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Necrotizing Enterocolitis Medication

  • Author: Shelley C Springer, JD, MD, MSc, MBA, FAAP; Chief Editor: Ted Rosenkrantz, MD  more...
 
Updated: Jan 02, 2016
 

Medication Summary

Pharmacologic therapy for necrotizing enterocolitis (NEC) includes agents to treat the developing disease and those to provide supportive and symptomatic relief.

As previously mentioned, placement of a central venous catheter for administration of pressors, fluids, antibiotics, and blood products is prudent because severely affected patients often have complications that include sepsis, shock, and DIC.

The initial course of treatment in stage I or II NEC consists of stopping enteral feedings, performing nasogastric decompression, and initiating broad-spectrum antibiotics. Historically, antibiotic coverage has consisted of ampicillin, gentamicin, and either clindamycin or metronidazole, although the specific regimen used should be tailored to the most common nosocomial organisms found in the particular NICU. Probiotics are emerging as a possible preventive therapy.[33]

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Antibiotics

Class Summary

Although no single infectious etiology is known to cause necrotizing enterocolitis (NEC), clinical consensus finds that antibiotic treatment is appropriate. Broad-spectrum parenteral therapy is initiated at the onset of symptoms after obtaining blood, spinal fluid, and urine for culture. Antibiotic coverage for staphylococcus should be considered in NICUs that have a high colonization rate. Antifungal therapy should be considered for premature infants with a history of recent or prolonged antibacterial therapy or for babies who continue to deteriorate clinically or hematologically despite adequate antibacterial coverage.

Various antibiotic regimens can be employed; one frequently used regimen includes ampicillin, aminoglycoside (eg, gentamicin) or third-generation cephalosporin (cefotaxime), and clindamycin or metronidazole. Vancomycin should be included if staphylococcus coverage is deemed appropriate. This combination provides broad gram-positive coverage (including staphylococcal species), excellent gram-negative coverage (with the exception of pseudomonads), and anaerobic coverage.

Doses are adapted from Neofax.[50] Postmenstrual age (PMA) is equivalent to gestational age plus postnatal age. Postnatal age is used as a secondary qualifier to determine dose.

Cefotaxime (Claforan)

 

Cefotaxime is a broad-spectrum, third-generation cephalosporin with excellent nonpseudomonal, gram-negative coverage at the expense of gram-positive effects. Its safety profile is more favorable than that for aminoglycosides. Cefotaxime penetrates cerebrospinal fluid to treat meningitis.

Ampicillin

 

Ampicillin is a broad-spectrum penicillin. It interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Ampicillin is an alternative to amoxicillin when medication cannot be taken orally. Previously, the HACEK bacteria were uniformly susceptible to ampicillin. However, beta-lactamase–producing strains of HACEK have been identified.

Gentamicin

 

Gentamicin is an aminoglycoside antibiotic for gram-negative coverage of bacteria, including Pseudomonas species. It is synergistic with beta lactamase against enterococci. Gentamicin interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits. Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as the body space into which the agent needs to distribute. Monitor gentamicin by serum levels obtained before the third or fourth dose (0.5 h before dosing); the peak level may be drawn 0.5 hour after a 30-minute infusion.

Vancomycin (Vancocin)

 

Vancomycin provides excellent gram-positive coverage, including of methicillin-resistant Staphylococcus species and Streptococcus species. The drug blocks bacterial cell wall synthesis. The parenteral formulation is widely bioavailable throughout all body tissues and fluids, including cerebrospinal fluid. Vancomycin is recommended for empiric use in patients with central lines and ventriculoperitoneal (VP) shunts, and for those with probable staphylococcal or streptococcal infection. Enteral administration is used for Clostridium difficile intoxication.

Clindamycin (Cleocin)

 

Clindamycin inhibits bacterial protein synthesis; it is bacteriostatic or bacteriocidal, depending on the drug concentration and organism. Coverage includes anaerobes commonly found in the intestinal tract and many staphylococcal and streptococcal species.

Metronidazole (Flagyl)

 

Metronidazole is used to treat susceptible anaerobic bacterial and protozoal intraabdominal, systemic, or central nervous system (CNS) infections.

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Vasopressors

Class Summary

Babies with serious illness may progress to shock and require pharmacologic blood pressure support.

