March 2017 FAQs

What evidence evaluates the use of procalcitonin to guide antibiotic duration in patients with hospital-acquired or ventilator-associated pneumonia?

The use of procalcitonin (PCT) as a predictive biomarker has evolved over the last 25 years since it was first noted to be elevated in patients with bacterial infections.¹ Procalcitonin is a precursor of calcitonin which is secreted by C cells in the thyroid and K cells of the lung as well as other organs such as the liver, kidney, and small intestine.^2-4 Levels have been shown to increase within 6 to 12 hours of bacterial infection and, importantly, PCT is usually not increased in patients with viral infection.

The use of PCT as an acute phase reactant indicative of bacterial infection has been evaluated in various infection types including those of the lung, heart, abdomen, and blood.^1-3 Among the recent updates to the hospital-acquired or ventilator-associated pneumonia (HAP/VAP) guidelines by the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) were recommendations for the use of PCT levels. The IDSA/ATS guidelines recommend that PCT levels should not be included in the decision of antibiotic initiation; however, they did make a weak recommendation for their use to assist in determining discontinuation of antibiotic therapy.⁴ This FAQ will evaluate the evidence for the use of PCT levels for antibiotic discontinuation in patients with HAP/VAP.

Literature evaluation

Meta-analyses have evaluated the use of PCT levels as a guide for antibiotic discontinuation in patients with pneumonia. Schuetz et al identified 14 trials that evaluated PCT-guided algorithms for either antibiotic initiation or discontinuation in 4221 patients with acute respiratory infections.^5,6 The majority of patients (48%) enrolled were diagnosed with community acquired pneumonia (CAP), 6% had VAP, less than 2% had HAP and the remaining subjects were diagnosed with upper respiratory infections such as common cold, rhino-sinusitis, pharyngitis, or tonsillitis. The study found no significant difference in mortality rates between the PCT group and the control group (5.7% vs. 6.3%; adjusted odds ratio [OR] 0.94; 95% confidence interval [CI], 0.71 to 1.23). However, patients treated based on PCT algorithms were at significantly lower risk for treatment failure compared to patients in the control group (19.1% vs. 21.9%; adjusted OR 0.82; 95% CI, 0.71 to 0.97). Patients in the PCT group also had approximately 3.5 fewer days of antibiotic exposure. The authors concluded that PCT-guided algorithms are safe and effective for reducing antibiotic exposure in patients with acute respiratory infections.

A 2011 meta-analysis included 3 studies that evaluated the use of PCT guidance on duration of antibiotic exposure in patients with HAP as part of a larger meta-analysis.⁷ Antibiotic therapy was significantly shorter (9.1 days vs. 12.1 days) in patients who were treated with PCT guidance. Mortality at 28 days (OR 0.66; 95% CI, 0.39 to 1.14), in-hospital mortality (OR 0.63; 95% CI, 0.25 to 1.58), and intensive care unit (ICU) mortality (OR 0.76; 95% CI, 0.26 to 2.22) were similar in the PCT-guided therapy group and the standard-therapy group. Pneumonia recurrence rates were increased in the PCT-based group compared to the standard group, but the results were not statistically significant (OR 2.06; 95% CI, 0.74 to 5.7).

Two randomized trials have investigated the effects of PCT-guided therapy on antibiotic duration in adults with HAP/VAP. The PRORATA trial was a prospective, multicenter, parallel-group, randomized, open-label trial.⁸ The main objective of the study was to determine whether a PCT-based treatment strategy for initiating and discontinuing antibiotics would result in reduced antibiotic exposure. In the PCT-guided group, antibiotic discontinuation occurred when the PCT level was less than 80% of the peak concentration or an absolute level less than 0.5 µg/L. The study included 630 ICU patients with suspected bacterial infections; however, the majority of patients in the study (over 70%) had pulmonary infections. Primary endpoints for the trial were death from any cause at 28 and 60 days, and the number of antibiotic-free days at 28 days after randomization. At 28 and 60 days the incidence of the primary outcome was similar between the PCT-guided treatment algorithm and the control group.  Mortality at 28 days was 21.2% in the PCT group vs. 20.4% in the control group (adjusted OR 0.89; 90% CI, 0.62 to 1.28) and 30% vs. 26.1% at 60 days (OR 1.09; 90% CI, 0.79 to 1.51). The PCT-guided group had more days without antibiotics at 28 days (14.3 vs. 11.6; p<0.0001).

