotension b. Urine output of 1 mL/kg per hour, fever, and hypotension c. Urine output of 0.3 mL/kg per hour, hypotension, and tachycardia d. Pulmonary edema, tachycardia, and hypotension 7. Which symptoms indicate recurrent pancreatitis? a. Abdominal pain with elevated amylase and lipase levels 2 weeks after the initial diagnosis b. Abdominal pain with elevated amylase level following a pain-free month c. Vomiting with elevated lipase level 3 weeks after the initial diagnosis d. A child experiencing 2 weeks of no abdominal pain with pain recurrence Test answers: Mark only one box for your answer to each question. You may photocopy this form. 1. a b c d 2. a b c d 3. a b c d 4. a b c d 5. a b c d 6. a b c d 7. a b c d 8. a b c d 9. a b c d 10. a b c d 11. a b c d 12. a b c d 13. a b c d Test ID: C1442 Form expires: August 1, 2017 Contact hours: 1.0 Pharma hours: 0.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 10 correct (77%) Synergy CERP Category A Test writer: Sarah A. Martin, RN, MS, CPNP-AC/PC, CCRN Name Program evaluation Yes For faster processing, take this CNE test online at www.ccnonline.org or mail this entire page to: AACN, 101 Columbia Aliso Viejo, CA 92656. Objective 1 was met Objective 2 was met Objective 3 was met Content was relevant to my nursing practice My expectations were met This method of CNE is effective for this content The level of difficulty of this test was: easy medium difficult To complete this program, it took me hours/minutes. No Member # Address City State Country ZIP Phone E-mail RN Lic. 1/St Payment by: Card # RN Lic. 2/St Visa M/C AMEX Discover Check Expiration Date Signature The American Association of Critical-Care Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. AACN has been approved as a provider of continuing education in nursing by the State Boards of Nursing of Alabama (#ABNP0062), California (#01036), and Louisiana (#ABN12). AACN programming meets the standards for most other states requiring mandatory continuing education credit for relicensure.
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