DOCSLIB.ORG

Pediatric Medical Nutrition Therapy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pediatric Medical Nutrition Therapy SECTION V Pediatric Medical Nutrition Therapy CHAPTER 12 Gastrointestinal Disorders ................... 267 CHAPTER 13 Critical Care. 313 CHAPTER 14 Cardiology ................................ 325 CHAPTER 15 Pulmonary Diseases ........................ 351 CHAPTER 16 Oncology and Hematology ................... 387 CHAPTER 17 Pediatric Surgical Nutrition: Principles and Techniques ............................ 423 CHAPTER 18 Chronic Kidney Disease ...................... 435 CHAPTER 19 Nutrition for Burned Pediatric Patients ......... 449 CHAPTER 20 Diabetes .................................. 465 © Gajus/istock/Getty Images. 265 © Gajus/istock/Getty Images. CHAPTER 12 Gastrointestinal Disorders Jennifer Autodore, Julia Driggers, and Rebecca Wilhelm LEARNING OBJECTIVES ■ Explain how to assess, diagnose, and manage common pediatric gastrointestinal nutrition related topics such as celiac disease, lactose intolerance, inflammatory bowel disease, and pancreatitis ■ Discuss normal digestion and absorption in the gastrointestinal tract ■ Identify diagnosis related at-risk macro and micronutrients ■ Interpret common diagnostic tests for pediatric gastrointestinal disorders particularly vulnerable to disease or surgical resection. ▸ Introduction FIGURE 12.1 graphically portrays the principal sites of The gastrointestinal tract is an organ system that absorption of macro- and micronutrients, vitamins, stretches from the mouth to the anus. It is a large and minerals. muscular tube designed to ingest, digest, and absorb Symptoms of gastrointestinal disease can arise nutrients before expelling waste as feces. Functions of from disorders located in a specific region of the bowel, the gastrointestinal tract may be disrupted by disease, the entire bowel, or distant sites (for example, vomit- injury, chemotherapeutic agents, antibiotics, parasites, ing can occur due to pyloric stenosis, gastroenteritis, environmental toxins, and/or bacterial overgrowth, or a brain tumor). Common pediatric disorders are resulting in alterations in nutritional requirements. listed in TABLE 12.1 and common diagnostic tests are Many nutrients are absorbed throughout the intesti- presented in TABLE 12.2. Many tests to evaluate gastro- nal tract, whereas others are absorbed only at specific intestinal function as well as the presence or absence of sites. Absorption of the latter class of nutrients is disease are available. 267 268 Chapter 12 Gastrointestinal Disorders FIGURE 12.1 Normal Digestion and Absorption in the GI Tract. Introduction 269 TABLE 12.1 Common Pediatric Gastrointestinal Disorders Presenting Symptom Differential Diagnosis Treatment Stomach and Esophagus Vomiting/regurgitation Congenital anomaly of the Surgery gastrointestinal tract Gastroesophageal reflux Infants: positioning, medications such as antacids, H2 blockers, and proton pump inhibitors (PPI). If preceding fails, consider surgical treatment. All ages: medications, antacids, H2 blockers, PPI, avoid caffeine-containing foods and other personal triggers Eosinophilic esophagitis Elimination diet, swallowed steroids Eosinophilic gastritis Steroids, immunosuppressive medication Peptic disease Medications such as antacids, H2 blockers, and PPI; avoid caffeine-containing foods and other personal triggers H. pylori Antibiotics, PPI Gastroparesis Prokinetics, diet changes such as multiple small low-fat meals per day, or postpyloric feeds Dysphagia (choking after Congenital anomalies, strictures, Surgery eating), odynophagia (pain with webs swallowing) Eosinophilic esophagitis Elimination diet, swallowed steroids Esophageal spasms/dysmotility Calcium channel blockers and nitrates; avoid extreme temperatures in foods Peptic strictures