Stolz and colleagues conducted a smaller, multicenter, randomized, open-label trial in 101 adult patients with documented VAP.⁹ Patients were randomized to either a PCT-guided antibiotic strategy or traditional antibiotic discontinuation guidelines. In the PCT-guided group, antibiotic discontinuation was “strongly encouraged” when PCT levels were under 0.25 µg/L. Discontinuation or reduction of antibiotics was “encouraged” when the PCT level was between 0.25 and 0.5 µg/L or there was at least an 80% decrease from baseline. Continuation of antibiotics was “encouraged” when PCT levels were 0.5 µg/L or greater or there was less than an 80% reduction in levels from day 0. The primary outcome for the study was the number of antibiotic-free days alive at 28 days after randomization. Patients in the PCT-guided group had significantly more antibiotic-free days alive than patients in the control group (13 vs. 9.5; p=0.049). There was a 27% reduction in antibiotic therapy duration in the PCT-guided group (15 vs. 10 days; p=0.038). Antibiotics were continued for more than 7 days in 82% of patients in the control group and in 65% of patients in the PCT group (p=0.044). Additionally, patients who died during hospitalization had significantly higher PCT levels compared to those who survived. This may be suggestive of a correlation between PCT levels and the severity of the disease.

Discussion

Pneumonia is a common nosocomial infection associated with significant mortality. Patients with HAP/VAP infections often require prolonged hospitalization and treatment with broad-spectrum antibiotics which are associated with significant adverse events. There are no clear and well-defined guideline recommendations regarding the duration of antibiotic therapy in HAP/VAP patients. Biomarkers such as PCT may be a useful aid in determining the appropriate duration of antibiotic therapy. Based on the data from the primary literature described above, PCT-guided algorithms result in reduction of antibiotic exposure without an increase in mortality. However, the trials evaluating PCT-guided therapy have a number of shortcomings associated with study design, patient population included, and issues with adherence to prespecified treatment protocols. One of the major limitations reported was non-adherence to PCT-based algorithms by the investigators. Also, the choice of antibiotic and antibiotic duration was left to the discretion of the investigator or attending physician which leads to inconsistency and potential bias. Based on the data in this review, PCT-guided discontinuation of antibiotics may be beneficial to decrease the duration of antibiotics which could reduce antibiotic resistance and minimize toxicities associated with these therapies. Larger and more robust trials are needed to explore the overall clinical benefit of utilizing PCT as a biomarker for patients with HAP/VAP.

