Organic causes include: Decreased appetite, e.g. psychological or secondary to chronic illn ess. Inability to ingest, e.g. GI structural or neurological problems. Excessive food loss, e.g. severe vomiting (gastro-oesophageal re \202 ux disease (GORD), pyloric stenosis, dys motility), diabetes mellitus (urine). Malabsorption (see Increased energy requirements, e.g . congenital heart disease, cystic \201 brosis, malignancy, sepsis. Impaired utilization, e.g. various syndromes, IEM, endocrinopathies. \200 \200 \200 b p.334). Causes may overlap, e.g. in cystic \201 brosis there is simultanous malabsorp- tion, incr eased energy requirements, anorexia, and chronic infection. Management \200 Detailed history: Consider asking pediatric dietitian to perform detailed dietary history. Full examination: If organic disease possible: \200 including age of onset of FTT, and timing of weaning. \200 including accurate measurement of growth. basic investigations should include: 2+, FBC, ESR/CRP, U&E, creatinine, total protein and albumin, Ca PO4 immunoglobulins; coeliac a ntibody screen; urinalysis, including M, C&S. 3 \200\223 , LFT; \200 \200 are indicated if there are suggestive symptoms Further investigations: or the faltering growth is severe, and include: IEM screen; karyotype; serum lead (pica); sweat t est; upper endoscopy and small intestinal biopsy; CXR; bone age, skeletal survey (NAI); abd ominal US; head CT/ MRI; oesophageal pH monitoring; ECG; fecal occult blood. If non-organic disease: pediatric dietitian: is likely, seek dietary advice, preferably by a 10_McClure_10.indd 308 11/14/2012 11:28:47 PM FALTERING GROWTH (FAILURE TO THRIVE) 309 If FTT resolves in the next few weeks, give positive reinforcement and supervise subsequent growth as an outpatient. If FTT persists, admit to hospital for basic investigations and o bserve the response to supervised adequate dietary input. Adequate growth in hospital sugge sts a non-organic cause; explore and support family dynamics. Should FTT occur again at hom e after improvement in hospital, and then refer to social services for family assessment an d appropriate intervention. If FTT continues in hospital despite adequate dietary input, oc cult organic disease is most likely and requires extensive investigation as above. Provide dietetic input, whatever the cause, to support nutritional correction and education . Identify and correct associated comorbidities, e.g. developmental delay or early presenta tion of neurological disorder such as cerebral palsy; fall off in head growth is suggestive . Prognosis The prognosis depends on the severity of FTT. It is good if mild. Severe FTT, wha tever the cause, may be associated with later developmental and behavioral impairment. 10_McClure_10.indd 309 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 310 Recurrent abdominal pain \200 De \201 ned as more than two discrete episodes in a 3mth period interfering with school an d/or usual activities. Incidence: 10 \200\22315% in school age children. Causes No organic cause is found in 90%. Organic causes include: constipation; dietary indi scretion; food intolerance (lactose or fructose); irritable bow- el syndrome; psychogenic p ain; peptic ulcer (H. pylori); coeliac disease; abdominal migraine (cyclic vomiting syndrom e); gallbladder disease; renal colic; dysmenorrhoea; UTI; mittleschmerz; and physical or se xual abuse. Presentation Non-organic disease This form occurs in a thriving, generally well child; with short episodes of peri-umbilical pain, good appetite, no other GI symptoms, no family his- tory of migraine or coeliac disease, and normal examination. Co-existent symptoms such as headache and fatigue are common and this is often referred to as recurrent abdominal pain s yndrome. Organic cause Likely if presentation is different to above or child <2yrs. \200\230Red \202 ag \200\231 symp- toms include weight loss, diarrhea, blood per rectum, joint symptoms , skin rashes, family history of in \202 ammatory bowel disease, or coeliac di- sease. Management History Ethnic origin (lactase de \201 ciency occurs in dark skinned races), at opy, rela- tionship to eating, precipitating events (e.g. cow \200\231s milk introduction i n milk protein enteropathy), social history (e.g. start of school, parental