Medications such as antacids, H2 blockers, and PPI; dilation Liver and Pancreas Jaundice Extrahepatic biliary tract Surgical correction; diet/formula with obstruction, such as biliary medium chain triglycerides (MCT), fat-soluble atresia vitamin supplementation, choleretic agents such as ursodeoxycholate Autoimmune hepatitis Steroids, evaluation for fat malabsorption, fat-soluble vitamin supplementation, protein restriction only if encephalopathic Jaundice with recurrent Gallstones Surgery abdominal pain Choledochal cyst Surgery Nausea, vomiting, abdominal Pancreatitis NPO; if severe or prolonged course expected pain then postpyloric tube feeds or parenteral nutrition; pain control, H2 blockers; when clinically able, resume low-fat oral diet Pancreatic pseudocyst Monitor cyst size; if cyst increases with enteral nutrition, may require parenteral nutrition (continues) 270 Chapter 12 Gastrointestinal Disorders TABLE 12.1 Common Pediatric Gastrointestinal Disorders (continued) Presenting Symptom Differential Diagnosis Treatment Chronic diarrhea, failure to thrive Pancreatic insufficiency, such as Enzyme replacement therapy, fat-soluble cystic fibrosis vitamin supplementation, high calorie balanced diet Cholestatic disease Diet/formula with MCT, fat-soluble vitamin supplementation Small Bowel and Colon Anemia, gastrointestinal Congenital malformations, Surgery bleeding such as Meckel’s diverticulum, duplication cysts Vomiting Food allergies Hydrolysate formula, elimination diet Infectious enteropathies Oral rehydration solutions, followed by lactose and/or sucrose restrictions Diarrhea in neonatal period Congenital disorders of Restriction of the problematic carbohydrate, carbohydrate absorption and balanced nutrition, vitamin/mineral transport supplementation, enzyme replacement Diarrhea, perioral and perianal rash Zinc deficiency Zinc supplementation Diarrhea Food allergies Elemental formula and/or elimination diet Infectious enteropathies Intravenous fluids, oral rehydration solutions, followed by lactose and/or sucrose restrictions if clinically indicated Crohn’s disease Enteral feeds for therapy and/or malnutrition, replete iron, fat-soluble vitamins, and zinc as necessary; monitor vitamin B12 if severe ileal disease or resection Ulcerative colitis Enteral feeds for weight gain, replete iron as necessary, low-residue diet if strictures Celiac disease Gluten-free diet Short bowel syndrome Parenteral nutrition progressing to enteral nutrition to oral feeds; vitamin and mineral supplements specific to patient’s condition Fructose intolerance Dietary restrictions of fructose-containing foods Lactose intolerance Dietary restrictions of lactose-containing foods Diarrhea, normal growth pattern Irritable bowel syndrome, Normal diet for age, increased soluble chronic nonspecific diarrhea, fiber intake, decreased intake of sorbitol- toddler’s diarrhea containing beverages (apple and pear juice) and other personal triggers Introduction 271 Presenting Symptom Differential Diagnosis Treatment Abdominal distention/pain Celiac disease Gluten-free diet Short bowel syndrome Total parenteral nutrition progressing to MCT- predominate hydrolysate formula; vitamin and mineral supplements Functional constipation Complete bowel clean-out using saline enemas, mineral oil, Miralax; high-fiber diet and adequate fluids; bowel habit training Congenital disorders of Restriction of the problematic carbohydrate, carbohydrate absorption and balanced nutrition, vitamin/mineral transport supplementation, enzyme replacement Fructose intolerance Dietary restrictions of fructose-containing foods Lactose intolerance Dietary restrictions of lactose-containing foods Constipation Hirschsprung’s disease; post- Surgery NEC strictures Functional constipation Complete bowel clean-out using saline enemas, mineral oil, Miralax; high-fiber diet