Dopamine

 

Dopamine is an adrenergic agonist that increases blood pressure by stimulating alpha-adrenergic vascular receptors, resulting in vasoconstriction. It has some inotropic effects via beta1 cardiac receptors and, at low doses, increases glomerular filtration via renal dopaminergic receptors. Dopamine is useful for babies with hypotension who are not responsive to volume repletion. It may be mixed in dextrose so that glucose delivery is not compromised.

Dobutamine

 

Dobutamine is an adrenergic agonist with specific effects on beta1-receptors in the heart, resulting in increased contractility. It has minimal alpha-adrenergic activity. Dobutamine can be used for babies in shock, usually adjunctively with dopamine, to increase cardiac output. It may be mixed in dextrose so that glucose delivery is not compromised.

Epinephrine (Adrenalin)

 

Epinephrine is a nonspecific adrenergic agonist that stimulates alpha receptors, beta1 receptors, and beta2 receptors. It can be used to support blood pressure in severe hypotension that is refractory to other treatment modalities.

Naloxone

 

Naloxone is an opioid receptor blocker. Experimental evidence suggests that it may increase blood pressure for babies in shock, perhaps by blocking the binding of endogenously produced endorphins released in sepsis, particularly from gram-negative organisms.

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Volume Expanders

Class Summary

Patients with severe illness may experience fluid shifts to the extracellular space, resulting in intravascular depletion that requires expansion.

Albumin (5% and 25%)

 

Albumin is used to increase intravascular oncotic pressure in hypovolemia and helps to mobilize fluids from the interstitial to the intravascular space. The concentration can be either 5% (5 g/100 mL) or 25% (25 g/100 mL), depending on the desired effect.

Sodium chloride hypertonic, ophthalmic (Normal saline, NS, Isotonic saline)

 

Sodium chloride can be used as a volume expander and can be as effective as albumin in acute hypovolemia.

Fresh frozen plasma

 

Fresh frozen plaza is especially helpful as a volume expander in patients with concomitant coagulopathy.

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Glucocorticosteroids

Class Summary

These agents correct the inappropriate adrenal response that is often present in very ill neonates. Once hydrocortisone therapy is initiated, hypotension typically resolves.

Hydrocortisone (Solu-Cortef)

 

Hydrocortisone elicits mineralocorticoid activity and glucocorticoid effects.

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Opioid Analgesics

Class Summary

Although difficult to assess, premature infants presumably experience pain with severe illness and invasive procedures. Narcotic analgesics are safe and effective in premature infants and have a long history of clinical experience.

Morphine sulfate (Duramorph, Astramorph, Oramorph SR, MS Contin)

 

Morphine sulfate is an opioid analgesic with a long history of safe and effective use in neonates. It inhibits ascending pain pathways by binding to the opiate receptors in the CNS, causing generalized CNS depression. Morphine sulfate is used for sedation and analgesia.

Fentanyl (Onsolis, Fentora, Actiq, Duragesic)

 

Fentanyl is an opioid analgesic that is 50-100 times more potent than morphine. Its mechanism of action and indications for use are similar to those of morphine; however, fentanyl has less hypotensive effect than morphine does, because of minimal to no associated histamine release. Fentanyl is administered as an IV bolus or as a continuous infusion. Because of the small volumes used in neonates for bolus administration, it is not usually cost-effective to administer as a bolus.

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Antifungal Agents

Class Summary

The mechanism of action in these agents may involve an alteration of ribonucleic acid (RNA) and deoxyribonucleic acid (DNA) metabolism or an intracellular accumulation of peroxide, which is toxic to the fungal cell.

If antifungal therapy is warranted, fluconazole can be initiated. Fluconazole is less toxic than amphotericin B, which is substituted if no clinical response to fluconazole occurs or if evidence of microbiologic resistance is present.

Fluconazole (Diflucan)

 

Fluconazole is an antifungal agent with good activity against Candida albicans. It is associated with less toxicity and is easier to administer than amphotericin B; however, fluconazole-resistant candidal species are being isolated with increasing frequency. This agent can be administered enterally or parenterally.

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Probiotics

Class Summary

A meta-analysis of published studies showed that oral administration of nonpathogenic bacterial species may result in beneficial alteration of intestinal bacterial flora, reducing the risk and severity of disease.[51, 52, 53, 54, 55, 56, 57, 58, 59] However, data are insufficient regarding the optimal time of initiation, type and dose of bacteria to be used, duration of administration, and potential adverse effects.