separa- tion), and family history. Full examination Investigation \200 If non-organic disease is likely: no or very little investigation is needed, e.g. FBC, ESR/ CRP, U&E, LFT, coeliac antibody screen, urine M, C&S, fecal M, C&S (if there is a recent hi story of foreign travel). If organic disease is likely: investigate as above, plus consider hydrogen breath test (lactose intolerance); C13 breath test (Helicobactor pylori); US; bar ium radiology; upper and lower GI endoscopy. Treatment Non-organic disease Con \201 dent reassurance; education that condition is commo n and pain is genuine (just like headaches); personal support; avoidance of associated stre ssful events (e.g. bullying); acknowledgement of symptom, whilst at same time down playing pain; minimize secondary gains from abdominal pain, e.g. school avoidance; increased dietar y \201 bre intake may be bene \201 cial; 10_McClure_10.indd 310 11/14/2012 11:28:47 PM RECURRENT ABDOMINAL PAIN 311 formal psychotherapy in complex and resistant cases. Multidisciplinary support and engageme nt of the family is essential. Organic disease: Treat the underlying cause. Prognosis Approximately 25% of children with functional recurrent abdominal pain continue t o have pain or headaches in adulthood. Functional sequelae are common. Abdominal migraine Abdominal pain is associated with pallor, headaches, anorexia, nausea, + / \200\223 vomiting. The condition overlaps with periodic syndrome and cyclic vom- iting sy ndrome. There is usually a strong family history of migraine. Treatment \200 Dietary cola), solid cheeses. Pharmacological: may be helpful. : avoid citrus fruits, chocolate, caffeine-containing drinks (e.g. pizotifen, sumatriptan, gabapentin, or amitriptyline 10_McClure_10.indd 311 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 312 Gastrointestinal hemorrhage This condition is relatively rare in childhood. Upper GI tract bleeding may present as haematemesis (vomiting of frank blood or \200\230coffee grounds \200\231) or melaena (black, tarry, foul-smelling stools). Haematochezia (bright or dark re d blood PR) indicates lower GI tract bleeding. Beware of spurious hemorrhage, e.g. black stools after bismuth/iron ingestion, red vomit af ter beetroot, urate crystals in nappies, or normal pseudomenstruation in newborns. Use Dips tix test or laboratory testing to con \201 rm blood you are if unsure. Causes Neonates \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Swallowed maternal blood, i.e. not GI hemorrhage. NEC. Dietary protein intolerance. Coagulo pathy. Stress ulcers. Gastritis, vascular. Malformations. Duplication cyst. Infectious coli tis, including pseudomembranous colitis. In \202 ammatory colitis. Infants Most of the above plus: \200 \200 \200 \200 \200 Oesophagitis. Swallowed blood from upper airway, e.g. epistaxis. Anal \201 ssure. Intussu sception ( Meckel \200\231s diverticulum (often presents as a massive painless rectal bleed ; b p.865). b p.860). Older children Most of the above plus: \200 Peptic ulcer disease. \200 Mallory \200\223 Weiss tear. \200 Oesophageal varices. \200 Nonsteroidal anti-in \202 ammatory drugs (N SAIDs). \200 Intestinal polyps. \200 b p.332). IBD ( \200 GI infection, e.g. dysenter y. \200 HSP ( \200 HUS ( b p.788). b p.376). 10_McClure_10.indd 312 11/14/2012 11:28:47 PM GASTROINTESTINAL hemorrhage 313 Management See Box 10.3 \200 \200 Detailed history: Examination: vessels); hepatic stigmata; ENT examination (e.g. epistaxis) ; organomegaly; abdominal tenderness; anal inspection (e.g. \201 ssure or \201 stula); rectal examination. Examine vomit or stool to con \201 rm nature of bleed. Supportive trea tment: protection with NGT or ETT as necessary. Drug \202 ow and, thereby, upper GI bleed ing. Therapeutic electrocautery, bleeding vessel ligation, paravariceal injection. Treat un derlying e.g. is there associated abdominal pain? speci \201 cally, vital signs; skin (pallor, abnormal blood \202 uids; blood product transfusion; airway treatment: somatostatin or vasopressin reduces splanchnic blood endoscopy: in severe bleeds, e.g. balloon tamponade, cause: e.g. surgical removal of Meckel \200\231s diverticulum. Box 10.3 Investigations for GI hemorrhage Guided by \201 ndings from examination and history, these may include: \200 \200 \200 \200 \200 \200 \200 \200 FBC U&E Coagulation studies LFT Albumin Protein ESR/CRP Apt \200\231s test in newborns (con \201 rms swallowed maternal blood by distinguishing adult from fetal Hb) Stool M,C&S Stoo l Formal ENT examination Abdominal US (e.g. intussusception or portal hypertension) Upper G I barium meal Nuclear medicine scan (Meckel \200\231s diverticulum) Labeled RBC scan (occul t bleeding) CXR (in case haemoptysis is true cause) Endoscopy (oesophago-gastro-duodenoscop y if melaena or haematemesis; \202 exible sigmoidoscopy or colonoscopy if haematochezia) \200 \200 \200 \200 \200 \200 \200 \200 Clostridia dif \201 cile toxin assay (pseudomembranous colitis) 10_McClure_10.indd 313 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 314 Jaundice See also b pp.130 \200\223131. Jaundice occurs when serum bilirubin >25 \200\22330 mmol/L. It is rare outside neonatal period. First determine the SBR and conjugated (direct) fraction. Unconjugated jaundice is rarely due to liver disease. Conjugated jaundice (>20mm ol/L) is due to liver disease and requires investigation. Unconjugated jaundice Due to excess bilirubin production, impaired liver uptake, or conjuga tion. Causes \200 Haemolysis (spherocytosis, G6PD de \201 ciency, sickle cell anemia, thalassaemia, HUS). De fective bilirubin conjugation (Gilbert syndrome, Crigler \200\223Najjar syndrome). Intrahepatic cholestasis Here, jaundice is due to hepatocyte damage +/ \200\223 cholestasis . There is un- conjugated +/ \200\223 conjugated hyperbilirubinaemia. Causes Infectious \200 \200 Viral hepatitis, including chronic hepatitis. Bacterial hepatitis (leptospirosis [Weil \200 \231s disease], septicaemia, Mycoplasma, liver abscess). Toxoplasma gondii. Toxic \200 Drugs or poisons, e.g. paracetamol overdose, sodium valproate, anti-TB drugs, cytotoxic dru gs. Amanita phalloides). Fungi ( Metabolic \200 \200 \200 A \200 \200 \200 \200 Galactosaemia, hereditary fructose intolerance. Tyrosinaemia type 1. Wilson \200\231s disea se. 1-antitrypsin de \201 ciency. Hypothyroidism. Peroxisomal disorders, e.g. Zellweger syndrome. Dubin \200\223Johnson syndr ome, Rotor syndrome. Biliary hypoplasia \200 \200 Non-syndromic. Syndromic, e.g. Alagille syndrome. Cardiovascular \200 \200 Budd \200\223Chiari syndrome. Right heart failure. Autoimmune hepatitis Autoimmune hepatitis. 10_McClure_10.indd 314 11/14/2012 11:28:47 PM JAUNDICE 315 Cholestatic (obstructive) jaundice Conjugated hyperbilirubinaemia is due to bile tract obst ruction. Causes \200 \200 \200 \200 \200 \200 \200 \200 Biliary atresia. Choledochal cyst. Caroli \200\231s disease. Primary sclerosing cholangitis (commonly associated with IBD). Cholelithiasis (may be secondary to chronic haemolysis). C holecystitis. Cystic \201 brosis. Obstructive tumors or cysts. Management of jaundice Full history e.g. medications, family history, overseas travel, past blood transfusions, jaundice contacts, pale stools, or dark urine (cholestasis). Examination Vital signs; conscious level (hepatic coma); hepatic stigmata (= chronic liver disease); pallor (haemolysis); hepatomegaly; splenomegaly; ascites; peripheral oedema. Investigations Depending on which of the above pattern presents these may include: \200 \200 \200 \200 FBC, blood \201 lm, reticulocyte count. Coagulation studies. U&E, SBR (total and conjugat ed), LFT, albumin, total protein, TFT. Viral serology (hepatitis A, B, C, EBV, CMV), blood culture, leptospira and toxoplasma antibody titres. IEM screen, ammonia, copper studies (se rum copper n, serum caeruloplasmin d in Wilson \200\231s disease), blood glucose, A 1-antit rypsin level, galactose-1-uridyl-phosphatase level. Immunoglobulins, anti-nuclear antibody, smooth muscle and liver/ kidney antibodies (autoimmune hepatitis); Abdominal US, abdominal CT/MRI, biliary scintigraphy, e.g. hepatoiminodiacetic acid [HIDA] scan). Liver biopsy. i, d, or Treatment \200 \200 \200 \200 Remove or treat underlying cause. Correct blood glucose if it is low. Correct any clotting abnormalities. Phototherapy may be helpful only if jaundice has a signi \201 cant unconjug ated component, e.g. Crigler \200\223Najjar syndrome. Treat any associated anemia if due to haemolysis. Treat liver failure as appropriate. \200 10_McClure_10.indd 315 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 316 Adverse reactions to food Food allergy De \201 ned as an abnormal immunological response t o food (incidence is 6 \200\2238% in children aged <3yrs). \200 Immediate allergic reactions involve production of food-speci \201 c IgE antibodies. 