NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES

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Carol Rees Parrish, R.D., M.S., Series Editor Reinfusion of Intestinal Secretions: A Viable Option for Select Patients Carol Rees Parrish Beth Quatrara Fifteen to 20% of patients with pancreatitis will
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Carol Rees Parrish, R.D., M.S., Series Editor Reinfusion of Intestinal Secretions: A Viable Option for Select Patients Carol Rees Parrish Beth Quatrara Fifteen to 20% of patients with pancreatitis will go on to develop a severe or complicated course requiring nutrition support. A small percentage of these patients will have an ongoing gastric outlet obstruction from duodenal inflammation and compression requiring gastric decompression; a few might even need an external biliary drain for a time. Enteral jejunal feeding has been demonstrated to be superior to parenteral nutrition in this patient population. For those patients with pseudocyst development needing extended nutrition support ( 30 days), enteral nutrition can be achieved by way of jejunal access as nasojejunal, PEG/J, or separate PEG and surgical jejunostomy tubes. This article focuses on the hydration aspects of these patients and shares one institution's experience of reinfusing gastric and/or pancreatobiliary secretions to maintain absorption, hydration and electrolyte status in the patient s own home environment. CASE A57-year-old female was admitted with nausea and vomiting due to gastric outlet obstruction as a result of duodenal compression from pancreatitis. A large pseudocyst was noted on CT exam. She was to undergo ERCP for common bile duct stone removal with placement of percutaneous endoscopic gastrostomy with a jejunal arm (PEG/J) for nutrition support while the pseudocyst resolved. She was 5 7 Carol Rees Parrish MS, RD, Nutrition Support Specialist and Beth Quatrara RN, MSN, ACNS-BC, Advanced Practice Nurse, Digestive Health Center of Excellence, University of Virginia Health System, Charlottesville, VA. and weighed 118#, down from her usual body weight of 145#. She was considered severely malnourished and at refeeding risk. After her PEG/J placement she tolerated tube feeding well and was discharged home 4 days later on a 1.5 cal/ml, non-fiber containing enteral product, full strength, at 100mL per hour over 12 hours at night via her j-port. She initially required venting of her gastric secretions, but was able to clamp her g-port prior to discharge. She was readmitted 3 weeks later with the following laboratory results: Na 107 mmol/l BUN 11 mg/dl K 1.9 mmol/l Cr 0.5 mg/dl Cl 74 mmol/l Glucose 133 mg/dl CO 2 34 mmol/l (continued on page 28) 26 (continued from page 26) The patient had been placed on a liquid proton pump inhibitor prior to discharge, but did not take it regularly after she returned home. In addition, the patient began venting off her gastric secretions due to nausea and occasional vomiting once she was at home. When queried by the GI nurse coordinator, her husband reported venting and discarding, maybe 1 2 cups of gastric juice every day. (Nutrition Editors note: This reminds me of Bill Cosby s, I know what I mean when I say oops, but what do you mean when you say oops?! Not to generalize, but I have noticed over the years that men have a different concept of what a cup is usually it runs anywhere from oz. I keep kitchen measuring cups in our GI nutrition clinic so patients/caregivers can show me what they mean by the portions that they eat or drink). The patient was, in fact, venting off 1 2, 16 oz. cups ( ml) of fluid from her gastric port each day with occasional vomiting also. She ultimately required a percutaneous external biliary drainage tube due to an infected gallbladder and the surgeons wanted to wait until she was better nourished before she went to the OR for a cholecystectomy. Her biliary drainage tube was putting out an average of 600 ml/day. INTRODUCTION Pancreatitis is not only a very painful process; it can also significantly ravage one s nutritional status (see Table 1). Nutrition support is needed in approximately 15 20% of patients enduring a severe course of pancreatitis. Enteral nutrition (EN) support has been clearly shown to be superior to parenteral nutrition (PN) with reductions in mortality, multiple organ failure, systemic infections and the need for surgical interventions (2,3), with the majority favoring the nasojejunal route. If the patient has ongoing emesis, gastric decompression will be required to relieve the patient of nausea and vomiting. Vigorous fluid resuscitation is the mainstay of supportive therapy in acute pancreatitis to prevent or minimize pancreatic necrosis (4). Hyperglycemia, if not well-controlled, can not only thwart efforts at nutrition support, but also accelerate dehydration. In the hospital setting, intravenous fluids are readily available; because of this, there are a few select patients who might remain Table 1 Factors Associated with Nutritional Deficits in Pancreatitis Functional Inability to eat as a