Some probiotic formulations used in these studies are not available in the United States, and no regimen or available preparation can be issued based on the meta-analysis. Because of these unknown factors, this therapy is experimental and is not accepted as a standard of care.

Lactobacillus acidophilus/Bifidobacterium infantis (Floranex, Bacid, Dofus, Culturelle)

 

These lactic acid–producing organisms are thought to acidify the intestinal contents and to prevent selective bacterial growth. Probiotic live cultures are intended to restore or maintain healthy microbial flora. Data are currently emerging regarding their use in NEC. Various products are available and doses may vary between products. Infloran has specifically been studied in very low birth weight (VLBW) infants with NEC. It has completed phase II clinical trials.

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Contributor Information and Disclosures
Author

Shelley C Springer, JD, MD, MSc, MBA, FAAP Professor, University of Medicine and Health Sciences, St Kitts, West Indies; Clinical Instructor, Department of Pediatrics, University of Vermont College of Medicine; Clinical Instructor, Department of Pediatrics, University of Wisconsin School of Medicine and Public Health

Shelley C Springer, JD, MD, MSc, MBA, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Coauthor(s)

David J Annibale, MD Professor of Pediatrics, Director of Neonatology, Director of Fellowship Training Program in Neonatal-Perinatal Medicine, Department of Pediatrics, Medical University of South Carolina

David J Annibale, MD is a member of the following medical societies: American Academy of Pediatrics, National Perinatal Association

Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD Professor, Departments of Pediatrics and Obstetrics/Gynecology, Division of Neonatal-Perinatal Medicine, University of Connecticut School of Medicine

Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Eastern Society for Pediatric Research, American Medical Association, Connecticut State Medical Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

Robert S Bloss, MD Clinical Associate Professor of Surgery and Pediatrics, University of Texas Medical School; Clinical Assistant Professor, Department of Surgery, Baylor College of Medicine; Consulting Staff, Houston Pediatric Surgeons

Robert S Bloss, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Southwestern Surgical Congress, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Li Ern Chen, MD Fellow, Pediatric Surgery, Children's Hospital of Wisconsin, Medical College of Wisconsin

Li Ern Chen, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, and Sigma Xi

Disclosure: Nothing to disclose.

David A Clark, MD Chairman, Professor, Department of Pediatrics, Albany Medical College

David A Clark, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Pediatric Society, Christian Medical & Dental Society, Medical Society of the State of New York, New York Academy of Sciences, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Diana Farmer, MD Associate Professor, Departments of Clinical Surgery, Pediatrics, Obstetrics, Gynecology and Reproductive Services, Division of Pediatric Surgery and the Fetal Treatment Center, University of California at San Francisco

Diana Farmer, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, and American Pediatric Surgical Association

Disclosure: Nothing to disclose.

Philip Glick, MD, MBA Professor, Departments of Surgery, Pediatrics, and Gynecology and Obstetrics, Vice-Chairperson for Finance and Development, Department of Surgery, State University of New York at Buffalo

Philip Glick, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, American Thoracic Society, Association for Academic Surgery, Association for Surgical Education, Central Surgical Association, Federation of American Societies for Experimental Biology, Medical Society of the State of New York, Phi Beta Kappa, Physicians for Social Responsibility, Royal College of Surgeons of England, Sigma Xi, Society for Pediatric Research, Society for Surgery of the Alimentary Tract, Society of Critical Care Medicine, and Society of University Surgeons

Disclosure: Nothing to disclose.

Andre Hebra, MD Chief, Division of Pediatric Surgery, Medical University of South Carolina; Professor of Surgery and Pediatrics, Medical University of South Carolina

Andre Hebra, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, Association for Academic Surgery, Society of Laparoendoscopic Surgeons, South Carolina Medical Association, Southeastern Surgical Congress, and Southern Medical Association

Disclosure: Nothing to disclose.

Oussama Itani, MD, FAAP, FACN Clinical Associate Professor of Pediatrics and Human Development, Michigan State University; Medical Director, Department of Neonatology, Borgess Medical Center

Oussama Itani, MD, FAAP, FACN is a member of the following medical societies: American Academy of Pediatrics, American College of Nutrition, American College of Physician Executives, and American Heart Association

Disclosure: Nothing to disclose.