70% o f cases have a family history of atopy. Allergy becomes less common as age increases. The c ommonest food allergens are cow \200\231s milk proteins, eggs, peanuts, wheat, soya, \201 sh, shell \201 sh, and tree nuts. \200 \200 Presentation \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Diarrhea +/ \200\223 blood/mucus. Vomiting. Dysphagia, gastro-oesophageal re \202 ux sympt oms. Abdominal pain. Faltering growth (FTT). Eczema. Urticaria. Erythematous rash, particul arly peri-oral. Asthma symptoms. Food induced anaphylaxis. Food intolerance Intolerance involves adverse reactions to food that are mediated by non- i mmunological responses. This condition is more common than food aller- gy. Its presentation is similar to that of food allergy. Fructose intolerance is very common due to usage of hi gh-fructose corn syrup in prepared foods and beverages. Other food intolerances may be due to: \200 b p.317), congenital GI enzyme de \201 ciency, e.g. lactose intolerance ( sucrase-isomaltase de \201 ciency. P harmacological reactions to agents contained in food, e.g. caffeine, histamine, tyramine, t artrazine, acetylsalicylic acid. Reactions to food toxins or microbes, e.g. haemagglutinins in soy or mycotoxin present in mold-contaminated cereals. Management of suspected food allergy or intolerance See Box 10.4 for clinical approach. Treatment \200 Dietary free, soya free, egg-free diet. \200 \200 \200 treatment: exclusion of offending food(s) from diet, e.g. milk Involve a pediatric dietitian in the diagnosis and management. Extensively hydrolysed or am ino acid based milks can be used. Dietary exclusion in the mother should be considered if b reast feeding. Drug cromoglicate, corticosteroids, and antihistamines. treatment: regular therapy may have a role, e.g. oral sodium 10_McClure_10.indd 316 11/14/2012 11:28:47 PM ADVERSE REACTIONS TO FOOD 317 IM adrenaline is used by the child or parents for emergency treatment of anaphylactic react ions, particularly if IgE mediated and there are respiratory or systemic symptoms and signs . After at least 6 \200\22312mths of being symptom-free on exclusion diet, consider food ch allenge if there is a food allergy. If the previous reaction was severe, this should only b e done in hospital with full resuscitation facilities available in the event of a serious a dverse reaction. Prophylaxis Data are not clear. In newborns with a \201 rst degree relative with con \201 rmed food allergy, exclusive breastfeeding to at least age 1yr reduces risk of allergy . If this is not possible then a hydrolysed milk formula can be used. After weaning tempora ry avoidance of at risk foods may also reduce risk. Box 10.4 Approach to adverse food reaction History Including diet history and examination. A food diary may be helpful. Investigations These may include: RAST or enzyme-linked immunosorbent assay (ELISA) test to detect speci \201 c food IgE antibodies; serum i total IgE or eosinophils; favorable resp onse to dietary elimination of speci \201 c suspected food protein and then recurrence aft er challenge; allergen prick or patch skin testing. If the diagnosis is still in doubt, a d ouble-blind, controlled food antigen challenge, or upper and lower gastrointestinal endosco py (non-speci \201 c in \202 ammatory in \201 ltrate) may be helpful in chil- dren with predominantly gut symptoms. In severe cases when allergen(s) cannot be identi \201 ed, start a full elimination diet i n which only a few hypoallergenic foods are given for 1 \200\2232wks, e.g. lamb, rice, wate r, pears, followed by a gradual reintroduction of increas- ingly allergenic foods until a f ood reaction(s) is detected. Prognosis of food allergy or intolerance The prognosis depends on the cause. The majority o f infantile food allergic reactions resolve by 2yrs. The exception is peanut allergy that t ends to persist. Allergies that develop in older children may become chronic. Lactose intolerance \200 This is most commonly due to post-viral