Diphenoxylate

Short bowel syndrome is characterized by severe dehydration and malnutrition and requires total parenteral nutrition (TPN). Prolonged TPN has serious complications. Caloric requirements can be met orally but oral fluid replacement is problematic. Noncompliance and an inability to discontinue TPN earlier increase the likelihood of complications. Discontinuation of parenteral support requires an assessment of gastrointestinal anatomy and absorption capacity. Fluids must be replaced independently of feedings because the osmotic gradients decrease fluid absorption. Nocturnal enteral rehydration is an intervention using oral rehydration solutions through percutaneous endoscopic gastrostomy tubes at night. Patients given nocturnal enteral rehydration discontinued TPN earlier and had improved fluid absorption.

Key words: short bowel syndrome, total parenteral nutrition, nocturnal enteral hydration, percutaneous endoscopic gastrostomy tube

© 2004 International Life Sciences Institute

doi: 10.1301/nr.2004.may.221-231

Introduction

Short Bowel Syndrome (SBS) in adults is defined by signs and symptoms of moderate to severe weight loss, macronutrient and micronutrient deficiencies, dehydration, and electrolyte anomalies, all of which occur as sequelae of congenital anomalies, dysfunction, dysmotility, and/or resection of the small bowel. Patients with SBS ultimately lose functioning surface area of the small intestine. In most adults, the type and severity of malabsorption and dehydration is quite variable, depending on the location, extent of resection, and function of remaining bowel, especially if the ileum and colon are involved. The most common causes in adults for surgical resection of the small intestine include Crohn's disease complicated by strictures or fistulous disease, malignancy, radiation enteritis, or strictures. Intestinal ischemia and infarction due to vascular insufficiency and/or embolic phenomenon were recently identified as the most prevalent causes of SBS in smokers and in aging persons. Other reasons for this condition may include chronic intestinal pseudo-obstruction syndrome, refractory sprue, and congenital villous hypoplasia, all of which qualify as functional SBS because the intestinal length is intact.1-4 SBS is more common than previously believed. More than 10,000 cases have been reported in the United States.4

SBS is generally seen when patients are left with

Even though total parenteral nutrition (TPN) plays an essential role, weaning off of TPN is an important goal. Complications of prolonged TPN present real and potentially devastating risks; in particular, catheter-related sepsis and abnormal liver function tests, and cirrhosis leading to hepatic failure. Each patient's requirement for TPN and intravenous hydration is unique. Variable clinical presentations of malnutrition and dehydration may help determine whether full or partial nutritional support is needed. In order to successfully wean off of TPN, a clear understanding of the absorptive capacity of the patient's jejunum, ileum, and colon is essential. Issues of malnutrition and dehydration must be addressed separately and warrant careful evaluation for each patient. In many cases, dehydration and inadequate absorption of electrolytes such as magnesium, phosphate, and trace elements, are significant limiting factors for successful weaning from TPN.

Hydration with oral rehydration solutions (ORSs) is important for the adequate delivery of fluids. ORSs are hypo-osmolar to isosmolar solutions that allow for greater fluid absorption by optimizing the ratio of sodium to glucose through the co-transport mechanism across the gut. Since the jejunum has leaky junctions, the flux of water into the intestine by osmotic loads can result in excessive fluid losses. Taking ORSs to replace losses can be very challenging and noncompliance may hinder the recovery process. Oral food intake may also affect the absorption of ORSs by altering the intraluminal composition needed for sufficient fluid absorption. Anti-dirrheals such as diphenoxylate HCL-atropine sulfate and loperamide HCL or tincture of opium have been used to slow the rapid progression of fluids in the small intestine and to enhance fluid absorption. Oral iso-osmolar liquid formulas can be used for patients who are unable to consume prescribed solid diets. However, many patients are unable to drink these formulas continuously.