Robert K Minkes, MD, PhD Professor of Surgery, University of Texas Southwestern; Chief of Surgical Services, Children's Medical Center of Dallas-Legacy

Robert K Minkes, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, American Pediatric Surgical Association, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Tapash K Palit, MD Assistant Professor of Surgery, Louisiana State University Health Sciences Center, New Orleans

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, Medscape Reference

Disclosure: Nothing to disclose.

References
  1. Scmid O, Quaiser K. Uer eine besondere schwere verlaufende Form von enteritis beim saugling. Oesterr Z Kinderh. 1953. 8:114.

  2. Berdon WE. Necrotizing enterocolitis in the premature infant. Radiology. 1964. 83:879.

  3. Hunter CJ, Bean JF. Cronobacter: an emerging opportunistic pathogen associated with neonatal meningitis, sepsis and necrotizing enterocolitis. J Perinatol. 2013 Aug. 33(8):581-5. [Medline].

  4. Hunter, CJ, Camerini V, Boyle A, et al. Bacterial Flora Enhance Intestinal Injury and Inflammation in the Rat Pup Model of Necrotizing Enterocolitis. Presented at PAS 2007, Toronto: Childrens hospital Los Angeles, CA; 2007.

  5. Pickard SS, Feinstein JA, Popat RA, Huang L, Dutta S. Short- and long-term outcomes of necrotizing enterocolitis in infants with congenital heart disease. Pediatrics. 2009 May. 123(5):e901-6. [Medline]. [Full Text].

  6. Been JV, Lievense S, Zimmermann LJ, Kramer BW, Wolfs TG. Chorioamnionitis as a risk factor for necrotizing enterocolitis: a systematic review and meta-analysis. J Pediatr. 2013 Feb. 162(2):236-42.e2. [Medline].

  7. Moya FR, Eguchi H, Zhao B, et al. Platelet-activating factor acetylhydrolase in term and preterm human milk: a preliminary report. J Pediatr Gastroenterol Nutr. 1994 Aug. 19(2):236-9. [Medline].

  8. Book LS, Herbst JJ, Atherton SO, Jung AL. Necrotizing enterocolitis in low-birth-weight infants fed an elemental formula. J Pediatr. 1975 Oct. 87(4):602-5. [Medline].

  9. Wan-Huen P, Bateman D, Shapiro DM, Parravicini E. Packed red blood cell transfusion is an independent risk factor for necrotizing enterocolitis in premature infants. J Perinatol. 2013 Oct. 33(10):786-90. [Medline].

  10. Bhandari V, Bizzarro MJ, Shetty A, Zhong X, Page GP, Zhang H, et al. Familial and genetic susceptibility to major neonatal morbidities in preterm twins. Pediatrics. 2006 Jun. 117(6):1901-6. [Medline].

  11. Moonen RM, Paulussen AD, Souren NY, Kessels AG, Rubio-Gozalbo ME, Villamor E. Carbamoyl phosphate synthetase polymorphisms as a risk factor for necrotizing enterocolitis. Pediatr Res. 2007 Aug. 62(2):188-90. [Medline].

  12. Franklin AL, Said M, Cappiello CD, et al. Are immune modulating single nucleotide polymorphisms associated with necrotizing enterocolitis?. Sci Rep. 2015 Dec 16. 5:18369. [Medline].

  13. Treszl A, Heninger E, Kalman A, Schuler A, Tulassay T, Vasarhelyi B. Lower prevalence of IL-4 receptor alpha-chain gene G variant in very-low-birth-weight infants with necrotizing enterocolitis. J Pediatr Surg. 2003 Sep. 38(9):1374-8. [Medline].

  14. Young C, Sharma R, Handfield M, Mai V, Neu J. Biomarkers for Infants at Risk for Necrotizing Enterocolitis: Clues to Prevention?. Pediatr Res. 2009 Jan 28. [Medline].

  15. More K, Athalye-Jape G, Rao S, Patole S. Association of inhibitors of gastric acid secretion and higher incidence of necrotizing enterocolitis in preterm very low-birth-weight infants. Am J Perinatol. 2013 Nov. 30(10):849-56. [Medline].

