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Deirdre Hartigan 13th November 2011
Neonatal Parenteral Nutrition- ‘There’s a hole in my ‘tummy’ dear Liza, dear Liza!’ Deirdre Hartigan 13th November 2011
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Overview of the workshop
Case study 12 questions IFALD NEC & SBS Lipid sources Parenteral Nutrition Complications of PN 2 2
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Overview Case study IFALD 12 questions Lipid sources NEC & SBS
Parenteral Nutrition Complications of PN 3 3
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Necrotising Enterocolitis
NEC is principally a disease of VLBW infants. The classical clinical triad consists of: Abdominal distension GI bleeding Pneumatosis intestinalis (gas in the bowel wall) Risk factors – prematurity, hypoxia, ischaemia, infection, exotoxin (from bacterial overgrowth and intestinal stasis), rapid advancement of feedings and exchange transfusions Nearly all infants with NEC have received enteral feeding. However NEC does not develop in the vast majority of infants who have been enterally fed and there is no evidence that delaying enteral feedings and providing PN prevent the development of NEC. Any part of the GIT can be involved but the ileum, colon and jejunum are the commonest sites. The spectrum of disease varies from a single, localised area ±perforation to involvement of the entire bowel. The pathology starts with coagulation necrosis of the mucosa, progressing to ulceration, oedema and haemorrhage with bacterial infiltration. In extensive cases, there is transmural necrosis and perforation.
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Definition Necrotising enterolcolitis (NEC) is a medical condition primarily seen in premature infants where portions of the bowel undergo necrosis (tissue death)
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Cause No definitive cause Infectious agent Weakened immune function
Intestinal flora Alterations in mesenteric blood flood Formula feeds
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Cause No definitive cause Infectious agent Weakened immune function
Intestinal flora Alterations in mesenteric blood flood Formula feeds NEC has no definitive known cause.3 An infectious agent has been suspected, as cluster outbreaks in neonatal intensive care units (NICUs) have been seen, but no common organism has been identified. Pseudomonas aeruginosa is suspected for causing necrotising enterocolitis in premature infants4 and neutropaenic cancer patients,5 often secondary to gut colonisation. A combination of intestinal flora, inherent weakness in the neonatal immune system, empirical antibiotic use for 5 days or more,6 alterations in mesenteric blood flow and milk feeding may be factors. The most common area of the bowel affected by NEC is near the ileocecal valve (the site of transition between the small and large bowel). NEC is almost never seen in infants before oral feedings are initiated. Formula feeding increases the risk of NEC by tenfold compared to infants who are fed breastmilk alone.7 Expressed breast milk protects the premature infant not only by its antiinfective effect and its immunoglobulin agents but also from its rapid digestion. A study by the Neonatal Research Network, published in the journal Pediatrics in January 2009, conducted a study regarding the administration of empirical antibiotics in extremely low birth weight infants. The research demonstrated that empirical antibiotic therapy over 5 days for extremely low birth weight babies increased the chance of necrotizing enterecolitis by 4% for each additional day over 5 days.6
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Once a child is born prematurely, thought must be given to decreasing the risk for developing NEC. Toward that aim, the methods of providing hyperalimentation and oral feeds are both important. A recent study, by researchers in Peoria, IL, published in Pediatrics in 2008, demonstrated that using a higher rate of lipid (fats and/or oils) infusion for very low birth weight infants in the first week of life resulted in zero infants developing NEC in the experimental group, compared with 14 % with NEC in the control group (They started the experimental group at 2 g/kg/d of 20% IVFE and increased within two days to 3 g/kg/d; Amino acids were started at 3 g/kg/d and increased to 3.5). (Drenckpohl D, McConnell C, Gaffney S, Niehaus M, Macwan KS. Randomized trial of very low birth weight infants receiving higher rates of infusion of lipid emulsions during the first week of life Pediatrics 2008;122; ). Neonatologists at the University of Iowa NICU reported on the importance of providing small amounts of trophic oral feeds of human milk starting ASAP, while the infant is being primarily fed intravenously, in order to prime the immature gut to mature and become ready to receive greater oral intake (Ziegler and Carlson, J Matern Fetal Neonatal Med Mar;22(3):191-7.) Human milk from a milk bank or donor can be used if mother's milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed.
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Alimentary tract of infant showing intestinal necrosis, pneumatosis intestinalis, and perforation site (arrow). Autopsy.