result of pain with food ingestion Gastric outlet obstruction due to duodenal compression from swollen pancreas Anatomical changes if surgery required (Whipple, etc.) Iatrogenic NPO for procedures/surgery Hospital Food Therapeutic hospital diets (insult to injury) Endocrine Poorly controlled hyperglycemia Exocrine Pancreatic insufficiency Malabsorption Steatorrhea Fat soluble vitamin loss Osteoporosis Vitamin D and calcium deficits Decrease in bicarbonate secretion Decrease normal pancreatic enzyme function due to inadequate rise in ph Decrease efficacy of exogenous enzymes enteric coated needs bicarbonate to be released Decrease efficacy of bile salts due to more acidic environment Medication Induced Acid reduction and Narcotics Predispose to small bowel bacterial overgrowth Constipation in the hospital because of problems caused by excess fluid loss from gastric decompression. Our case demonstrates the metabolic complications that can arise when patients have excessive loss Table 2. Secretion of Fluid within the Gastrointestinal Tract Source ml/24 hours Saliva Stomach Bile 1000 Pancreas 1000 Intestine 1000 Used with permission from (7) 28 Table 3. Fluid and Electrolyte Content of Gastrointestinal Secretions (meq/l) Body Fluid Na K HCO 3 H Cl ph Sweat Saliva Gastric Pancreas Bile Jejunum/Ileostomy Diarrhea Normal stool Used with permission from (8) Table 4. Electrolyte Content of IV Solutions / Liter IV Fluid Na K Chloride 0.9 NS* NS Lactated Ringers (LR) D 5 W D 5 W 0.45 NS Table 5. Causes of Pancreato-biliary Insufficiency or Deficiency Potential causes of Pancreatic enzyme deficiency or insufficiency Pancreatic cancers Severe acute or chronic pancreatitis Cystic fibrosis External loss of pancreatic secretions due to distal duodenal tumor compression or enterocutaneous fistula Gastric acid dumped into the upper gut can inhibit lipases activity as well as decreased bicarbonate secretion from the pancreas, both result in a lowering of the luminal ph thereby affecting enzyme function. Potential causes of bile salt deficiency or insufficiency Primary biliary cirrhosis Primary sclerosing cholangitis Cirrhosis Cholestatic processes External biliary drains Gastric hypersecretion Small bowel bacterial overgrowth Obstruction distal to the common bile duct requiring decompression above the site Disruption in enterohepatic circulation of bile salts due to resection of terminal ileum or small bowel enterocutaneous fistula of upper GI tract secretions that are not adequately replaced. With the placement of a percutaneous endoscopic gastrostomy with jejunal arm (PEG/J), malabsorption can be averted, medication delivery can be preserved, and patients can maintain their hydration and nutritional needs without the use and risks of a central line. Successful jejunal feeding in this patient population has been described elsewhere (5,6). Devising an effective plan that allows these patients to return to the comfort of their home is the focus of this article. While the article presents our experience with patients with severe pancreatitis complicated by pseudocysts, the same process can be used for patients with refractory gastroparesis, obstructing GI lesions or external biliary drains. THE VALUE OF UPPER GUT SECRETIONS Role of Gastric Secretions Normal endogenous secretions produced daily above the pylorus include both salivary and gastric secretions and amount to ml per day (see Table 2). These secretions as well as the others listed in Table 2 are essentially recycled in the GI tract and contribute to the overall hydration status of the individual. Saliva and gastric secretions are stimulated by the cephalic phase of eating that is, just thinking about eating as well as taking the first bite of food. In addition to initiating protein digestion in the stomach, gastric secretions contain significant acid and are front line protection in terms of its bacteriocidal action. If significant gastric secretions are lost, then dehydration and hypochloremic metabolic alkalosis can result from excessive loss of acid, chloride and fluid (see 29 Table 6. Cost Comparison of Elemental & Semi-elemental Formulas Vs Standard Formula* with Pancreatic Enzymes** Cost/ Cost / w/ 4 tabs g Fat/ g MCT:LCT/ Enteral Product cal/ml 1000 kcal 1500 kcal Viokase /can 1000 & 1500 kcal MCT/LCT 1500 kcal Select Elemental and Semi-elemental Peptamen^ / Peptamen OS 1.5^ / Peptamen 1.5^ / Perative / Optimental / Vital HN / Vivonex TEN^ / Standard Polymeric Fibersource HN^ / Jevity / Osmolite / Promote / TwoCal HN / *Cost information obtained from company toll-free # (March 2010) ^Nestle: ; online: +Ross: ; online: Note: 4 tabs of Viokase 8000 IU lipase crushed = 1/2 teaspoon of Viokase powder (the powder goes off the market in 4/2010). **Wal-Mart $96.68/ 100 tabs of 8000 IU (4 tabs = $4.04) Used with permission from the University of Virginia Health System Traineeship Manual (1). Table 3 for electrolyte content of gastrointestinal secretions as compared to Table 4 with standard repletion IV solutions). Hypochloremic Metabolic Alkalosis Metabolic alkalosis is