References

1. Maruna P, Nedelníková K, Gürlich R. Physiology and genetics of procalcitonin. Physiol Res. 2000;49(Suppl 1):S57-S61.
2. Manasia A, Narimasu J. Biomarkers in decision making. In: Oropello JM, Pastores SM, Kvetan V, eds. Critical Care. New York, NY: McGraw-Hill; 2016. http://accessmedicine.mhmedical.com/content.aspx?bookid=1944&sectionid=143515798. Accessed February 07, 2017.
3. Gilbert DN. Procalcitonin as a biomarker in respiratory tract infection. Clin Infect Dis. 2011;52(Suppl 4):S346-S350.
4. Kalil AC, Metersky ML, Klompas M, et al. Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis. 2016;63(5):e61-111.
5. Schuetz P, Briel M, Christ-Crain M, et al. Procalcitonin to guide initiation and duration of antibiotic treatment in acute respiratory infections: an individual patient data meta-analysis. Clin Infect Dis. 2012;55(5):651-662.
6. Schuetz P, Muller B, Christ-Crain M, et al. Procalcitonin to initiate or discontinue antibiotics in acute respiratory tract infections. Cochrane Database Syst Rev. 2012;(9):CD007498.
7. Pugh R, Grant C, Cooke RP, Dempsey G. Short-course versus prolonged-course antibiotic therapy for hospital-acquired pneumonia in critically ill adults. Cochrane Database Syst Rev. 2011;(10):CD007577.
8. Bouadma L, Luyt CE, Tubach F, et al. Use of procalcitonin to reduce patients' exposure to antibiotics in intensive care units (PRORATA trial): a multicenter randomized controlled trial. Lancet. 2010;375(9713):463-474.
9. Stolz D, Smyrnios N, Eggimann P, et al. Procalcitonin for reduced antibiotic exposure in ventilator-associated pneumonia: a randomized study. Eur Respir J. 2009;34(6):1364-1375.

Prepared by:

Tetyana Melnyk, PharmD

PGY1 Pharmacy Practice Resident

College of Pharmacy

University of Illinois at Chicago

March 2017

The information presented is current as of January 16, 2017. This information is intended as an educational piece and should not be used as the sole source for clinical decision-making.

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What is the usual clinical presentation, diagnosis, and management of norovirus infection?

Introduction

Noroviruses are a group of nonenveloped, single-stranded ribonucleic acid (RNA) viruses that are currently one of the leading causes of gastroenteritis globally.^1-3 In the United States, approximately 21 million cases of norovirus infection occur annually resulting in > 70,000 hospitalizations and 800 deaths.^2,3 As with many infectious diseases, the elderly, young children, and immunocompromised patients tend to be the most severely affected by norovirus.^4,5 The virus is extremely contagious and is spread through a variety of mechanisms including aerosol dispersal following vomiting, direct contact with infected individuals or contaminated surfaces, and the fecal-oral route.⁵ A majority of norovirus outbreaks reported in the media are due to this final transmission route via an infected food handler or through contamination with human waste in the food distribution system, as has been most notably seen with outbreaks involving oysters or raspberries.¹ Norovirus outbreaks occur in many settings but are most commonly observed where there are high levels of person-to-person contact and potentially compromised hygiene such as schools, child care centers, prisons, cruise ships, restaurants, long-term care facilities, and hospitals.^1,5 Although an outbreak can occur at any time, a seasonal pattern of increased activity during the winter months is well documented.¹ 

Clinical Presentation

Although norovirus infection can be asymptomatic, particularly in children, the onset of symptomatic disease is usually quite abrupt.^1,6 The illness generally begins following a 12 to 48 hour incubation period.¹ Diarrhea (90%), vomiting (75%), nausea, and abdominal cramps are commonly observed and may be quite severe in nature.^1,6,7 Patients may also report body aches, headache, chills and a low grade fever.  Due to these symptoms, norovirus infection is often referred to as the “stomach flu”, although there is no biologic association between influenza and norovirus.¹ Symptom resolution typically happens within 1 to 3 days in healthy individuals, but prolonged symptomatic infection lasting 4 to 6 days may occur in at risk patients such as young children, the elderly, and hospitalized patients. Fatalities associated with norovirus infection are rare; however, severe norovirus-related effects have been reported including necrotizing enterocolitis in neonates, chronic diarrhea in immunosuppressed patients, and postinfectious irritable bowel syndrome.