gastroenteritis lactase de \201 ciency, e.g. rotav irus. Most cases are transient and short lasting (<4 \200\2236wks). In older healthy childr en and adults, lactase levels commonly decline with subsequent variable severity intoleranc e (especially in certain populations, e.g. South-east Asian and Afro-Caribbean). Rarely due to genetic congenital lactase de \201 ciency (primary). Infants present with severe diarr hea after lactose exposure (present in high quantities in breast milk). Presentation: stool pH <5. diarrhea; excessive \202 atus; colic; peri-anal excoriation; 10_McClure_10.indd 317 11/14/2012 11:28:47 PM CHAPTER 10 Gastroenterology and nutrition 318 Treatment: children under 6/12). lactose-free formula milk (soya milk not recommended in Cow \200\231s milk protein allergy \200 \200 Commonest food allergy in infancy. Symptoms depend on where the allergic in \202 ammation is. \200 \200 \200 \200 stools, rarely, chronic constipation. Limited use for RAST or skin testing in infants. May occur in breast-fed infants, the reaction is to cow \200 \231s milk protein secreted into breast milk following maternal ingestion. Usually presents as allergic colitis in an otherwise healthy happy infant. In infants, \201 rst treat by limiting cow \200\231s milk protein intake (and commonly soy protein): \200 Upper GI tract \200\224 Small intestine enteropathy, FTT. Large intestine \200\224 vomiting, feeding aversion, pain. \200\224diarrhea, abdominal pain, protein-losing diarrhea, acute colitis with blood and mucus in \200 \200 In exclusively breast-fed infants, this is achieved by a maternal exclusion diet to these p roteins. In formula fed infants feed with a hydrolysed formula (short peptides). If symptoms severe, or unresponsive to hydrolysed formula, then an elemental (amino acid) f ormula may be required. Anti-in \202 ammatory medications are very rarely needed. Avoid us ing goat \200\231s or sheep \200\231s milk as a cow \200\231s milk substitute, as 25% will also develop allergy to these milks (cross-reactivity). Similar cross- reactivity also ofte n occurs with soya milk. Use of soya milk is not recommended under age 6mths. After weaning , introduce a cow \200\231s milk protein free diet (supplement with oral calcium if require d). Consider a cow \200\231s milk protein challenge after 6 \200\22312mths (see p.317). \200 b 10_McClure_10.indd 318 11/14/2012 11:28:48 PM ADVERSE REACTIONS TO FOOD 319 10_McClure_10.indd 319 11/14/2012 11:28:48 PM CHAPTER 10 Gastroenterology and nutrition 320 Nutritional disorders Malnutrition is a common cause of child mortality and morbidity. Ther e is a wide spectrum of nutritional disorders, varying from protein-energy malnutrition to micronutrient nutritional de \201 ciencies to morbid obesity (see Table 10.1). In non-indu strialized nations malnutrition and associated infection are leading causes of child death. Causes \200 \200 \200 Diets low in protein, energy, or speci \201 c nutrients. Strict fad or vegetarian diets. D iseases causing malabsorption (e.g. coeliac disease, cystic \201 brosis, Crohn \200\231s disease), severe GORD, immunode \201 ciency, chronic infection. Eating disorders, e.g. ano rexia nervosa (see b Chapter 16). Assessment of nutritional status Refer to a pediatric dietician and review the following: \200 (cid:2)10% over 3mths is suggestive of impaired Recent weight loss ( nutritional status). Accurately plot serial height and weight (falling across 2 centile lines or below 3rd centile may indicate nutritional impairment). Percenta ge weight for height (= [actual weight/expected weight for height centile] x 100); a value of (cid:1)90% may indicate impairment. 2. Body mass index (BMI) = weight (kg)/height (m) Mi d-arm circumference divided by head circumference (malnutrition if <0.31). Detailed dietary assessment of 5 \200\2237-day food diary. Serum albumin. \200 \200 Protein \200\223energy malnutrition Kwashiorkor and marasmus usually occur together. Becaus e of oedema, mid-upper arm circumference is a better guide to malnutrition than weight. Kwa shiorkor is due to severe de \201 ciency of protein/essential amino acids. \200 \200 \200 \200 Clinical features: oedema; skin/hair depigmentation; abdominal distension with fatty liver. Investigations: d Ca2+, d Mg2+, d PO3 \200\223 Marasmus: Clinical features: height is rela tively preserved compared to weight; wasted appearance; muscle atrophy; listless; diarrhea; constipation. d Serum albumin, Hb, U&E, Ca2+, Mg2+, PO4 Investigations: glucose; stool M,C &S for intestinal ova, cysts, and parasites. growth retardation; diarrhea; apathy; anorexia; hypoalbuniaemia, normo- and microcytic anemia, 4 , and d glucose. \200 is due to severe energy (calories) de \201 ciency. 