and adequate fluids; bowel habit training TABLE 12.2 Common Diagnostic Tests for Pediatric Gastrointestinal Disorders Test Description Useful to Help Diagnose Barium enema Barium sulfate administered by ■ Colonic strictures and obstructions enema; colonic lumen and mucosa ■ Hirschsprung’s disease visualized by fluoroscopy. ■ Polyps Barium swallow Barium sulfate administered orally; ■ Aspiration upper gastrointestinal tract is ■ Dysmotility disorders visualized by fluoroscopy. ■ Hiatal hernias ■ Strictures ■ Varices Breath hydrogen test Oral administration of sugar and ■ Fructose malabsorption expiratory collection of hydrogen ■ Lactose malabsorption as an indirect measure of bacterial ■ Bacterial overgrowth fermentation of unabsorbed carbohydrate. DXA (dual energy X-ray Measures bone density in the spine, ■ Osteomalacia absorptiometry) hip, or forearm. ■ Osteopenia ■ Osteoporosis Colonoscopy Insertion of flexible fiber optic tube ■ Colitis via anus into large bowel; visual ■ Polyps examination of colonic lining, biopsies obtained. (continues) 272 Chapter 12 Gastrointestinal Disorders TABLE 12.2 Common Diagnostic Tests for Pediatric Gastrointestinal Disorders (continued) Test Description Useful to Help Diagnose CT (computed tomography Multiple radiographs of abdomen ■ Areas of inflammation (e.g., abscess) scan) of abdomen with or without intraluminal and/or ■ Blood vessel anatomy and intravenous contrast; computer obstructions reconstructs multiple images ■ Organ size and consistency to generate “slices” through the ■ Tumors abdomen. EGD Fiber optic tube is inserted into ■ Celiac disease (esophagogastroduodenoscopy) upper gastrointestinal tract ■ Duodenitis allowing mucosal lining of upper ■ Esophagitis, including eosinophilic GI tract to be visualized and esophagitis (EE) biopsies to be taken. ■ Gastritis ■ Peptic ulcer disease Fecal fat test Concurrent 3-day diet record of ■ Fat malabsorption fat intake and stool collection; ■ Pancreatic insufficiency comparison as percentage
Load more

Recommended publications
  • Prevalence of Fructose Malabsorption in Patients with Irritable Bowel Syndrome After Excluding Small Intestinal Bacterial Overgrowth
    J Neurogastroenterol Motil, Vol. 24 No. 2 April, 2018 pISSN: 2093-0879 eISSN: 2093-0887 https://doi.org/10.5056/jnm17044 JNM Journal of Neurogastroenterology and Motility Original Article Prevalence of Fructose Malabsorption in Patients With Irritable Bowel Syndrome After Excluding Small Intestinal Bacterial Overgrowth Kee Wook Jung,1 Myeognsook Seo,1 Young Hwan Cho,1 Young-Ok Park,2 So-Yoon Yoon,2 Jungbok Lee,3 Dong-Hoon Yang,1 In Ja Yoon,1 So Young Seo,1 Hyo Jeong Lee,1 Sang Hyoung Park,1 Kyung Jo Kim,1 Byong Duk Ye,1 Jeong-Sik Byeon,1 Hwoon-Yong Jung,1 Suk-Kyun Yang,1 Jin-Ho Kim,1 and Seung-Jae Myung1* Departments of 1Gastroenterology, 2Clinical Nutrition, and 3Clinical Epidemiology and Biostatistics, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea Background/Aims Fructose malabsorption (FM) mimics symptoms of irritable bowel syndrome (IBS), and its prevalence has increased. Diagnosing FM in IBS is challenging because of its overlap with small intestinal bacterial overgrowth (SIBO). We assessed the prevalence of FM by comparing patients with IBS with asymptomatic control individuals after excluding SIBO using the glucose hydrogen breath test (HBT). Methods Patients diagnosed with IBS and asymptomatic control individuals were enrolled prospectively. Dietary habits were assessed with the Food Frequency Questionnaire. After excluding SIBO, participants underwent HBTs with both 15 g and 25 g of fructose. Results Thirty-five patients with IBS and 35 age- and sex-matched asymptomatic control individuals were enrolled. The 15-g fructose HBT yielded positive results in 7 of the 35 (20.0%) patients with IBS and in 2 of 35 (5.7%) controls (P = 0.070).