Diagnosis

Rapid identification of norovirus is key to management of the disease process particularly in outbreak settings.⁶ Currently, most public health and clinical virology laboratories use the real-time reverse transcription-polymerase chain reaction (RT-qPCR) assay as the “gold standard” for norovirus detection.^4,6 The RT-qPCR assay is extremely sensitive (detecting as few as 10 to 100 norovirus copies per reaction),  provides an approximation of viral load, and detects the virus in a variety of specimens (eg, vomit, foods, and water).⁴ An assortment of enzyme immunoassays (EIAs) are also commercially available.⁶ Although EIAs detect norovirus antigen, these assays have limited sensitivity (50 to 75%) and are not recommended for routine diagnosis of sporadic norovirus cases.⁴ Although the RT-qPCR assay establishes a definitive norovirus diagnosis, access to this diagnostic method may be limited in some settings. In these situations, clinicians may utilize Kaplan’s criteria (Table 1) to distinguish outbreaks of gastroenteritis caused by noroviruses from those caused by bacteria.

Table 1.  Kaplan’s criteria for norovirus outbreaks.^6,8

Management

In order to control unfettered transmission of the norovirus, appropriate hand hygiene remains of utmost importance.¹ The 2011 Centers for Disease Control and Prevention (CDC) updated norovirus outbreak management and disease prevention guideline recommends “thorough hand washing with running water and plain or antiseptic soap” for at least 20 seconds. The utilization of alcohol-based and other hand sanitizers against norovirus remains controversial. Currently, the CDC guideline states that these products may serve as effective adjuncts in between proper hand washings with soap and water, but should not be considered substitutes.

Beyond hand washing, isolating infected individuals is another vital mechanism for breaking the norovirus transmission cycle.^1,5 This is especially important in outbreaks involving facilities where many people reside such as college dormitories, long term care facilities, and hospitals. In these settings, isolating infected patients in single occupancy rooms without shared toilet facilities may be an effective option to curtail transmission. Along with isolation, environmental disinfection of bathrooms and high-touch surfaces (eg, door knobs, hand rails) with sodium hypochlorite (chlorine bleach) is strongly recommended.¹ 

As of now, there is no specific treatment for norovirus infection; dehydration is the most commonly reported complication that may require medical assistance.⁴ Severe dehydration from diarrhea and vomiting may require treatment with intravenous fluids or oral rehydration. Additionally, electrolytes should be monitored closely and corrected if disturbances are found.  Older children and adults may benefit from antimotility agents in conjunction with rehydration, but these agents should be avoided in children < 3 years of age. The administration of antiemetics should generally be limited to adults only. Additionally, antibiotic therapy is of no benefit in treating norovirus infection.

A variety of antivirals are under development for the treatment of norovirus due to the potentially serious complications of the disease in at risk populations.^5,9,10  These include nitazoxanide (a broad-spectrum anti-infective), favipravir (an investigational influenza antiviral), ribavirin, and a wide assortment of nucleoside analogues, protease inhibitors, entry inhibitors, and other compounds.¹⁰ Vaccine development is also underway and recently took a major step forward when the human norovirus was successfully grown in a laboratory for the first time.¹¹

Conclusion

Norovirus is an extremely contagious infection that spreads rapidly and is often seen in outbreak situations involving individuals who live in close quarters such as dormitories, long term care facilities, and hospitals. Although the disease process is fairly self-limiting in healthy people, young children, the elderly, and the immunocompromised may be particularly at risk for severe complications. No specific treatment of norovirus exists currently; the focus of clinical intervention is on appropriate rehydration. Additionally, proper hand washing, patient isolation, and environmental disinfection are key to halting the spread of norovirus. There are a number of investigational antivirals under development and vaccine progress took a major leap forward recently when human norovirus was successfully grown in a laboratory setting.