Given the severe complications of being on long-term TPN, another possible solution to prevent dehydration and allow earlier weaning from TPN is nocturnal enterai rehydration (NER) through a PEG (percutaneous endoscopic gastrostomy) tube. ORS intake is maintained through the PEG tube and reliance on volitional ORS intake is minimized. Oral intake potentially increases the intraluminal osmotic load in the gut when compared to the fasting state. Fluid absorption through NER is less affected by osmotic loads from daytime food intake, thereby providing for the optimal absorption of ORSs. After reading through the following case studies, the reader should better understand the complex problems related to weaning from TPN. For the reader's reference, information relevant to the management of SBS is provided in Appendixes 1 through 5.

Case 1

VG, a 72-year-old female status-post transverse colectomy/chemotherapy for colon cancer 30 years ago, presented to Loyola University Medical Center in February of 1995 for a second opinion regarding the repair of an enterocutaneous fistula and an ileostomy takedown. Her medical history included a hysterectomy, long-standing hypertension, chronic obstructive pulmonary disease from smoking, osteoarthtritis, paroxysmal atrial fibrillation, Groshong catheter infection with methicillin-resistant Staphylococcus aureus, and an ileostomy complicated by cellulitis and abscess. She was on long-term TPN since 1994.

Clinical Course

In March of 1995, she had her fistula repaired and was discharged. She was re-admitted three times for dehydration at her local hospital. Her fluid maintenance consisted of 1 L IV 0.9% normal saline infusions 4 times a week with oral intake of 3-5 quarts of Gatorade®. Her ileostomy output was between 3 and 5 L per day. A small-bowel-follow-through showed that she had 70% of her colon and 20% of her small bowel removed (a small amount of jejunum and ileum was removed). She was anemic with a hemoglobin of 11.1 g/dL; she was mildly hypoalbuminemic and had an albumin of 3.4 g/dL. She was also hypomagnesemic and had an iron saturation of only 4.8%. Her initial alkaline phosphatase was high at 224. She was encouraged to obtain more of her calories from an oral diet. Despite the administration of oral rice rehydration solution, antidiarrheal medication, apple pectin, acid-suppressing agents, and oral glutamine, her ostomy output continued to be 3-4 L. She continued to have diarrhea on her hyperosmolar intake and still required IV fluid support. She was losing weight and had concurrent diarrhea. An esophago-gastro-duodenoscopy failed to show any evidence of celiac disease.

In April of 1996, VG was referred to our Clinical Nutrition Unit for further management. Oral WHO (World Health Organization) solution replaced her oral rice hydration with club soda and Gatorade® regimen. In the following two-and-a-half months, the oral WHO solution was gradually increased to 3 L/day with a decrease in IV fluid infusions from 4 to 3 times per week with favorable results. Her diarrhea improved and her weight stabilized. Eventually, her fluids were titrated to 800 mL of IV fluids 5 times per week. In late 1998, and in addition to her hydration regimen, NER was discussed in order to wean off parenteral hydration. VG had been stable and had started to gain weight until November 1999 when she developed cholecystitis and had a cholecystectomy in January 2000. She agreed to a PEG tube and had it placed at the time of surgery (Appendix 1). Shortly after her surgery, she was started on NER (Appendix 2) with the WHO solution. Her IV hydration was discontinued. She maintained her nutrition with oral feedings and continued on NER. Her ostomy outputs decreased to 2-3 L/day. She had a stable clinical course following the discontinuation of TPN and remains relatively healthy.

Implications

This case demonstrates the importance of addressing the patient's dehydration separately from her nutritional needs in order to manage her ostomy fluid losses and wean from TPN. An attempt to minimize fluid losses with loose stools also proved to be of significance. In addition, NER reduced the cost of her care, which had become a significant burden on her family.