    [Show full text]
  • Limiting Fructose, Fructans Intake May Ease IBS
    36 Digestive Disorders FAMILY P RACTICE N EWS • July 1, 2008 Limiting Fructose, Fructans Intake May Ease IBS BY MARY ANN MOON “marked and sustained global improve- of irritable bowel syndrome (IBS) in patients prove symptoms. In the current study, the Contributing Writer ment in gastrointestinal symptoms,” re- who also have fructose malabsorption. researchers focused on osmotic load with- searchers noted. A subsequent study of The results also demonstrate that re- in the lumen and fermentative gas content. atients with irritable bowel syn- the patients revealed that symptom relief stricting intake of these substances may Poorly absorbed short-chain carbohy- drome and fructose malabsorption was not specific to restricted intake of lead to durable symptomatic improve- drates, including fructose and lactose, are Pappeared to benefit from a diet that fructose, but was achieved by limiting the ment, wrote Ms. Shepherd, a dietician at highly fermentable. They exert a strong restricted intake of fructose and fructans, intake of poorly absorbed short-chain Australia’s Monash University, Clayton, osmotic effect in people who have malab- Susan J. Shepherd and her colleagues re- carbohydrates. Victoria, and her colleagues. sorption of these two sugars—about 40% ported in an article appearing in the July These findings “represent the first high- They theorized that, because many ab- of the population in the case of fructose, 2008 issue of Clinical Gastroenterology level evidence” that poorly absorbed short- dominal symptoms may originate from and between 15% to 100% of the popula- and Hepatology. chain carbohydrates—fructose and fruc- bowel distension, addressing factors that tion for lactose. In the 25-patient study, the diet led to tans—are dietary triggers for the symptoms contribute to the distension would im- To minimize or eliminate intake of poor- ly absorbed short-chain carbohydrates, the investigators created a diet that omitted Brief Summary—see package insert for full prescribing information.
    [Show full text]
  • Oxalate Loading Test: a Screening Test for Steatorrhoea
    Gut: first published as 10.1136/gut.20.12.1089 on 1 December 1979. Downloaded from Gut, 1979, 20, 1089-1094 Oxalate loading test: a screening test for steatorrhoea D. S. RAMPTON', G. P. KASIDAS, G. ALAN ROSE, AND MARTIN SARNER2 From University College Hospital, London, St. Peter's Hospitals and Institute of Urology, London SUMMARY To investigate the possibility of measuring urinary oxalate output instead of faecal fat excretion as an outpatient screening test for steatorrhoea, we determined 24 hour urinary oxalate and five day faecal fat excretion before and during an oral load of sodium oxalate 600 mg daily (oxalate 4-44 mmol), in 32 patients with suspected malabsorption on a diet containing oxalate 30 mg (0-33 mmol), fat 50 g (180 mmol), and calcium 1 g (25 mmol). Nineteen patients proved to have steatorrhoea (mean faecal fat 62 mmol/24 h, range 19-186 mmol) of varying aetiologies. On the diet alone, urinary oxalate was raised in only nine of these patients (mean 0 25 mmol/24 h, range 0-08-059 mmol) (normal <0 20). By contrast, when the diet was supplemented with oral sodium oxalate, all 19 patients with steatorrhoea had hyperoxaluria (mean 0-91 mmol/24 h, range 046- 1P44 mmol) (normal <0-44). There was a significant positive linear relationship between urinary oxalate and faecal fat when the 32 patients were on the high oxalate intake (r=0*73, P <0.001), but not when they were on the low oxalate intake. Mean percentage absorption of orally administered oxalate was 58+09% (±1 SD) in normal subjects and 14-7+6-0% (P <0.002) in patients with steatorrhoea.