References

1. Division of Viral Diseases, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention. Updated norovirus outbreak management and disease prevention guidelines. MMWR Recomm Rep. 2011;60(RR-3):1-18.
2. Kambhampati A, Koopmans M, Lopman BA. Burden of norovirus in healthcare facilities and strategies for outbreak control. J Hosp Infect. 2015;89(4):296-301.
3. Arias A, Emmott E, Vashist S, Goodfellow I. Progress towards the prevention and treatment of norovirus infections. Future Microbiol. 2013;8(11):1475-1487.
4. Norovirus. Centers for Disease Control and Prevention website. https://www.cdc.gov/norovirus/. Accessed February 17, 2017.
5. Iturriza-Gomara M, Lopman B. Norovirus in healthcare settings. Curr Opin Infect Dis. 2014;27(5):437-443.
6. Robilotti E, Deresinski S, Pinsky BA. Norovirus. Clin Microbiol Rev. 2015;28(1):134-164.
7. Belliot G, Lopman BA, Ambert-Balay K, Pothier P. The burden of norovirus gastroenteritis: an important foodborne and healthcare-related infection. Clin Microbiol Infect. 2014;20(8):724-730.
8. Kaplan JE, Feldman R, Campbell DS, Lookabaugh C, Gary GW. The frequency of a Norwalk-like pattern of illness in outbreaks of acute gastroenteritis. Am J Public Health. 1982;72(12):1329-1332.
9. Pringle K, Lopman B, Vega E, Vinje J, Parashar UD, Hall AJ. Noroviruses: epidemiology, immunity and prospects for prevention. Future Microbiol. 2015;10(1):53-67.
10. Kaufman SS, Green KY, Korba BE. Treatment of norovirus infections: moving antivirals from the bench to the bedside. Antiviral Res. 2014;105:80-91.
11. Ettayebi K, Crawford SE, Murakami K, et al. Replication of human noroviruses in stem cell-derived human enteroids. Science. 2016 Aug 25. doi 10.1126/science.aaf5211.

March 2017

The information presented is current as February 2, 2017.  This information is intended as an educational piece and should not be used as the sole source for clinical decision-making.

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Which is the best method for administration of pancreatic enzyme replacement products by enteral feeding tube?

Introduction

Pancreatic enzyme replacement therapy (PERT) is recommended for patients with a variety of conditions that lead to pancreatic insufficiency, including chronic pancreatitis, pancreatic cancer, and cystic fibrosis.¹ Non-pancreatic causes of pancreatic insufficiency may also arise in patients with celiac disease, Crohn’s disease, diabetes mellitus, short bowel syndrome, or history of gastric surgery. Currently, available pancreatic enzyme replacement products include Creon^®, Pancreaze^®, Pertzye^®, Ultresa^®, Viokace^®, and Zenpep^®.^2-6 With the exception of Viokace, all of the other agents are formulated as capsules that contain amylase, lipase, and protease microspheres surrounded by an enteric coating. The enteric coating shields the microspheres from gastric acid in the stomach, allowing them to remain intact until they reach the duodenum.⁷ In the duodenum, the alkaline environment dissolves the enteric coating and activates the enzymes. While Viokace contains the same enzymes, this agent is formulated as a tablet without an enteric coating and requires co-administration with a proton pump inhibitor (PPI).⁸

Appropriate timing and administration technique are fundamental components of successful PERT, as these biologically active agents work in conjunction with administered macronutrients.⁷ Without effective PERT, patients with pancreatic insufficiency may suffer from malnutrition as a result of the malabsorption of dietary fat, protein, and other nutrients.⁹ For these reasons, patients who have an enteral feeding tube present an additional challenge in relation to the effective administration of PERT.

Currently, there is no best practice guidance for administering PERT via enteral feeding tubes. The 2009 American Society for Parenteral and Enteral Nutrition (ASPEN) enteral nutrition practice guideline specifically mention an increased risk of enteral tube clogs with enteric coated products that are crushed and diluted with water.¹⁰ In regards to patients with cystic fibrosis, a 2001 consensus report states that further research is needed in order to define appropriate dosing and optimal method of administration of PERT with enteral feedings.⁹ It is well known that the administration of drugs through feeding tubes is prone to drug errors as a result of improper absorption, preparation, and administration of products.¹¹ Therefore, patients with pancreatic insufficiency who are receiving enteral tube feedings are vulnerable to experiencing delays in therapy or receiving inappropriate therapy. The remainder of this review will summarize published literature and manufacturer-provided recommendations for the administration of PERT via enteral feeding tubes.