3 \200\223, and Treatment \200 \200 \200 \200 \200 Correct dehydration and electrolyte imbalance (IV if required). Treat underlying infection and/or parasitic infections. Treat concurrent/causative disease. Treat speci \201 c nutrit ional de \201 ciencies. Orally refeed slowly- watch out for refeeding syndrome ( b p.322). 10_McClure_10.indd 320 11/14/2012 11:28:48 PM 1 0 _ M c C l u r e _ 1 0 . i n d d 3 2 Table 10.1 Speci \201 c nutritional de \201 ciencies 1 Name Causes Presentation Treatment i Morbidity and mortality from infections, follicular hyperkeratosis, xerophthalmia, night blindness. Plasma retinol <0.7mmol/l. Rickets (limb x-rays: distal bony cupping and fraying ), d serum Ca2+ and PO4 <25nmol/l. Vitamin A Fat malabsorption states, e.g. cystic \201 brosis; de \201 cient indigenous diet. Oral vitamin A supplementation. Vitamin D Dietary de \201 ciency; low UV light; fat Oral 40 \200\223125 micrograms/day vitamin D, Ca2+ and PO 4 3 \200\223 supplements. IV 1mg vitamin K1. 3 \200\223, i alkaline phosphatase, plasma 25-hydroxy cholecalciferol malabsorption, hepatic or renal failure. Vitamin K Congenital, fat malabsorption states, small bowel bacterial overgrowth. Bleeding, including haemorrhagic disease of the newborn. Vitamin B1 Dietary de \201 ciency (particularly when polished Beri-beri (muscle weakness, oedema, heart failure), Wernicke \200\231s encephalopathy. Red cell thiamine pyrophosphate <150nmol/l. Oral 5mg vitamin B1 daily. rice staple diet). Vitamin B12 Vegan diets, distal small bowel disease (e.g. Macrocytic megaloblastic anemia, peripheral neuropathy, motor weakness. Vitamin B12 level < 75pmol/l, Schilling test of B12 absorption. IM vitamin B12 1mg every 1 \200\2233mths. Crohn \200\231s disease), pernicious anemia. Vitamin C Lack of fresh fruit and vegetables. Scurvy: petechiae, ecchymosis, bleeding gums, painful sub-periosteal bleeding of legs, moto r weakness. Plasma vitamin C level <6 \200\22311 mol/l. Oral vitamin C 25mg QDS for 4 days then BD. N U T R Vitamin E Prematurity, fat malabsorption. Haemolytic anemia. Serum vitamin E level <5mg/l. Oral 75 \200\223100mg vitamin E daily. Folic acid Small bowel disease, malignancy, drugs (anticonvulsants, cytotoxics). Macrocytic megaloblastic anemia, irritability, failure to thrive, thrombocytopenia. Red cel l folate <160ng/ml. Common (710% in UK children). Microcytic hypochromic anemia, developmen tal delay, angular stomatitis, koilonychia, serum ferritin <7mg/l, serum iron <5nmol/l, tot al iron binding capacity >90mmol/l. Oral 0.5 \200\2231mg folic acid daily. I T O N A L I Iron Low dietary intake, chronic blood loss (e.g. intestinal parasites or malaria), prematurity. Oral 4 \200\2236 mg/kg/day iron. D I S O R D E R S Zinc Prematurity, dietary insuf \201 ciency, intestinal disease or chronic diarrhea, acrodermat itis enteropathica (inborn error of zinc absorption). Peri-orifacial and anal dermatitis, diarrhea, alopecia, failure to thrive, neurological dys function. Serum zinc <11 mol/l. Infants oral 1mg/kg/day zinc, children 1 \200\2235yrs 5mg/day, >10yrs 10mg/day. Iodine Dietary de \201 ciency. Endemic in some regions. Hypothyroidism and retarded development. Low urine iodine: creatinine ratio. Oral 100 \200\223300 micrograms/day iodine and oral levothyroxine replacement. 