    [Show full text]
  • 16. Questions and Answers
    16. Questions and Answers 1. Which of the following is not associated with esophageal webs? A. Plummer-Vinson syndrome B. Epidermolysis bullosa C. Lupus D. Psoriasis E. Stevens-Johnson syndrome 2. An 11 year old boy complains that occasionally a bite of hotdog “gives mild pressing pain in his chest” and that “it takes a while before he can take another bite.” If it happens again, he discards the hotdog but sometimes he can finish it. The most helpful diagnostic information would come from A. Family history of Schatzki rings B. Eosinophil counts C. UGI D. Time-phased MRI E. Technetium 99 salivagram 3. 12 year old boy previously healthy with one-month history of difficulty swallowing both solid and liquids. He sometimes complains food is getting stuck in his retrosternal area after swallowing. His weight decreased approximately 5% from last year. He denies vomiting, choking, gagging, drooling, pain during swallowing or retrosternal pain. His physical examination is normal. What would be the appropriate next investigation to perform in this patient? A. Upper Endoscopy B. Upper GI contrast study C. Esophageal manometry D. Modified Barium Swallow (MBS) E. Direct laryngoscopy 4. A 12 year old male presents to the ER after a recent episode of emesis. The parents are concerned because undigested food 3 days old was in his vomit. He admits to a sensation of food and liquids “sticking” in his chest for the past 4 months, as he points to the upper middle chest. Parents relate a 10 lb (4.5 Kg) weight loss over the past 3 months.
    [Show full text]
  • Chronic Pancreatitis: What the Clinician Want to Know from Mri
    HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Magn Reson Manuscript Author Imaging Clin Manuscript Author N Am. Author manuscript; available in PMC 2019 August 01. Published in final edited form as: Magn Reson Imaging Clin N Am. 2018 August ; 26(3): 451–461. doi:10.1016/j.mric.2018.03.012. CHRONIC PANCREATITIS: WHAT THE CLINICIAN WANT TO KNOW FROM MRI TEMEL TIRKES, M.D. Department of Radiology and Clinical Sciences, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA Keywords Pancreas; Chronic Pancreatitis; Magnetic Resonance Imaging; Magnetic Resonance Cholangiopancreatography; Computerized Tomography INTRODUCTION Chronic pancreatitis (CP) is a low prevalence disease.1–3 In 2006, there were approximately 50 cases of definite CP per 100,000 population in Olmsted County, MN 3, translating to a total of 150,000–200,000 cases in the US population. Clinical features of CP are highly variable and include minimal, or no symptoms of debilitating pain repeated episodes of acute pancreatitis, pancreatic exocrine and endocrine insufficiency and pancreatic cancer. CP profoundly affects the quality of life, which can be worse than other chronic conditions and cancers.4 Natural history studies for CP originated mainly from centers outside the U.S.5−910,11 conducted during the 1960–1990’s and consisted primarily of males with alcoholic CP. Only one large retrospective longitudinal cohort study has been conducted in the US for patients seen at the Mayo Clinic from 1976–1982.12 While these data provide general insights into disease evolution, it is difficult to predict the probability of outcomes or disease progression in individual patients.