Case 2

BD, a 53-year-old female with a history of diet-controlled diabetes, presented to an outside hospital for abdominal pain. A computerized tomography scan of her abdomen revealed ischemic gangrenous bowel from a superior mesenteric artery thrombosis. Fatty infiltration of her liver was also noted. She was diagnosed with Protein C and S deficiency. Subsequently, she underwent two bowel resections in March of 1999 with an ileostomy placement, which resulted in SBS. During the resections, the terminal ileum and cecum were removed, leaving 42 cm of viable small bowel. Other pertinent medical history included dyspepsia with bloating and a cholecystectomy. She was placed on coumadin, acid suppression, and TPN. Six weeks later, she was transferred to Loyola University Medical Center for further management of SBS. Her height is 165cm (5.5 ft), and her weight 81 kg (141% of ideal body weight). Her initial evaluation in April 1999 showed an albumin of 2.1 g/dL, total protein of 4.9 g/dL, alkaline phosphatase of 329 (IU/L), AST of 22 IU/L, and a total bilirubin of 0.9 mg/dL. The trends of her alkaline phosphatase, AST, ALT, and total bilirubin are found in Figure 1.

Clinical Course

BD was started on a maintenance TPN regimen (1730 kcal and 95 g protein in 5 L) and was discharged after being started on oral glutamate supplements and other standard pharmacologic agents for SBS to optimize gut adaptation. She was pleased with this regimen. Her ostomy output was 5-6 L at the time of discharge in part due to noncompliance with dietary suggestions. In the following month, she was admitted twice for line sepsis, and was treated with IV antibiotics and pressors for septic shock. Throughout her clinical course of TPN, she developed four additional episodes of central line infection with Gram-positive, coagulase-negative cocci. In July 1999, her fluid and nutritional status were stabilized, and her weaning from TPN began. An improvement in her hypoalbuminemia was seen after she started an oral diet. In early 2001, she still had elevated alkaline phosphatase levels (~200-300, Figure 1A). At this time, she was put on supplementation with vitamins A, E, and D, and pancreatic supplements. Given persistent liver function test abnormalities, BD was started on ursodeoxycholic acid (given to help prevent cholelithiasis). A right-upper-quadrant ultrasound did not reveal any abnormalities other than changes consistent with fatty infiltration of the liver seen before on CT scan. Her oral diet was advanced slowly and she gained some weight. At this time she had been on long-term TPN for 3 years.

In August of 2002, the idea of nocturnal feeding was entertained. Initially, she was reluctant to try another regime since the onset of her diarrhea after intestinal resection had resolved her long-standing dyspepsia. She delayed her decision, but within 4 months, she agreed to receive a gastrostomy tube. By October 2002, after she was placed on ORS and a short bowel diet, her TPN was reduced to 187 kcal and 20 g protein in 2 L (from 4.4 L). At this time, a small-bowel-follow-through was performed to better determine the absorptive surface of her small intestine. She had 90-120 cm of remaining small bowel, which was significantly different from what her operative report stated. There was also a large hiatal hernia and thickened mucosal folds in her stomach. In February 2003, 1 L of NER was started and BD's TPN was replaced with 2 L of IV 0.9% normal saline with other electrolytes. Subsequently, NER was increased to 2.5 L and IV normal saline requirements were reduced to an as needed basis. NER was increased to 4 L, and her dependency on IV support was eliminated in early September 2003. BD tolerated this very well and she stayed on an oral diet with NER through her PEG tube. Her liver function tests, especially her AP, improved markedly from the time that she was dependent on TPN (Figure 1A). Her weight stabilized at 76 kg (167 lbs) and she has been without adverse events.

Implications

This case demonstrates the complications of catheter-related sepsis and elevations of liver function tests in patients who require long-term TPN. In the preceding 3 years, BD could not be weaned off TPN because of her extensive fluid requirements. The use of NER was again successful in eliminating parenteral dependency without further sequelae of catheter-related sepsis or hepatic failure.