General recommendations

The size of the feeding tube, its position in the gut, and the type of feeding regimen should all be considered prior to administering PERT by an enteral feeding tube, as these factors can significantly impact absorption and tube blockage.¹² An overview of the administration of enteric-coated PERT products through a gastrostomy tube (G-tube) is provided in Table 1.^7,11,12,14 Although some tertiary drug information references recommend that capsule contents be dispersed in water immediately prior to administration, enteric-coated medications are susceptible to increased adhesiveness when combined in this manner.^13,14 Therefore, mildly thickened fruit juice is recommended over water for suspension of capsule contents, as it has shown to be less likely to clump and clog tubes.¹² Clogging can also be caused by the interaction between the acidic juice and the feed formula; therefore, tubes should be flushed with 15 to 30 mL water before and after administration.^12,14,15 If other medications are provided via feeding tube, they should be administered separately, and the tube should be flushed with 5 to 30 mL of water between each individual administration.¹⁵ In general, PERT should be provided before and immediately after each bolus feed.¹⁴ For patients receiving continuous feeds, therapy should be provided at the beginning of the feed and at regular intervals thereafter.

Table 1. Instructions for the administration of enteric-coated PERT products through a G-tube.*^7,11,12,14

Instructions for administration of enteric-coated PERT via a duodenal or jejunal feeding tube are provided in Table 2.¹² Generally, sodium bicarbonate is utilized to compound an activated enzyme solution when administering PERT via feeding tubes placed in these locations. Some enzyme activity is likely to be lost as a result of this preparation; therefore, PERT dosage may need to be adjusted to compensate. Of note, the dissolution of enteric-coated granules in sodium bicarbonate varies with each specific PERT product and dose.⁷ In a 2015 study, several PERT products were dissolved in 20 mL of an 8.4% sodium bicarbonate solution and evaluated for their ability to successfully dissolve at pre-specified time points. After 30 minutes, both Zenpep^® 20,000 and 40,000 lipase unit doses were completely dissolved. Investigators noted that success with both doses might have been due to the consistent size of the granules along with a visibly thinner and uniform enteric coating. The only dose of Creon^® and Ultressa^® that was completely dissolved after 30 minutes was the 24,000 and 23,000 lipase unit dose, respectively. None of the doses of Pancreaze^® were completely dissolved at 30 minutes.

Table 2. Instructions for the administration of enteric-coated PERT products by a duodenal or jejunal feeding tube.^12,14

Activated enzyme solutions have also been mixed directly with enteral feeding formulas, although published literature related to this practice is mostly limited to the neonatal and pediatric patient populations.^9,12 This method of administration also poses a risk for the granules to clump together or become activated in the enteral formula container, increasing the risk for tube obstruction and premature digestion of nutrients.¹³ For patients with sufficient gastric acid suppression, such as those receiving a PPI, it may be possible to give an activated enzyme solution via a G-tube in a similar method to that which would be given via a duodenal or jejunal feeding tube; this method may be preferred for small-bore feeding tubes that are likely to be clogged with whole microspheres.¹²

Product specific recommendations

The Food and Drug Administration approved product labeling does not include recommendations for administering PERT via an enteral feeding tube for any of the currently available products. However, some manufacturers provide off-label guidance for administration. Table 3 provides a summary of information gathered from published literature and personal communication with PERT manufacturers.^13,16-18 The full-text for each citation should be consulted for further information related to specific enteral formulas and infusion equipment (eg, pumps, tubing). Of note, some of the published product-specific data involves the preparation of an activated-enzyme product.¹³ Consideration should be given to whether or not the intended recipient is a candidate for this type of therapy. If not, the guidance for general administration of enteric-coated PERT products should be consulted (see General recommendations).