  16. Terrin G, Passariello A, De Curtis M, et al. Ranitidine is Associated With Infections, Necrotizing Enterocolitis, and Fatal Outcome in Newborns. Pediatrics. 2012 Jan. 129(1):e40-5. [Medline].

  17. Kawase Y, Ishii T, Arai H, Uga N. Gastrointestinal perforation in very low-birthweight infants. Pediatr Int. 2006 Dec. 48(6):599-603. [Medline].

  18. Kovacs L, Papageorgiou, A. Incidence, Predisposing Factors and Outcome of NEC in Infants <32 Weeks' Gestation. Presented at PAS 2007, Toronto: SMBD-Jewish General Hospital, McGill University, Montreal; 2007.

  19. Wiswell TE, Robertson CF, Jones TA, Tuttle DJ. Necrotizing enterocolitis in full-term infants. A case-control study. Am J Dis Child. 1988 May. 142(5):532-5. [Medline].

  20. Brotschi B, Baenziger O, Frey B, Bucher HU, Ersch J. Early enteral feeding in conservatively managed stage II necrotizing enterocolitis is associated with a reduced risk of catheter-related sepsis. J Perinat Med. 2009 Aug 13. [Medline].

  21. McKeown RE, Marsh TD, Amarnath U, et al. Role of delayed feeding and of feeding increments in necrotizing enterocolitis. J Pediatr. 1992 Nov. 121(5 Pt 1):764-70. [Medline].

  22. Shorter NA, Liu JY, Mooney DP, Harmon BJ. Indomethacin-associated bowel perforations: a study of possible risk factors. J Pediatr Surg. 1999 Mar. 34(3):442-4. [Medline].

  23. Adderson EE, Pappin A, Pavia AT. Spontaneous intestinal perforation in premature infants: a distinct clinical entity associated with systemic candidiasis. J Pediatr Surg. 1998 Oct. 33(10):1463-7. [Medline].

  24. Stark AR, Carlo WA, Tyson JE, et al. Adverse effects of early dexamethasone in extremely-low-birth-weight infants. National Institute of Child Health and Human Development Neonatal Research Network. N Engl J Med. 2001 Jan 11. 344(2):95-101. [Medline].

  25. Sylvester KG, Ling XB, Liu GY, Kastenberg ZJ, Ji J, Hu Z, et al. Urine protein biomarkers for the diagnosis and prognosis of necrotizing enterocolitis in infants. J Pediatr. 2014 Mar. 164(3):607-612.e7. [Medline].

  26. Bohnhorst B. Usefulness of abdominal ultrasound in diagnosing necrotising enterocolitis. Arch Dis Child Fetal Neonatal Ed. 2013 Sep. 98(5):F445-50. [Medline].

  27. Deeg KH, Rupprecht T, Schmid E. Doppler sonographic detection of increased flow velocities in the celiac trunk and superior mesenteric artery in infants with necrotizing enterocolitis. Pediatr Radiol. 1993. 23(8):578-82. [Medline].

  28. Harding A. Slow feeding helps prevent necrotizing enterocolitis in smallest preemies. Reuters Health. October 27, 2014. Available at http://www.pediatricsconsultant360.com/story/slow-feeding-helps-prevent-necrotizing-enterocolitis-smallest-preemies. Accessed: November 1, 2014.

  29. Viswanathan S, McNelis K, Super D, Einstadter D, Groh-Wargo S, Collin M. A Standardized Slow Enteral Feeding Protocol and the Incidence of Necrotizing Enterocolitis in Extremely Low Birth Weight Infants. JPEN J Parenter Enteral Nutr. 2014 Oct 14. [Medline].

  30. Kapoor V, Glover R, Malviya MN. Alternative lipid emulsions versus pure soy oil based lipid emulsions for parenterally fed preterm infants. Cochrane Database Syst Rev. 2015 Dec 2. 12:CD009172. [Medline].

  31. Hoyos AB. Reduced incidence of necrotizing enterocolitis associated with enteral administration of Lactobacillus acidophilus and Bifidobacterium infantis to neonates in an intensive care unit. Int J Infect Dis. 1999. 3(4):197-202. [Medline].