Case 3

TM is a 45-year-old male with a prothrombin protein mutation who suffered a thrombosed portal vein and superior mesenteric vein requiring intestinal resection and left him with ~35 cm of small bowel. In December 2002, he was referred to Loyola University Medical Center by his surgeons for advice on nutritional management and TPN requirements for SBS. The operative reports stated that he had 20 cm of jejunum and 15 cm of ileum left with terminal ileum sparing. His colon was intact and functional. He presented to our institution one month after having a gastrostomy tube placed at the time of surgery. His diet consisted of three small meals a day. He had significant diarrhea (8-12 bowel movements/day) with occasional lower-quadrant abdominal pain. His review of systems revealed occasional dyspnea and wheezing, a >2.27 kg (~5 lbs) weight loss in the last 6 months, and a change in appetite. He weighed 107 kg and is 183 cm (6 ft) tall. On physical examination, he had right-lower-quadrant tenderness and a palpable hepatic margin, 1 cm below the right costal margin. He had a past medical history of rheumatic fever, nephrolithiasis with multiple urinary tract infections, hypertension, depression, strokes with resultant paralysis and seizures, and recently diagnosed anemia. He was anemic with a hemoglobin of 10.1 g/dL and the following liver function tests (albumin of 2.9 g/dL, total protein of 5.6 g/dL, total bilirubin of 0.8 mg/dL, alkaline phosphatase 124 IU/L, ALT 29 IU/L, and AST 28 IU/L). His total cholesterol was 110, triglycerides 121, high-density lipoprotein 25, and low-density lipoprotein 61.

Clinical Course

TM was on TPN since his surgery. He was referred to the Hematology service for his prothrombin mutation and continued to take coumadin. A CT scan of the abdomen and pelvis in late December 2002 showed small bowel ischemia. He was given anti-diarrheals and multivitamins for frequent stooling. A TPN taper was planned depending on oral intake. He started on nocturnal feeding. A small-bowel-follow-through to confirm the actual length of remaining small intestine showed that the patient actually had 60-90 cm (2-3 ft) of small bowel with an intact terminal ileum. One blind loop was noted but the area was ill defined. Malabsorption was suspected given his diarrhea. The patient recalled that he was only eating two meals a day with vanilla soymilk. In an effort to decrease stool frequency and facilitate colonic adaptation, he was started on the SBS II diet with ORS (Appendix 3). The SBS II diet is low in lactose and insoluble fiber, moderate in fat, high in soluble fiber, and limited in concentrated sweets. The goal of this diet is six small meals a day. The vanilla soymilk was changed to the unsweetened variety to decrease monomeric sugar sources and 2-3 L of Pedialyte® was recommended for hydration. With an intact colon, the optimal diet composition for TM included 20% protein, 50-60% carbohydrates with limited simple sugars, 20-30% fat, and 5-10 grams of soluble fiber per day with isotonic or hypoosmolar fluid. His compliance with the SBS diet and ORS was unparalleled and he kept a precise log of his oral intake and stool frequency. He then returned to the nutrition clinic in March of 2003 with a stable weight and reported a decrease in the number of bowel movements to 2-4 per day. He now consumed 3 meals per day averaging ~1500-1700 kcal/day. His TPN provided 1180 kcal with 110 g of protein (68 grams of amino acids) in order to supplement oral intake and meet a total caloric goal of 2400-2600 kcal/day for weight maintenance. Once TM tolerated an oral diet while keeping his bowel movements to a minimum, weaning him from TPN was initiated. Because he had an intact colon and terminal ileum, G-tube feedings were initiated. He was started on Osmolite® (a fiber-free, isotonic enteral formula) at 10 mL/hr, which was increased as tolerated. Two weeks later, TM's estimated intestinal absorption was found to be 70-80% based on clinical observation and caloric/weight assessment. Because he still required supplemental nutrition along with fluid and electrolyte replacement, our Clinical Nutrition Unit provided a modified enteral feeding formula. He was started on one can of Ultracal® mixed with ¼4 level tsp of table salt and 150 mL of water infusion over 6-8 hours every night via his G-tube. The feeding was advanced to meet a goal of 6 cans of Ultracal® mixed with a total of 900 mL of water and 1½ tsp of table salt. This provided 1526 kcal, 64 g of protein, and 1195 mL of free water. This regimen contained a high amount of soluble fiber to increase transit time and adequate sodium to maximize the sodium-glucose co-transport process in the intestine (sodium = 90 meq/L). The calculated osmolality of this solution is 326 miliosmoles/L, therefore, providing a minimal osmotic load to the intestine. His TPN was weaned by 250 kcal and 15 g of protein for each additional can of Ultracal® infused enterally. He was seen at the end of May with an improvement of his diarrhea and had successfully transitioned to enteral feeding from TPN with continued NER. Subsequent follow up in September 2003 demonstrated stability in his health and resolution of his symptoms of weight loss and diarrhea.