Table 3. Product specific data for PERT administration via feeding tubes.^13,16-18

Remarks

Successful administration of PERT through a feeding tube has been reported for the following products: Creon^®, Pancreaze^®, Pertzye^®, Viokace^®, and Zenpep^®. Administration of Ultressa^® may be done by following the general recommendations for administration of enteric-coated PERT products via G-tube (see General recommendations). While published data and product manufacturers propose several methods for PERT administration through feeding tubes, each present unique challenges and none should be considered “ideal.” Nonetheless, mixing capsule contents or tablet with a diluent solution and administering through a large bore feeding tube generally leads to successful administration. Additional research is warranted in order to gain further insight into clinical outcomes and pharmacokinetic changes with alternate methods of PERT administration.

References:

1.         Struyvenberg MR, Martin CR, Freedman SD. Practical guide to exocrine pancreatic insufficiency – Breaking the myths. In: BMC Med. 2017;15(29):1-8.

2.         Creon [package insert]. North Chicago, IL: Abbvie, Inc.; 2017.

3.         Pancreaze [package insert]. Titusville, NJ: Janssen Pharmaceuticals, Inc.; 2016.

4.         Pertzye [package insert]. Bethlehem, PA: Digestive Care, Inc.; 2016.

5.         Ultresa [package insert]. Bridgewater, NJ: Aptalis Pharma US, Inc.; 2014.

6.         Zenpep [package insert]. Bridgewater, NJ: Aptalis Pharma US, Inc.; 2014.

7.         Boullata AM, Boullata JI. Pancreatic enzymes prepared in bicarbonate solution for administration through enteral feeding tubes. Am J Health Syst Pharm. 2015;72(14):1210-1214.

8.         Viokace [package insert]. Birmingham, AL: Aptalis Pharma US, Inc.; 2014.

9.         Borowitz D, Baker RD, Stallings V. Consensus report on nutrition for pediatric patients with cystic fibrosis. J Pediatr Gastroenterol Nutr. 2002;35(3):246-259.

10.       Bankhead R, Boullata J, Brantley S, et al. Enteral nutrition practice recommendations. JPEN J Parenter Enteral Nutr. 2009;33(2):122-167.

11.       Boullata JI. Drug administration through an enteral feeding tube. Am J Nurs. 2009;109(10):34-42; quiz 43.

12.       Ferrie S, Graham C, Hoyle M. Pancreatic enzyme supplementation for patients receiving enteral feeds. Nutr Clin Pract. 2011;26(3):349-351.

13.       Nicolo M, Stratton KW, Rooney W, Boullata J. Pancreatic enzyme replacement therapy for enterally fed patients with cystic fibrosis. Nutr Clin Pract. 2013;28(4):485-489.

14.       White R, Bradnam V. Handbook of drug administration via enteral feeding tubes. London: Pharmaceutical Press; 2007.

15.       Wohlt PD, Zheng L, Gunderson S, Balzar SA, Johnson BD, Fish JT. Recommendations for the use of medications with continuous enteral nutrition. Am J Health Syst Pharm. 2009;66(16):1458-1467.

16.       Hollander S, Harrington E, Woo MS. What g-tube size is required for successful administration of enteric-coated  pancreatic enzymes beads? Pediatr Pulmonol. 2015;50(suppl 41):S193-453. Abstract 568.

17.       Severson M, Phillips J. Flow characteristics of three different pancrelipase pellets through a gastrostomy feeding  tube. Pediatr Pulmonol. 2015;50(suppl 41):S193-453. Abstract 585.

18.       Shlieout G, Koerner A, Maffert M, Forssmann K, Caras S. Administration of CREON® pancrelipase pellets via gastrostomy tube is feasible with no loss of gastric resistance or lipase activity: an in vitro study. Clin Drug Investig. 2011;31(7):e1-7.

March 2017

The information presented is current as February 20, 2017. This information is intended as an educational piece and should not be used as the sole source for clinical decision-making. 

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