    [Show full text]
  • The Practice of Gastrointestinal Motility Laboratory During COVID-19 Pandemic
    J Neurogastroenterol Motil, Vol. 26 No. 3 July, 2020 pISSN: 2093-0879 eISSN: 2093-0887 https://doi.org/10.5056/jnm20107 JNM Journal of Neurogastroenterology and Motility Review The Practice of Gastrointestinal Motility Laboratory During COVID-19 Pandemic: Position Statements of the Asian Neurogastroenterology and Motility Association (ANMA-GML-COVID-19 Position Statements) Kewin T H Siah,1,2* M Masudur Rahman,3 Andrew M L Ong,4,5 Alex Y S Soh,1,2 Yeong Yeh Lee,6,7 Yinglian Xiao,8 Sanjeev Sachdeva,9 Kee Wook Jung,10 Yen-Po Wang,11 Tadayuki Oshima,12 Tanisa Patcharatrakul,13,14 Ping-Huei Tseng,15 Omesh Goyal,16 Junxiong Pang,17 Christopher K C Lai,18 Jung Ho Park,19 Sanjiv Mahadeva,20 Yu Kyung Cho,21 Justin C Y Wu,22 Uday C Ghoshal,23 and Hiroto Miwa12 1Department of Medicine, Yong Loo Lin School of Medicine, The National University of Singapore, Singapore; 2Division of Gastroenterology and Hepatology, Department of Medicine, National University Hospital, Singapore; 3Department of Gastroenterology, Sheikh Russel National Gastroliver Institute and Hospital, Dhaka, Bangladesh; 4Department of Gastroenterology and Hepatology, Singapore General Hospital, Singapore; 5Duke-NUS Medical School, Singapore; 6School of Medical Sciences, Universiti Sains Malaysia, Malaysia; 7St George and Sutherland Clinical School, University of New South Wales, Kogarah, NSW, Australia; 8Department of Gastroenterology and Hepatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; 9Department of Gastroenterology, GB Pant Hospital, New Delhi, India;
    [Show full text]
  • Blueprint Genetics Primary Hyperoxaluria Panel
    Primary Hyperoxaluria Panel Test code: KI0801 Is a 3 gene panel that includes assessment of non-coding variants. Is ideal for patients with a clinical suspicion of hyperoxaluria. About Primary Hyperoxaluria The primary hyperoxalurias are rare disorders of glyoxylate metabolism, which result in markedly increased endogenous oxalate synthesis by the liver. They are characterized by an excess of oxalate resulting in manifestations ranging from occasional renal stones, recurrent nephrolithiasis and nephrocalcinosis to end-stage renal disease (ESRD) and systemic oxalosis. Presenting ranges from the neonatal period to adulthood. Among disorders causing hyperoxaluria, the primary hyperoxalurias are the most severe, ultimately leading to ESRD and if untreated, death in most patients. Type I primary hyperoxaluria (PH1), is caused by deficient or absent activity of liver-specific peroxisomal alanine glyoxylate aminotransferase (AGT). In some patients with PH1 type disease, the enzyme is present but mistargeted to mitochondria where it is metabolically inactive. The severe infantile form is characterized by a failure to thrive, nephrocalcinosis with or without nephrolithiasis and early ESRD. Onset in childhood and adolescence is often characterized by recurrent urolithiasis (with or without nephrocalcinosis) and progressive renal failure. The late onset form is characterized by occasional renal stones with onset in adulthood, but acute renal failure caused by bilateral obstruction of the kidneys by oxalate stones may occur. Other manifestations include urinary tract infections, dysuria and hematuria. The ongoing systemic oxalosis also may lead to other clinical manifestations such as cardiac conduction defects, vascular calcification with distal gangrene, disturbed vision, specific brown colored retinal deposits, skin nodules, joint involvement and bone disease leading to fractures in long-term dialysis-dependent patients.