Implications

In this case, the importance of accurately assessing the length of small bowel was re-demonstrated as it was essential to his nutritional management. Because he had a short remaining small bowel, the presence of his full colon, and particularly the terminal ileum, played a significant role in his nutritional recovery and wean from TPN. The osmolarity of his feedings and hydration were tailored in a manner as to minimize fluid losses while maintaining caloric requirements.

Discussion

In these three cases, NER played a crucial role in maintaining proper hydration while effectively weaning from TPN and reducing morbidity from associated complications. Maintaining nutritional intake and hydration was difficult in the face of diarrheal losses, ostomy outputs, and infection-related complications. This approach provides a way to address hydration with greater effectiveness. TPN is not without multiple and serious consequences and requires careful monitoring of the patient.5,6 Catheter-related sepsis and elevation of liver function tests were seen with BD in case 2. Her course had been quite severe and weaning from TPN was imperative for her survival. Bacterial overgrowth from the lack of or little peristalsis of the alimentary tract was also considered with TM in case 3, especially because he had a blind loop identified on small-bowel-follow-through.

In patients with SBS, physicians encounter three physiologie phases of recovery and stages in nutritional management. Phase I is acute and usually occurs at 1-3 months after surgical resection of short bowel and/or loss of functioning small bowel, during which time the absorption of nutrients is very poor and intestinal output may exceed 5 L/day. Sodium losses are significant and stomal and fecal losses should be recorded. Gastric hypersecretion should be treated with H^sub 2^ blockers or proton pump inhibitors as needed. Pancreatic supplements may also be needed. Elevated liver function tests are common initially and may be due to microbial translocation and gangrenous tissue during the healing period.4 Cyclical parenteral nutrition is usually started and antibiotics can be used for suspected intraluminal bacterial translocation. Enteral feeding is usually initiated in this phase to maximize intestinal adaptation. This is done slowly keeping in mind the extent of resection and its adaptive physiology. An important goal in choosing enterai feeding is to minimize diarrhea due to hyperosmolar formulas while still maintaining adequate caloric intake, and instituting an oral diet with iso-osmolar liquid nutritional supplements sometimes makes for an easier transition. Enteral feedings must also be modified or changed in order to minimize microbial overgrowth and prevent excessive diarrhea and/or malabsorption. It is in this phase that TPN becomes an important intervention in the recovery of the patient. For the lengths of remaining intestine that have been identified with a certain clinical pattern of malnutrition requiring TPN, see appendix 4.

Phase II involves adaptation of the residual intestine as well as the pancreas, stomach, and colon. In this phase, the transition from parenteral to enteral nutrition is maximized using various enteral nutrients such as glutamine to stimulate the intestinal epithelium growth1,3,4,7; glutamine therapy is still being studied, however, and its use in SBS is controversial. Various growth factors such as growth hormone, insulin-like growth factor, epidermal growth factor, and enteroglucagon have been studied and are also being investigated further.3-5 Adaptation is also enhanced through oral diet but can unfortunately provoke diarrhea due to hyperosmolarity. Increasing fluid losses are a sign that enteral feedings are not being tolerated.