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Close up of intestine of infant showing necrosis and pneumatosis intestinalis. Autopsy.
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Multi-system organ failure
Gut Necrosis Perforation Peritonitis Respiratory Abdominal distension Acidosis RDS Circulation Septic shock Hypotension Blood Coagulopathy Platelets Anaemia Renal Electrolyte imbalance Fluid retention Brain Hypoxia Perfusion injury Typical recovery from NEC if medical, non-surgical treatment succeeds, includes 10–14 days or more without oral intake and then demonstrated ability to resume feedings and gain weight. Recovery from NEC alone may be compromised by co-morbid conditions that frequently accompany prematurity. Longterm complications of medical NEC include bowel obstruction and anemia. Despite a significant mortality risk, long-term prognosis for infants undergoing NEC surgery is improving, with survival rates of 70-80%. "Surgical NEC" survivors are at-risk for complications including short bowel syndrome, and neurodevelopmental disability.
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Short bowel syndrome SBS
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Short Bowel Syndrome “malabsorption resulting from loss of part of the small intestine; inadequate absorptive area, and the physiological consequences” “a reduction in the functioning intestinal mass below the amount necessary for adequate absorption to allow for growth” Spectrum of malabsorption that occurs after resection of a major portion of small intestine Need for prolonged parental nutrition secondary to intestinal failure Short Bowel Syndrome: epidemiology and etiology Wales et al Toronto 2009
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PIN THE TAIL ON THE DONKEY!
(…….kind of!)
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Duodenum Jejunum Ileum Ileocaecal valve Descending colon
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Severe malnutrition pre-PN era.
Successful long term PN in such a patient first described in 1968 by Wilmore and Dudrick Severe malnutrition pre-PN era.
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Overview Case study IFALD 12 questions Lipid sources NEC & SBS
Parenteral Nutrition Complications of PN 17 17
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SBS Outcomes Numerous series of SBS patients have been reported
survivals ranging from 50% to 80%. Greater than 38cm good survival 1,2 and again 2004 1. Wilmore DW. Factors correlating with a successful outcome following extensive intestinal resection in newborn infants. Pediatr 1972;80:88-9 2. LONG-TERM PARENTERAL NUTRITIONAL SUPPORT AND INTESTINAL ADAPTATION IN CHILDREN WITH SHORT BOWEL SYNDROME: A 25-YEAR EXPERIENCE RUBE´N E. QUIRO´ S-TEJEIRA, MD,MARVIN E. AMENT, MD, LAURIE REYEN, RN, FAYEHERZOG, RN,MICHELLEMERJANIAN, MD, NANCYOLIVARES-SERRANO, MD, AND JORGE H. VARGAS, MD The Journal of Pediatrics August 2004 Short gut – 38cm Very short gut - <38cm Ultra Short gut <15cm 18
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Outcomes ¾ survived in 2004 study with < 15cm bowel
50% survival in 1970s 15-38cm ICV improved outcome 19
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Outcomes Survival (neonatal) < 40 cm (n = 35) 67%
(Goulet et al, 1991) ¾ survived in 2004 study with bowel <15cm 20
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Outcomes Prognosis newborn, full enteral feeding established:
<40 cm mean 27 months (3 - 84) cm mean 14 months (1 - 70) (Goulet et al, 1991)
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Outcomes 4 year old girl, 12cm jejunum following midgut volvulus; survived without PN! (Surana et al. JPGN 1994;19: ) survival 8/9 patients without ileocaecal valve and < 40 cm small bowel (Chaet et al. JPGN 1994;19: )
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Surgery To get off PN: Bianchi (bowel lengthening)
STEP (serial transverse enteroplasty) Indications poorly defined. Need dilated bowel
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Bianchi bowel lengthening procedure
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STEP procedure
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Selective Decontamination of Digestive system (SDDS)
Cyclical antibiotics Metronidazole + Trimethoprim + fluconazole (LTH) Gentamicin + Metronidazole + Co-trimoxazole Polymyxin E/Colistin + Tobramicin + Amphoteracin Rifaximin > 2 years of age (LTH) 2 weeks on, 2 weeks off (LTH)
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Overview Case Study IFALD 12 questions Lipid sources NEC & SBS
Parenteral Nutrition Complications of PN 27 27
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Intestinal Failure Associated Liver Disease (IFALD)
Parenteral Nutrition Associated Cholestasis (PNAC) Parenteral Nutrition Associated Liver Disease (PNALD) Intestinal failure occurs when the gastrointestinal tract is unable to ingest, digest and absorb sufficient macronutrients and/or water and electrolytes to maintain health and growth clinical presentation most commonly as jaundice (type 2) conjugated bilirubin >50 μmol/L is a manifestation of significant liver disease urgent review by NST with access to specialist hepatology advice diagnosis of IFALD should prompt multi-professional review of enteral and parenteral nutrition
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IFALD – Risk factors Prematurity IUGR Lack of enteral intake Lipid
Early CVC infection Co-morbidity Early = < 4 weeks.