a relatively common clinical problem that is often induced by the loss of chloriderich gastric secretions due to vomiting or nasogastric suctioning. With vomiting or nasogastric suctioning, loss of acid initiates the alkalosis, but volume contraction along with hypochloremia and an increase in aldosterone secretion contributes to the reduction in bicarbonate excretion in the kidney by increasing proximal tubule reabsorption of bicarbonate and increasing hydrogen ion secretion in the distal tubule (aldosterone effect) (9). Hypokalemia is common in this setting also and further aggravates the alkalosis by enhancing bicarbonate absorption. Many patients are asymptomatic, or, if they have symptoms (weakness, muscle cramps, postural dizziness), it is typically a result of the hypovolemia that accompanies the excess loss of gastric fluid. Sodium loss can also be significant, and patients can be admitted with life-threatening hyponatremia. Intravenous saline corrects both volume contraction, hypochloremia and the alkalosis. In our case, homeostasis was achieved by collecting and reinfusing the vented gastric secretions via the jejunal tube. Role of Pancreato-biliary Secretions Pancreatic enzymes and bile salts work in tandem to efficiently and effectively digest macronutrients, especially fat, in preparation for absorption across the brush border. Alterations in either one of these important digestive agents can significantly alter absorption. Pancreato-biliary secretion deficiency, impairment, (continued on page 32) 30 (continued from page 30) or exclusion can arise under several conditions (see Table 5). Pancreatic Secretions. Pancreatic exocrine insufficiency occurs in 35 86% of patients with severe pancreatitis (5). It should be noted that diarrhea does not always accompany steatorrhea, particularly in the patient requiring narcotics for pain management. Bicarbonate secretion from the pancreas provides the ideal environment for pancreatic enzymes to function most effectively; a damaged pancreas may not secrete adequate bicarbonate, further aggravating pancreatic enzyme dysfunction and malabsorption. Pancreatic insufficiency can be very effectively treated with pancreatic enzyme supplementation. In the enterally fed patient, low fat elemental or semi-elemental products can be used, however it is important to note that some of the semi-elemental products have considerable fat, despite a large percentage of medium chain triglycerides, and pancreatic enzymes may still be needed. Although this institution commonly used standard enteral formulas, new cost analysis and the loss of Viokase powder from the market, has made us reevaluate our practice (see Table 6 with new cost data of enteral products with and without pancreatic Table 7. Another Institution s Practice of Using Creon with Enteral Feeding For Creon capsules: Gastrically-fed pts: minimicrospheres are whole in a slurry of mildly thickened fruit juice down the feeding tube. Postpylorically-fed, we crush and activate the minimicrospheres using bicarbonate of soda. Use one Creon 10 capsule or two Creon 5000 capsules to one Sodibic capsule (840 mg sodium bicarbonate) (made by Aventis or Aspen- Pharmacare) + 10 ml warm water or 1 teaspoon of sodium bicarbonate (baking soda). Procedure: use a mortar and pestle to mix 10 ml warm tap water with the contents of 1 Sodibic capsule. Empty the Creon capsules into this mixture and crush well. Add a little more lukewarm water as needed. This mixture is then instilled into the feeding tube with a 10 ml syringe, and given every 2 hours or so. Submitted by: Suzie Ferrie, AdvAPD, CNSC Critical Care Dietitian, Royal Prince Alfred Hospital, Australia enzymes). Although enteric coated enzymes are not to be crushed, at least one institution has been doing this for several years (see Table 7 for their practice). Clinical progress with whatever plan will be most telling if nutrient absorption is in question, the plan will need to be reevaluated. Bile Salts. Bile salts are not only important for digestion and absorption of fat, but also of fat soluble vitamins. The bile salt pool is maintained via the enterohepatic circulation in the last 100 cm of ileum, such that 95% is recycled daily. Loss of bile salts for any reason decreases fat absorption up to 50% (10). There are no commercially available bile salt replacers, hence the only recourse the clinician has is to decrease the fat content in the diet or enteral formula, unless the patient s bile salt loss is due to an external drain and this can be collected and reinfused in a feeding port below. Reinfusion Gastrointestinal Secretions Venting gastrostomies have been used successfully in both palliative situations as well as in aggressive treatment of disease processes as an alternative to salem sump type nasogastric tubes (5,11 15). Salem sump type tubes routinely used for gastric or intestinal decompression are very uncomfortable, and are associated with nasal necrosis, esophageal and gastric erosions. In most circumstances, patients use the venting port to relieve nausea, vomiting, abdominal