Patients enter Phase III, which is a maintenance state, after achieving maximal adaptation and absorptive capacity. Dietary supplementation is usually necessary as is occasional pharmacologic therapy for prevention and/or management of complications. The establishment of oral diet is an important factor in maintaining caloric requirements and weaning from TPN. Short bowel diets (I and II) at Loyola University Medical Center were designed to reduce malabsorption and minimize intestinal fluid losses (appendix 2). Compliance with these diets can be challenging. However, optimizing the dietary management of SBS is the first step and a corner stone of our approach to treating SBS.

Functional Anatomy and Physiologic Assessment

In the human body, the small intestine ranges from 300 to 800 cm in length, depending on its physiologic or pathologic state and technique of measurement. In general, the small intestine is ~600 cm long with the colon measuring ~150 cm.4 SBS is usually seen in patients with

The jejunum is ~200 to 300 cm, has a large concentration of digestive enzymes and transporter proteins, and provides for a large surface capacity to absorb most nutrients.5 Water fluxes occur across gradients set up by luminal contents due to leaky junctions and water loss in the jejunum can be significant. Enterohormonal regulation of the ileum also depends on a viable jejunum. 1,4,7-11 If less than 200 cm of jejunum remains, the presence of an intact colon can allow for a successful transition to oral feeding after the initial phases of recovery are complete. In the absence of a colon, the patient with a jejunal length less than 200 cm can transition to oral intake only if adherence to a strict short bowel dietary regimen and complete ileal adaptation occurs. The ileum is ~300 to 400 cm long. The terminal ileum is the primary site for vitamin B12 and bile acid absorption. The reabsorption of water released from the jejunum occurs in the ileum along with some unabsorbed nutrients. This requires active transport across luminal surfaces due to tight junctions of enterocytes. An important feature of the ileum is that it slows transit time in the face of unabsorbed fat, which allows for greater contact of luminal contents with the intestinal epithelium resulting in increased absorption. This is known as the ileal brake phenomenon. The ileocecal valve acts as a physiologic sphincter preventing reflux of colonie bacterial flora into the small intestine. If the ileum is

The colon is ~150 cm and its functions are relevant to SBS and its management as well. The ascending colon has the ability to absorb water and electrolytes up to 5 times its normal absorptive capacity and can exhibit adaptive responses to small bowel resection.4,12 Colonic flora are responsible for vitamin K production as well as fermentation of 75 to 80% of starches and soluble fiber into short-chain fatty acids, acetate, butyrate, and propionate. These short-chain fatty acids provide a caloric source and trophic factors for colonic enterocytes. Therefore, the colon has a significant function in fluid and nutrient absorption. The absence of the colon can result in fecal energy losses and dehydration especially when

Water Absorption

Luminal water absorption occurs across gradients that depend on luminal nutrient absorption as discussed above. The challenge of hydrating the patient against macronutrient gradients in the duodenum, and especially in the jejunum, is quite formidable. Water homeostasis and electrolyte absorption are intimately linked in varying relationships throughout the segments of small bowel, which have been described above. Several hypothetical models for the movement of water have been studied.13 Sodium movement is responsible for water absorption. Sodium is transported into the enterocyte with the transport of organic solutes such as amino and organic acids, and bile salts through an electrogenic solute-linked phenomenon, and accounts for much of the absorptive capacity of the small bowel. The small bowel can absorb up to 22 L of water a day with the colon accounting for ~6L.4,13 Water transport is entirely dependent on Na+-Cl- transport as there is no primary water transport system. The jejunum is unable to maintain an osmotic gradient due to its leaky junctions. Therefore, osmotic gradients formed by luminal nutrients determine the amount of nutrients and water absorbed. The movement of monomeric and polymeric nutrients across intestinal mucosa has been reviewed by Thillainayagam et al.13 Polymeric glucose, starches, and proteins need to be hydrolyzed by brush border enzymes, allowing for more time to transport resultant monomers across, the luminal surface. This lowers intraluminal osmolarity and therefore attenuates water losses. This is opposed to fluid losses and malabsorption of other nutrients caused by osmotic fluxes from the hyperosmolarity of monomeric glucose content in the lumen of the small intestine, especially the jejunum. It is with this concept in mind that ORSs have shown added benefit in maintaining greater water absorption in the jejunum. The specific differences in osmolality of the ORSs are still being debated.13-15