    [Show full text]
  • Redalyc.The Nutritional Limitations of Plant-Based Beverages in Infancy
    Nutrición Hospitalaria ISSN: 0212-1611 [email protected] Sociedad Española de Nutrición Parenteral y Enteral España Vitoria, Isidro The nutritional limitations of plant-based beverages in infancy and childhood Nutrición Hospitalaria, vol. 34, núm. 5, 2017, pp. 1205-1214 Sociedad Española de Nutrición Parenteral y Enteral Madrid, España Available in: http://www.redalyc.org/articulo.oa?id=309253341026 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Nutr Hosp. 2017; 34(5):1205-1214 ISSN 0212-1611 - CODEN NUHOEQ S.V.R. 318 Nutrición Hospitalaria Revisión The nutritional limitations of plant-based beverages in infancy and childhood Limitaciones nutricionales de las bebidas vegetales en la lactancia y la infancia Isidro Vitoria Unit of Nutrition and Metabolopathies. Hospital Universitario y Politécnico La Fe. Valencia, Spain Abstract Breastfeeding, infant formula and cow’s milk are basic foods in infant nutrition. However, they are being increasingly replaced either totally or partially by plant-based beverages. The composition of 164 plant-based beverages available in Spain was reviewed based on the nutritional labeling of the package and the man- ufacturers’ webpages. This was compared to the composition of cow’s milk and infant formula. In addition, the nutritional disease associated with consumption of plant-based beverages in infants and children was reviewed by means of a literature search in Medline and Embase since 1990 based on the key words “plant-based beverages” or “rice beverages” or “almond beverages” or “soy beverages” and “infant” or “child”.
    [Show full text]
  • Navigating Home Care: Parenteral Nutrition—Part Two
    NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #11 Series Editor: Carol Rees Parrish, M.S., R.D., CNSD Navigating Home Care: Parenteral Nutrition—Part Two by Gisela Barnadas Parenteral nutrition (PN) is often used for patients who are unable to absorb suffi- cient nutrition through the gastrointestinal tract. PN can be safely administered in the home setting with proper assessment and monitoring of the patient. An interdiscipli- nary team approach is used to identify and avoid potential complications, which may occur. This article provides the physician with specific guidelines for evaluating, ordering and monitoring PN therapy in the home patient. It also addresses financial and reimbursement considerations with emphasis on understanding the often con- fusing, Medicare guidelines. CASE 1 • What resources are available to help manage this JR is a 65-year-old female with vascular disease, patient in the home? hypertension, diabetes and history of a hysterectomy. • What resources are there available for the patient? She presents with severe abdominal pain, vomiting and • Will insurance pay for this? diarrhea. A small bowel series documents a bowel obstruction, most likely due to bowel ischemia. Find- Providing total parenteral nutrition in the home ings during surgical intervention included: twisted, (HPN) is by no means a new treatment option. The gangrenous small bowel with multiple adhesions first record of a patient receiving HPN was a 36-year- resulting in resection of her distal jejunum, ileum and old woman with extensive metastatic ovarian carci- right colon, leaving an intact duodenum, approximately noma in 1968.(1) While the exact number of people 100 cm of the jejunum and most of her left colon.
    [Show full text]
  • Fructose As an Endogenous Toxin
    HEPATOCYTE MOLECULAR CYTOTOXIC MECHANISM STUDY OF FRUCTOSE AND ITS METABOLITES INVOLVED IN NONALCOHOLIC STEATOHEPATITIS AND HYPEROXALURIA By Yan (Cynthia) Feng A thesis submitted in the conformity with the requirements for the degree of Master of Science Graduate Department of Pharmaceutical Sciences University of Toronto © Copyright by Yan (Cynthia) Feng 2010 ABSTRACT HEPATOCYTE MOLECULAR CYTOTOXIC MECHANISM STUDY OF FRUCTOSE AND ITS METABOLITES INVOLVED IN NONALCOHOLIC STEATOHEPATITIS AND HYPEROXALURIA Yan (Cynthia) Feng Master of Science, 2010 Department of Pharmaceutical Sciences University of Toronto High chronic fructose consumption is linked to a nonalcoholic steatohepatitis (NASH) type of hepatotoxicity. Oxalate is the major endpoint of fructose metabolism, which accumulates in the kidney causing renal stone disease. Both diseases are life-threatening if not treated. Our objective was to study the molecular cytotoxicity mechanisms of fructose and some of its metabolites in the liver. Fructose metabolites were incubated with primary rat hepatocytes, but cytotoxicity only occurred if the hepatocytes were exposed to non-toxic amounts of hydrogen peroxide such as those released by activated immune cells. Glyoxal was most likely the endogenous toxin responsible for fructose induced toxicity formed via autoxidation of the fructose metabolite glycolaldehyde catalyzed by superoxide radicals, or oxidation by Fenton’s hydroxyl radicals. As for hyperoxaluria, glyoxylate was more cytotoxic than oxalate presumably because of the formation of condensation product oxalomalate causing mitochondrial toxicity and oxidative stress. Oxalate toxicity likely involved pro-oxidant iron complex formation. ii ACKNOWLEDGEMENTS I would like to dedicate this thesis to my family. To my parents, thank you for the sacrifices you have made for me, thank you for always being there, loving me and supporting me throughout my life.