1 1 / 1 4 / 3 2 1 2 0 1 2 1 1 : 2 8 : 4 8 P M CHAPTER 10 Gastroenterology and nutrition 322 Nutritional support Nutritional support can be either enteral or parenteral. Enteral nutrit ion, when possible, is preferred as it is cheaper, technically less demanding, more physiol ogical, and associated with fewer complications. \200 Involve a pediatric dietitian to assess nutritional status, requirements, and support. Bewa re of \200\230refeeding syndrome \200\231 (potentially fatal respiratory and cardiac failu re induced by electrolyte disturbance following overzealous nutritional therapy in severe m alnutrition) and be prepared to use PN in severe cases. Indications \200 \200 \200 \200 \200 \200 Severely ill patients, e.g. ill preterm infants. Nutritional supplementation is required, e .g. FTT, cystic \201 brosis. Swallowing dif \201 culty, e.g. severe cerebral palsy. Meta bolic diseases, e.g. phenylketonuria. Gastrointestinal failure, e.g. malabsorption, short b owel syndrome. Other primary disease state, e.g. chronic renal failure. Oral supplementation Includes high energy milks, mineral/vitamin supplementation. Specializ ed foods Huge range of specialized milk and feeds exist for many different conditions, (mod ular elemental diets for IBD, hypoaller- genic milk for milk protein allergy). Enteral tube feeding \200 \200 \200 Can be orogastric, NG, nasojejunal, and gastrostomy. Liquid feeds are given as boluses or c ontinuously, e.g. overnight. Indications: prematurity), cardiorespiratory compromise, GORD, anorexia, generalized debilitation, e.g. trauma. Feeds: standard polymeric diets (e.g. rea dy to feed nutritionally complete whole protein products); elemental diets and semi-element al diets requiring little or no digestion; or disease-speci \201 c formulations. Gastrosto my reduces orofacial complications/discomfort, but complications include: Gastric leakage; localized skin infection or in \202 ammation; GI perforation/trauma/hemorrhage. swallowing problems (e.g. severe cerebral palsy, Trophic feeding \200 \200 \200 Synonyms: Indications: Rationale structure and function despite PN-induced anabolic body st ate. Small milk volumes appear to prevent this. Also promotes GI development in newborn inf ants. Typically 0.5 \200\2231mL/kg/h milk is fed within 2 \200\2233 days of birth. Evidence of bene \201 cial effects (in newborns) includes: sepsis; fewer days of PN; improved grow th; improved gut function. minimal enteral feeding, gut priming. during PN in newborn infants, particularly if preterm . : prolongation of enteral starvation leads to loss of normal GI \200 fewer episodes of 10_McClure_10.indd 322 11/14/2012 11:28:48 PM NUTRITIONAL SUPPORT 323 10_McClure_10.indd 323 11/14/2012 11:28:48 PM CHAPTER 10 Gastroenterology and nutrition 324 Parenteral nutrition IV parenteral nutrition may be supplemental or provide TPN. Parents ca n be trained to give prolonged PN at home to children. Indications \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Post-operative, e.g. abdominal or cardiothoracic. Treatment of IBD. After severe trauma or burns. Acute pancreatitis. Oral feeds are contraindicated, e.g. NEC. Intestinal failure, e. g. short bowel syndrome, congential enteropathy. Protracted vomiting or diarrhea. GI obstru ction, e.g. chronic intestinal pseudo-obstruction. Very preterm infants. Oncology patients, e.g. severe mucositis, graft versus host disease. Administration \200 A multidisciplinary team of clinician, pharmacist, and pediatric dietitian should be involv ed in supervising PN. Follow unit/hospital dietetic/drugstore guidelines for individual nee ds. Allowance should be made of body weight (you may need to estimate a working weight, e.g . if oedematous or gross ascites), recent weight trends, clinical condition, \202 uid and nutritional requirements, additional infused \202 uids. \200 Method Once requirements are calculated, sterile drugstore-prepared solutions are given via central (preferable) or peripheral venous lines. Rapid com- mencement of PN may risk \200 \230refeeding syndrome \200\231 in chronically under- nourished patients (see b p.320). Whe n signi \201 cant malnutrition exists, measure and correct electrolyte abnormalities befor e commencing PN and introduce slowly. PN is usually supplied and administered as two components. Lipid and fat soluble vitamins. Usually infused over 20hr. component: contains carbohydrate (glucose solution), protein Aqu eous (crystalline L-amino acid solution), electrolytes, water soluble vitamins, minerals, t race elements (zinc, copper, manganese, selenium, +/ \200\223 iron). Usually infused over 2 4hr. component: contains fat (triglyceride emulsion, e.g. Intralipid 20%) Monitoring Serious, unexpected biochemical disturbances occur rarely as a result of PN. An appropriate monitoring regimen is suggested in Table 10.2. Weaning PN should be weaned slowly so that hypoglycaemia is avoided. This also allows GI mu cosal recovery as enteral feeding is increased. When wean- ing is protracted parenteral nut rition can be administered over shortened periods. A pediatric dietitian should assess the contribution of both enteral and parenteral feeds to ensure nutritional adequacy. 