In case 1, the length of VG's remaining intestine indicated sufficient surface area for appropriate adaptation and fluid absorption. VG had approximately 45 cm of her colon and 480 cm of her small intestine left. Her ostomy losses were significant and were compounded by the fact that she had some evidence of malabsorption (see Table 1 for measured losses and appendix 5 for method of assessing ORS tolerance). Attempts at minimizing her diarrhea were important as she had nutrient losses given duodenal disease, jejunal and ileal compromise, and colonic resection. Ileal adaptation and the ileal brake still allowed for her to absorb nutrients despite her fluid losses through her ostomy. However, it was difficult for her to keep up with oral fluid replacement even while adjusting the osmolarity of ORSs (Gatorade®, boiled rice hydration, and club soda with salt and with or without pectin). The fiber in her lactose-free/low-fat diet was increased to minimize osmotic diarrheal losses. Once NER began through a PEG tube, her ostomy output/hour did not significantly increase. By instituting this method, her nutritional requirements were separated from her fluid losses. By addressing these issues separately, it allowed for her to wean off of TPN and even IV hydration for the following reasons: the luminal osmolarity was significantly reduced when she received hydration during the night; oral fluids of relative hypo-osmolality were being consumed throughout the day; oral fluid absorption was increased by slowing down luminal transit through several dietary maneuvers as discussed (i.e., SBS Diet I and II); and nocturnal gastrointestinal motility is slower, which allows for greater water absorption from NER. Her small intestine was able to absorb enough fluids and nutrients once the osmolarity of luminal contents was addressed through the use of ORS.

In case 2, the reported length of her GI tract was 42 cm based on the operative report. It would have been impossible to discontinue her TPN given the fact that she had less than 60 cm of small intestine without a full colon. Reassessing her remaining bowel length was a priority in an attempt to wean her from TPN given her repeated bouts of catheter-related sepsis and unresolved elevations of liver function tests. Through radiographie survey, it was found that 90 to 120 cm (3-4 ft) of small bowel remained, making it possible to discontinue TPN at some point in time. The measurement of fluid losses and an assessment of ORS tolerance were performed as well (Table 1 and appendix 5). Her diarrheal losses were minimized similarly to case 1. However, her fluid losses remained challenging due to repeated bouts of sepsis, sequelae of repeated and extended antibiotic use, and difficulty in adequate oral intake, which thereby delayed ileal adaptation. Additionally, she feared the return of her dyspepsia (which was present prior to her intestinal resection) if her diarrhea was controlled, attributing to her reluctance in starting NER. After the start of NER through a PEG tube, her fluid losses were minimized, thereby allowing faster weaning of IV hydration with resultant decline in liver function tests, notably alkaline phosphatase (Figure 1A). She was pleased. Without an accurate assessment of her remaining gastrointestinal tract, it would have been unrealistic to anticipate weaning her off parenteral support. It is possible that she would have progressed to hepatic failure due to continued bouts of line-related sepsis along with bowel stasis and resultant bacterial toxin production. Hepatic and small bowel transplantation have been reported in prolonged courses of TPN along with the aforementioned complications.1,2