    [Show full text]
  • Short Bowel Syndrome with Intestinal Failure Were Randomized to Teduglutide (0.05 Mg/Kg/Day) Or Placebo for 24 Weeks
    Short Bowel (Gut) Syndrome LaTasha Henry February 25th, 2016 Learning Objectives • Define SBS • Normal function of small bowel • Clinical Manifestation and Diagnosis • Management • Updates Basic Definition • A malabsorption disorder caused by the surgical removal of the small intestine, or rarely it is due to the complete dysfunction of a large segment of bowel. • Most cases are acquired, although some children are born with a congenital short bowel. Intestinal Failure • SBS is the most common cause of intestinal failure, the state in which an individual’s GI function is inadequate to maintain his/her nutrient and hydration status w/o intravenous or enteral supplementation. • In addition to SBS, diseases or congenital defects that cause severe malabsorption, bowel obstruction, and dysmotility (eg, pseudo- obstruction) are causes of intestinal failure. Causes of SBS • surgical resection for Crohn’s disease • Malignancy • Radiation • vascular insufficiency • necrotizing enterocolitis (pediatric) • congenital intestinal anomalies such as atresias or gastroschisis (pediatric) Length as a Determinant of Intestinal Function • The length of the small intestine is an important determinant of intestinal function • Infant normal length is approximately 125 cm at the start of the third trimester of gestation and 250 cm at term • <75 cm are at risk for SBS • Adult normal length is approximately 400 cm • Adults with residual small intestine of less than 180 cm are at risk for developing SBS; those with less than 60 cm of small intestine (but with a
    [Show full text]
  • Nutrition Options in Short-Bowel Syndrome Upmcphysicianresources.Com/GI Instructions: Services
    In This Issue 1 Nutrition Options in Short-Bowel Syndrome SPRING 2017 Division of Gastroenterology, 3 Gastric Carcinoids with Duodenal Ulcers Hepatology, and Nutrition 4 Living Donor Liver Transplant (LDLT) 6 PancreasFest 2017 / Honors and Awards 7 Pittsburgh Gut Club 8 What Is This? Nutrition Options in Short-Bowel Syndrome By David G. Binion, MD, and Zachary Zator, MD Intestinal transplantation is an option for select patients with short-bowel syndrome- associated intestinal failure (SBS-IF) who fail or do not tolerate nutritional rehabilitation. There are a range of factors to consider in the nutritional management of patients before and after intestinal transplantation. SBS-IF can be defined as the inability to maintain proper nutritional balance — including of proteins, electrolytes, macronutrients, micronutrients, and fluids — while adhering to a conventional diet in the face of an anatomically or functionally limited gut surface. The ideal management of patients with SBS-IF involves a multidisciplinary team of gastro enterologists, nurses, dietitians, pharmacists, and surgeons. Pharmacotherapeutic agents aimed at minimizing fluid losses have been routinely employed to support these patients. For instance, antidiarrheal agents, such as loperamide or diphenoxylate, are used alongside proton pump inhibitors. Somatostatin analogs, like octreotide, inhibit gastrointestinal secretions from the stomach, pancreas, and intestines and have been proven beneficial in the past. However, their role can be limited, as somatostatin can actually
    [Show full text]