10_McClure_10.indd 324 11/14/2012 11:28:48 PM PARENTERAL NUTRITION 325 Complications/problems \200 \200 \200 \200 \200 \200 Sepsis Demanding: Central-line: Electrolyte/metabolic Vascular Cardiac atrium. From amino a cids: cholestasis, or, rarely cirrhosis or portal hypertension. From lipids hypertension. M etabolic bone disease: : usually S. epidermidis, S. aureus, Candida, Pseudomonas, E. coli. in expertise, cost, etc. occlusion, breakage, displacement. disturbances: e.g. glucose i or d. : thrombophlebitis, thromboembolism, extravasation injuries. tamponade: avoid by placing IV line tip proximal to right PN-associated liver disease, including, steatosis, : platelet dysfunction, hyperlipidaemia, fatty liver, pulmonary 3 \200\223. due to insuf \201 cient Ca2+ and PO4 Table 10.2 Guidelines for monitoring stable patients during short- term PN During Measurements Pre-PN 1st week 2nd week 3rd and subsequent weeks x 2 (cid:2) x 2 x 2 Creatinine, urea, Na, K (cid:2) x 1 x 1 x 2 x 1 x 1 x 1 x 1 x 1 x 2 Mthly x 2 x 2 Calcium (cid:2) Magnesium (cid:2) Phosphate (cid:2) ALP, ALT, bilirubin, albumin (cid:2) Glucose Daily blood glucose Urine dipstick daily Urine dipstick daily Cu, Zn, Se \200\224 \200\224 \200\224 x 1 x 1 Daily Mthly x 1 x 1 Daily FBC \200\224 (cid:2) (cid:2) \200\224 x 1 Daily Triglycerides Weight 10_McClure_10.indd 325 11/14/2012 11:28:48 PM CHAPTER 10 Gastroenterology and nutrition 326 Oesophageal disorders See also b pp.276, 295. Gastro-oesophageal re \202 ux (GORD) Gastro-oesophageal re \202 ux occurs when there is i nappropriate effort- less passage of gastric contents into the esophagus. GORD exists when re \202 ux is repeated and severe enough to cause harm. Re \202 ux is very com- mon in in fancy and is associated with slow gastric emptying, liquid diet (milk), horizontal posture, and low resting lower oesophageal sphincter (LOS) pressure. Other causes in infancy and in older children include: LOS dysfunc- tion (e.g. hiatus herni a); i gastric pressure (e.g. delayed gastric emptying); external gastric pressure; gastric hypersecretion (e.g. acid); food allergy; and CNS disorders (e.g. cerebral palsy). Presentation of GORD \200 Gastrointestinal: oesophagitis (heartburn, dif \201 cult feeding with crying, painful swal lowing, haematemesis), faltering growth (calorie de \201 ciency due to profuse re \202 ux of ingested calories). Respiratory: disease (aspiration pneumonia, asthma, BPD). Neurobeha vioural and lateral turning of head, dystonic postures). Complications: \200 \200 \200 \200 \200 regurgitation, non-speci \201 c irritability, rumination, apnoea, hoarseness, cough, stridor, lower respiratory symptoms: e.g. Sandifer \200\231s syndrome (bizarre extension oesophageal stricture (dysphagia); barrett \200\231s esophagus (premalignant intestinal met aplasia); faltering growth; anemia (chronic blood loss); lower respiratory disease. Management of GORD \200 \200 \200 History: Examination: Investigations response to treatment, or complications occur) may inc lude: upper GI endoscopy; oesophageal biopsy; 24hr oesophageal pH probe; barium swallow wit h \202 uoroscopy; radioisotope \200\230milk \200\231 scan (aspiration); oesophageal mano metry (oesophageal dysmotility); and CXR (associated respiratory disease). e.g. effortless regurgitation, relationship to feeds. including growth, possible anemia, respiratory. (appropriate when diagnosis is uncertain, t here is a poor Treatment Treatment is carried out in a stepwise fashion. \200 \200 nurse infants on head-up slope of 30* 9 prone. Positioning: Dietary: food before sleep; avoid fatty foods, citrus juices, caffeine, carbon ated drinks, \200\230alcohol and smoking \200\231. Drugs: oesophagitis); Gaviscon (conta ins antacids and an alginate that forms thickened milk feeds (infants); small frequent meals; avoid gastric acid reducing drugs, e.g. ranitidine or omeprazole (if 10_McClure_10.indd 326 11/14/2012 11:28:48 PM