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IFALD – Risk factors Short bowel Dysmotility Bacterial overgrowth
Frequent CVC infections (>3/year) Poor aseptic technique Long hospital in-patient stays
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Overview Case study IFALD 12 questions Lipid NEC & SBS sources
Parenteral Nutrition Complications of PN 31 31
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Intralipid 20% Developed in the 1960s Purified soybean oil
Mainly Omega 6 fatty acids 60% polyunsaturated fatty acids (PUFA) 23% monounsaturated fatty acids (MUFA) Reliable source of essential fatty acids Long chain PUFAs play a crucial role in pathogenesis of PNALD. phytosterols in soy emulsions ω-6 pro-inflammatory; oxidative damage
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Clinoleic 20% Olive oil based lipid soybean + olive oil
long chain fatty acids 20% PUFA 65% MUFA intake PUFA Clinoleic – more physiological in his fatty acid profile. Clinoleic has a fatty acid profile that closely matches the recommended normal diet.
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Fish Oil ‘Reversal of Parenteral Nutrition-Associated Liver Disease in Two Infants With Short Bowel Syndrome Using Parenteral Fish Oil: Implications for Future Management’ Gura et al. Paediatrics 2006; 118; ‘The rationale for the use of parenteral omega-3 lipids in children with Short bowel syndrome and liver disease’ Diamond et al.Pediatr Surg Int (2008) 24: ‘Rescue treatment of infants with intestinal failure and parenteral nutrition-associated cholestasis (PNAC) using a parenteral fish- oil-based lipid’ Cheung at al. Clinicl Nutrition 28 (2009)
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Omegaven 10% Fish oil based lipid Rich in Omega 3 Improves bile flow
Decreased steatosis Immunomodulatory effects High percentage of very long chain omega 3 fatty acids.
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SMOF Lipid® Soybean oil Medium-chain triglycerides (MCT) Olive oil
Fish oil (with additional vitamin E to counteract lipid peroxidation and oxidative stress) 37
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Overview 38 Case study IFALD 12 questions NEC & SBS Lipid sources
Parenteral Nutrition Complications of PN 38 38
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Complications of PN - CVC
Occlusion Infection Catheter misplacement Haemorrhage Thrombosis Air embolism Breakage/leakage Prevention of CRBSI is extremely important in order to save precious lines and venous access
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Line Locks Taurolock® - 2% Taurolidine (antimicrobial)
- 4% citrate (prevents thrombus formation) All LTH line locks = 2mL Instil 2ml into each lumen of line and leave for as long as possible. Aspirate before connecting PN or using the line eg to give next dose of antibiotics Taurolock – a catheter lock solution for tunelled and non-tunnelled CVCs and ports. 2% Taurolidine as the antimicrobial component and 4% citrate to prevent clots. antiseptic with a broad range of activity against gram positive and gram negative bacteria and fungi. It is a derivative of taurinamide, a naturally occurring aminosulphonic acid and formaldehyde. In vitro experiments have demonstrated efficacy in preventing and eradicating the catheter bio-film caused by a variety of Gpos and Gneg bacteria and Candida albicans
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Taurolock® Broad spectrum bactericidal activity Not an antibiotic
gram negative & positive organisms fungi Not an antibiotic No antimicrobial resistance Irreversible binding of its methylol groups to the cell walls of the organism Prevents biofilm formation
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Taurolock ® Minimal side effects
Reversible thrombocytopenia & neutropenia Severe localised pain Unusual taste in mouth
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LTH Data Patient Total catheter days CRBSI episodes pre Taurolock® post Taurolock® CRBSI/1000 catheter days 1 1064 2 4394 3 0.87 3290 12 4.4 4 2018 5.26 5 914 8.7 6 1340 9 10.9
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And Finally Thank you! 44 44
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