In case 3, we re-emphasize the importance of assessing the length of remaining bowel by small-bowel-follow-through. He was reported to have only 20 cm of jejunum and 15 cm of ileum including the terminal ileum by intra-operative measurement. We speculated that due to sympathetic responses of the bowel, the measurement of intestinal length intra-operatively, was not reliable. By small-bowel-follow-through, we determined that he had ~60 to 90 cm (2-3 ft) of small intestine (with some terminal ileum remaining) and an intact colon. With these measurements, we were optimistic in our attempts to wean his TPN while addressing his caloric requirements in the face of his diarrhea. The presence of his terminal ileum was very important in preventing cholerrheic diarrhea since he had a full colon. His diarrhea appeared to be from malabsorption as he had a short bowel and a blind loop in the distal ileum. But since his ILCV was intact, it made bacterial translocation from the colon to the small bowel less likely. Due to his frequent bowel movements, he was placed on anti-diarrheal agents. In addition, fiber intake had been increased, monomeric sugar sources were reduced, and a low-fat diet was initiated. Bowel stasis with bacterial overgrowth was also considered but as the frequency of his bowel movements decreased, this also seemed less likely. Treatment of bacterial overgrowth becomes critical in the face of malabsorption and fluid losses. In fact, it can prevent effective weaning from TPN, setting up a viscous cycle of using TPN to treat malnutrition with recurrent overgrowth and malabsorption. A hydrogen breath test can be used to document bacterial overgrowth and, if the results are positive, a trial of antibiotics can be used to treat this condition. Other methods exist as well including probiotics, colonic flushes, etc.16 Diarrhea related to hypermotility can also be addressed using loperamide and/or codeine. All methods were not used as they were not indicated. His oral feedings were started early in an attempt to initiate small bowel and colonic adaptation. The ascending colon served as a digestive organ and allowed for short-chain fatty acids to provide added caloric intake, which had been accounted for. As discussed earlier, minimizing his diarrhea through the control of osmotic physiology of his small intestine, a modified enteral feeding formula through his PEG was initiated early in his case. The composition of the modified enteral feeding formula was optimized to deliver a relatively iso-osmolar solution and to maximize sodium-glucose transport while providing adequate calories as well. This solution was designed specifically for his caloric and hydration needs. He was closely monitored by our Clinical Nutrition Unit and improved without complications.

Conclusion

Short bowel syndrome has become more prevalent. The sequelae of malnutrition and dehydration are formidable challenges in the face of weaning TPN and IV hydration. The complications of malnutrition/dehydration combined with recurrent bouts of central catheter-related sepsis and liver function test abnormalities provided impetus to develop a method of circumventing these issues related to SBS and TPN. NER through PEG tube made it feasible to overcome these complications that resulted in greater nutritional independence from parenteral support for the patients in a faster and effective manner. Assessing the overall gastrointestinal function, its anatomy, and absorptive capacity were essential in the face of caloric and fluid deficits. Attention to individual nutritional needs, taking into account the osmolality of ORSs, was critical for shortening the transition off of TPN to enteral feeding and reducing the period required for ileal adaptation. Implementing this method can also be a significant cost benefit for the individual and health care institution given the complications of treating sepsis, cost of TPN, and medical services. The physical and mental burden on the patient can be effectively reduced as they gain further autonomy and return to their personal lives sooner. As discussed in these cases, NER with PEG tubes show promise at effective weaning of TPN and in the treatment of SBS, as discussed in these cases. Investigation and in-depth studies at utilizing this method may provide added insight into further uses or enhanced benefit of this modality.

Justin Nauth, D.O., Chih Wen Chang, Pharm.D., Sohrab Mobarhan, M.D., Sherri Sparks, R.D., L.D., C.N.S.D., Margaret Borton, R.N., B.S.N., C.R.N.I., C.N.S.N., and Sheryl Svoboda, R.D., L.D., C.N.S.D.

Dr. Nauth is with the Department of Internal Medicine, Loyola University Medical Center; Dr. Chang is with the Clinical Nutrition Unit, Loyola University Medical Center; Dr. Mobarhan is Chief of the Division of Gastroenterology, Hepatology, and Nutrition; Ms. Sparks, Borton, and Svoboda are with the Clinical Nutrition Unit, Loyola Unviersity Medical Center, Maywood, IL, USA.

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