distension and gas. Some patients are able to take some liquids by mouth and vent only as needed; while others require NPO status as part of the treatment of the disease process. Regardless of the circumstance, adequate hydration, nutrition and medication delivery of the patient will require attention from the clinician depending on the total volume lost in a 24 hour period. While no prospective studies exist supporting the practice of reinfusing intestinal secretions, many case reports are available in the literature. Procedures or devices to preserve biliary secretions, in particular, have been accomplished using PEGs (16 18), percutaneous endoscopic duodenostomy (PED) (19), external transhepatic biliary drainage tubes connected to PEG/J or PEG/D tubes (20 23), gastric secretions or external 32 Table 8. Cases of Reinfusion of Gastric or Biliary Secretions Study Population N Access for Reinfusion Comments Cheong, 1993 Cholangio CA; 2 PTC drainage tube to j-port Pt 1 survived 3.8 months; 2 bouts of sepsis; one w/lung mets of PEG/J^ Pt 2, length of survival not reported Decher, 2009 Pancreatic CA 1 PEG/J^ & external biliary drain Bile collected and bolused into j-port. Foutch, 1989 Unresectable 2 PTBD* to PEG Pt 1 survived 4 weeks; Pt 2 survived pancreatic CA 4 months Friman, 1989 CBD stones 1 T-tube collection and replaced Temporary replacement of bile via NGT; via nasogastric tube volume & tolerance not reported; pt discharged after 4 weeks Lenthall, 1970 Cirrhosis 7 Gastrostomy Only 1 pt reinfused bile (up to 2 liters/day) Levy, 1983 All w/ peritonitis w/enterocutaneous fistulas Intestinal losses can be decreased during w/distal mucous fistula; 14 had 1 the early phase of treatment; as sepsis is or more temp double enterotomies controlled, optimal utilization of remaining absorptive area for EN is permitted Makola, 2006 Pancreatitis w/ 18/ Venting of gastric secretions and Avg of 4.4 months to resolution of large pancreatic 126 reinfusion via j-port of PEG/J^ pancreatitis; 500 ml gastric secretions pseudocysts reinfused/ 24 hours Mohandas, 1991 GB CA 1 PTBD* & 18 Fr PEG w/ 8 Fr Bile and tube feedings were both infused into feeding tube placed duodenally*** 8 Fr duodenal tube Morita, 1988 Pancreatic CA 1 PTBD* to PED*** Pt survived 4 months; external drain converted to internal Ponsky, 1982 Inoperable gall 2 PTBD* to PEG Pt 1 drained mL of bile/day; bladder & pancreatic survived 4 months; Pt 2 drained ml; CA absorption improved w/replacement Rumley, 1985 All w/unresectable 12 Stamm gastrostomies connected All pts tolerated bolus jejunal feeding of malignancies to jejunostomies by T-connector ml q 2 hours; 8 pts needed reinfusion gastric juices 7 went home doing this; 1 pt had jejunal irritation as ph of reinfused secretions was 2. Shike, 1989 Unresectable 1 PTBD to PED*** Pt survived 5 months pancreatic CA Tokumo, 1997 Pancreatic CA 1 PEG for feeding PTBD* Nutritional status & daily living activities connected to PEG/J^ improved Wolfer, 1935 Review of jejunal Various Jejunostomy Report experience w/ reintroducing feeding since 1885 case ml of gastric aspirates daily; along reports w/pabulum, it improved results of feeding. All reported on cases of bile reinfusion into the jejunum. *Percutaneous transhepatic biliary drain (PTBD) **Percutaneous transhepatic cholangio-drain (PTCD) ***Percutaneous endoscopic duodenostomy (PED) ^Percutaneous endoscopic gastrostomy w/ jejunal extension (PEG/J) 33 biliary drainage bolused periodically into a jejunal port of PEG/J (5,24), gastrostomy with separate jejunostomy (25,26) and via nasogastric tube (27). One study even described a cohort of patients with double enterotomies where the effluent from the upper enterotomy was infused into the lower enterotomy resulting in an overall net decrease in fluid lost from the above site (28). See Table 8 for a summary of published reports. Despite the number of case reports published, the clinician is still left with surmising how one might orchestrate the collection, followed by the reinfusion of these electrolyte, enzyme, and bile salt rich secretions. REINFUSING INTESTINAL SECRETIONS ONE INSTITUTION S EXPERIENCE AND PRACTICE Although reinfusing gastric secretions may seem benign to a healthcare provider, the mere concept of reinfusing intestinal secretions can be shocking to a patient. Taking the time to thoroughly explain the rationale for the intervention, answer questions and allay anxieties facilitates the reinfusion process. Similarly, asking the patient to notify you of any difficulties with the reinfusion establishes a concrete role for the patient and builds support for the procedure. Creating a partnership with the patient on this venture reduces the need for extended hospitalizations, central access or the need for periodic intravenous fluids after discharge. This procedure can be achieved with either a PEG/J, separate g and j tubes, or a nasogastricjejunal tube (NG-J). Below describes our experience using PEG/J tubes; see Table 9 for the type of equipment u
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