  32. Alfaleh K, Anabrees J, Bassler D. Probiotics Reduce the Risk of Necrotizing Enterocolitis in Preterm Infants: A Meta-Analysis. Neonatology. 2009 Aug 25. 97(2):93-99. [Medline].

  33. Olsen R, Greisen G, Schrøder M, Brok J. Prophylactic probiotics for preterm infants: a systematic review and meta-analysis of observational studies. Neonatology. 2015 Dec 2. 109 (2):105-112. [Medline].

  34. Sharma D, Shastri S. Lactoferrin and neonatology - role in neonatal sepsis and necrotizing enterocolitis: present, past and future. J Matern Fetal Neonatal Med. 2016 Mar. 29 (5):763-70. [Medline].

  35. Pammi M, Abrams SA. Oral lactoferrin for the prevention of sepsis and necrotizing enterocolitis in preterm infants. Cochrane Database Syst Rev. 2011 Oct 5. CD007137. [Medline].

  36. Haque KN, Pammi M. Pentoxifylline for treatment of sepsis and necrotizing enterocolitis in neonates. Cochrane Database Syst Rev. 2011 Oct 5. CD004205. [Medline].

  37. Vaughan WG, Grosfeld JL, West K, Scherer LR 3rd, Villamizar E, Rescorla FJ. Avoidance of stomas and delayed anastomosis for bowel necrosis: the 'clip and drop-back' technique. J Pediatr Surg. 1996 Apr. 31(4):542-5. [Medline].

  38. Martin LW, Neblett WW. Early operation with intestinal diversion for necrotizing enterocolitis. J Pediatr Surg. 1981 Jun. 16(3):252-5. [Medline].

  39. Ein SH, Marshall DG, Girvan D. Peritoneal drainage under local anesthesia for perforations from necrotizing enterocolitis. J Pediatr Surg. 1977 Dec. 12(6):963-7. [Medline].

  40. Moss RL, Dimmitt RA, Barnhart DC, Sylvester KG, Brown RL, Powell DM, et al. Laparotomy versus peritoneal drainage for necrotizing enterocolitis and perforation. N Engl J Med. 2006 May 25. 354(21):2225-34. [Medline].

  41. Premkumar MH, Carter BA, Hawthorne KM, King K, Abrams SA. High rates of resolution of cholestasis in parenteral nutrition-associated liver disease with fish oil-based lipid emulsion monotherapy. J Pediatr. 2013 Apr. 162(4):793-798.e1. [Medline].

  42. Lucas A, Cole TJ. Breast milk and neonatal necrotising enterocolitis. Lancet. 1990 Dec 22-29. 336(8730):1519-23. [Medline].

  43. Eyal F, Sagi E, Arad I, Avital A. Necrotising enterocolitis in the very low birthweight infant: expressed breast milk feeding compared with parenteral feeding. Arch Dis Child. 1982 Apr. 57(4):274-6. [Medline].

  44. Chowning R, Radmacher P, Lewis S, Serke L, Pettit N, Adamkin DH. A retrospective analysis of the effect of human milk on prevention of necrotizing enterocolitis and postnatal growth. J Perinatol. 2015 Dec 3. [Medline].

  45. Berseth CL. Effect of early feeding on maturation of the preterm infant's small intestine. J Pediatr. 1992 Jun. 120(6):947-53. [Medline].

  46. Meetze WH, Valentine C, McGuigan JE, et al. Gastrointestinal priming prior to full enteral nutrition in very low birth weight infants. J Pediatr Gastroenterol Nutr. 1992 Aug. 15(2):163-70. [Medline].

  47. Rayyis SF, Ambalavanan N, Wright L, Carlo WA. Randomized trial of "slow" versus "fast" feed advancements on the incidence of necrotizing enterocolitis in very low birth weight infants. J Pediatr. 1999 Mar. 134(3):293-7. [Medline].

  48. Kennedy KA, Tyson JE, Chamnanvanakij S. Rapid versus slow rate of advancement of feedings for promoting growth and preventing necrotizing enterocolitis in parenterally fed low-birth-weight infants. Cochrane Database Syst Rev. 2000. (2):CD001241. [Medline].

  49. [Guideline] Cincinnati Children's Hospital Medical Center. Evidence-based care guideline for necrotizing enterocolitis (NEC) among very low birth weight infants. Cincinnati (OH): Cincinnati Children's Hospital Medical Center; 2007 Feb.

  50. Young TE, Mangum B. Neofax. Twenty-first edition. Montvale, NJ: Thomson Reuters; 2008.

  51. Alfaleh K, Bassler D. Probiotics for prevention of necrotizing enterocolitis in preterm infants. Cochrane Database Syst Rev. 2008 Jan 23. CD005496. [Medline].

  52. Bin-Nun A, Bromiker R, Wilschanski M, et al. Oral probiotics prevent necrotizing enterocolitis in very low birth weight neonates. J Pediatr. 2005 Aug. 147(2):192-6. [Medline].

  53. Carlson K, Schy RB, Jilling T, Lu J, Caplan MS. The Two Probiotic strains, L acidophilus and S thermophilus, down-regulate Toll-like Receptor 4 Expression in Enterocytes. Presented at PAS Toronto, 2007: Evanston Northwestern Hospital, IL; 2007.

  54. Dani C, Biadaioli R, Bertini G, Martelli E, Rubaltelli FF. Probiotics feeding in prevention of urinary tract infection, bacterial sepsis and necrotizing enterocolitis in preterm infants. A prospective double-blind study. Biol Neonate. 2002 Aug. 82(2):103-8. [Medline].

  55. Hammerman C, Bin-Nun A, Kaplan M. Germ warfare: probiotics in defense of the premature gut. Clin Perinatol. 2004 Sep. 31(3):489-500. [Medline].

  56. Lin HC, Su BH, Chen AC, et al. Oral probiotics reduce the incidence and severity of necrotizing enterocolitis in very low birth weight infants. Pediatrics. 2005 Jan. 115(1):1-4. [Medline].

  57. Millar M, Wilks M, Costeloe K. Probiotics for preterm infants?. Arch Dis Child Fetal Neonatal Ed. 2003 Sep. 88(5):F354-8. [Medline].

  58. Lin HC, Hsu CH, Chen HL, et al. Oral probiotics prevent necrotizing enterocolitis in very low birth weight preterm infants: a multicenter, randomized, controlled trial. Pediatrics. 2008 Oct. 122(4):693-700. [Medline].

  59. Alfaleh K, Anabrees J, Bassler D, Al-Kharfi T. Probiotics for prevention of necrotizing enterocolitis in preterm infants. Cochrane Database Syst Rev. 2011 Mar 16. 3:CD005496. [Medline].

  60. Hand L. NICU: Probiotics Reduce NEC, Should Be Routine, Experts Say. Available at http://www.medscape.com/viewarticle/820814. Accessed: February 24, 2014.

  61. Janvier A, Malo J, Barrington KJ. Cohort Study of Probiotics in a North American Neonatal Intensive Care Unit. J Pediatr. 2014 Jan 7. [Medline].

  62. Tarnow-Mordi W, Soll RF. Probiotic Supplementation in Preterm Infants: It Is Time to Change Practice. J Pediatr. 2014 Feb 8. [Medline].

  63. Groer MW, Gregory KE, Louis-Jacques A, Thibeau S, Walker WA. The very low birth weight infant microbiome and childhood health. Birth Defects Res C Embryo Today. 2015 Dec 10. [Medline].

 
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Normal (top) versus necrotic section of bowel. Photo courtesy of the Department of Pathology, Cornell University Medical College.
Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
Pneumatosis intestinalis. Photo courtesy of Loren G Yamamoto, MD, MPH, Kapiolani Medical Center for Women & Children, University of Hawaii, with permission.
Pneumoperitoneum. Photo courtesy of the Department of Pathology, Cornell University Medical College.
Resected portion of necrotic bowel. Photo courtesy of the Department of Pathology, Cornell University Medical College.
Micrograph of mucosal section showing transmural necrosis. Photo courtesy of the Department of Pathology, Cornell University Medical College.
Histologic section of mucosal wall demonstrating pneumatosis. Photo courtesy of the Department of Pathology, Cornell University Medical College.
Histologic section of bowel mucosa showing regeneration of normal cellular architecture. Photo courtesy of the Department of Pathology, Cornell University Medical College.
Extensive pneumatosis intestinalis.
Necrotizing enterocolitis totalis. Pneumatosis intestinalis and multiple areas of perforation were seen.
Pneumatosis intestinalis.
 
 
 
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