Neonatal necrotizing enterocolitis
NEC is the most common life-threatening emergency of the gastrointestinal tract in the newborn period. The disease is characterized by various degrees of mucosal or transmural necrosis of the intestine. The cause of NEC remains unclear but is most likely multifactorial. The incidence of NEC is 1-5% of infants in neonatal intensive care units (NICUs). Both incidence and case fatality rates increase with decreasing birthweight and gestational age. Because very small, ill preterm infants are particularly susceptible to NEC, a rising incidence may reflect improved survival of this high-risk group of patients.
Clinical Manifestations
Infants with NEC have a variety of signs and symptoms and may have an insidious or sudden catastrophic onset (Table 96-1). The onset of NEC is usually in the 2nd or 3rd week of life but can be as late as 3 mo in VLBW infants. Age of onset is inversely related to gestational age. The 1st signs of impending disease may be nonspecific, including lethargy and temperature instability, or related to gastrointestinal pathology, such as abdominal distention and gastric retention. Obvious bloody stools are seen in 25% of patients. Because of nonspecific signs, sepsis may be suspected before NEC. The spectrum of illness is broad, ranging from mild disease with only guaiac-positive stools to severe illness with bowel perforation, peritonitis, systemic inflammatory response syndrome, shock, and death. Progression may be rapid, but it is unusual for the disease to progress from mild to severe after 72 hr.
Diagnosis
A very high index of suspicion in treating preterm at-risk infants is crucial. Plain abdominal radiographs are essential to make a diagnosis of NEC. The finding of pneumatosis intestinalis (air in the bowel wall) confirms the clinical suspicion of NEC and is diagnostic; 50-75% of patients have pneumatosis when treatment is started (Fig. 96-4). Portal venous gas is a sign of severe disease, and pneumoperitoneum indicates a perforation (Figs. 96-4 and 96-5). Hepatic ultrasonography may detect portal venous gas despite normal abdominal roentgenograms .
Neonatal necrotizing enterocolitis
NEC is the most common life-threatening emergency of the gastrointestinal tract in the newborn period. The disease is characterized by various degrees of mucosal or transmural necrosis of the intestine. The cause of NEC remains unclear but is most likely multifactorial. The incidence of NEC is 1-5% of infants in neonatal intensive care units (NICUs). Both incidence and case fatality rates increase with decreasing birthweight and gestational age. Because very small, ill preterm infants are particularly susceptible to NEC, a rising incidence may reflect improved survival of this high-risk group of patients.
Clinical Manifestations
Infants with NEC have a variety of signs and symptoms and may have an insidious or sudden catastrophic onset (Table 96-1). The onset of NEC is usually in the 2nd or 3rd week of life but can be as late as 3 mo in VLBW infants. Age of onset is inversely related to gestational age. The 1st signs of impending disease may be nonspecific, including lethargy and temperature instability, or related to gastrointestinal pathology, such as abdominal distention and gastric retention. Obvious bloody stools are seen in 25% of patients. Because of nonspecific signs, sepsis may be suspected before NEC. The spectrum of illness is broad, ranging from mild disease with only guaiac-positive stools to severe illness with bowel perforation, peritonitis, systemic inflammatory response syndrome, shock, and death. Progression may be rapid, but it is unusual for the disease to progress from mild to severe after 72 hr.
Diagnosis
A very high index of suspicion in treating preterm at-risk infants is crucial. Plain abdominal radiographs are essential to make a diagnosis of NEC. The finding of pneumatosis intestinalis (air in the bowel wall) confirms the clinical suspicion of NEC and is diagnostic; 50-75% of patients have pneumatosis when treatment is started (Fig. 96-4). Portal venous gas is a sign of severe disease, and pneumoperitoneum indicates a perforation (Figs. 96-4 and 96-5). Hepatic ultrasonography may detect portal venous gas despite normal abdominal roentgenograms .
Definition of neonatal sepsis,type of neonatal sepsis ,early onset neonatal sepsis,late onset neonatal sepsis,Pathophysiology of neonatal sepsis,,sign and symptoms of neonatal sepsis, diagnosis of neonatal sepsis,management of neonatal sepsis, antibiotic used for neonatal sepsis,prevention of neonatal sepsis, prognosis of neonatal sepsis ,and A summary
Definition of neonatal sepsis,type of neonatal sepsis ,early onset neonatal sepsis,late onset neonatal sepsis,Pathophysiology of neonatal sepsis,,sign and symptoms of neonatal sepsis, diagnosis of neonatal sepsis,management of neonatal sepsis, antibiotic used for neonatal sepsis,prevention of neonatal sepsis, prognosis of neonatal sepsis ,and A summary
Streptococcus mutans in the oral cavity as a risk factor for threatened misca...komalicarol
we have found that the presence of Streptococcus mutans in the
oral cavity of a pregnant woman may be a risk factor for miscarriage. We observed that Streptococcus mutans is significantly more
widespread in the oral cavity of women with threatened abortion
than in those undergoing a healthy pregnancy.
Streptococcus Mutans in the Oral Cavity as a Risk Factor for Threatened Misca...komalicarol
we have found that the presence of Streptococcus mutans in the
oral cavity of a pregnant woman may be a risk factor for miscarriage. We observed that Streptococcus mutans is significantly more
widespread in the oral cavity of women with threatened abortion
than in those undergoing a healthy pregnancy
A randomised, double-blind clinical trial was undertaken in order to assess the effectiveness of probiotics in
the prevention of necrotising enterocolitis (NEC) in newborns weighing <1500 g.
This presentation is part of and education series to pediatric healthcare providers in Syria and it may be useful to all practitioners working in low resource settings.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
1. NECROTIZING
ENTEROCOLITIS
By
AYMAN ABOU MEHREM, MD, CABP
Assistant Consultant
Department of pediatrics
King Abdulaziz Hospital, Al-Ahsa
November 25, 2007
3. Definitions
Necrotizing Enterocolitis:
an acquired neonatal acute intestinal necrosis
of unknown etiology
NEC is neither a uniform nor a well-defined
disease entity.1
1 Gordon PV et al, Emerging trends in acquired neonatal intestinal disease: is it time to abandon Bell's
criteria?, J Perinatol. 2007 Nov;27(11):661-71.
4. Definitions
Isolated spontaneous intestinal perforation
(SIP): ill-defined clinical syndrome of undetermined
cause resembling NEC with less systemic involvement
and a less severe clinical course. It may present a variant
of classical NEC.
The National Institute of Child Health and Human
Development Neonatal Network (NICHD): intestinal
perforation without evidence of pneumatosis since 2002.1
1 Gordon PV et al, Emerging trends in acquired neonatal intestinal disease: is it time to abandon Bell's
criteria?, J Perinatol. 2007 Nov;27(11):661-71.
5. Definitions
Acquired neonatal intestinal diseases (ANIDs)1
Wider umbrella includes different pathologies affecting
gastrointestinal tract in preterm and term infants. Some
which do lead to the common final pathology of NEC and
some which do not.
Includes:
NEC
SIP
Viral enteritis of infancy
Cow’s milk protein allergy
1 Gordon PV et al, Emerging trends in acquired neonatal intestinal disease: is it time to abandon Bell's
criteria?, J Perinatol. 2007 Nov;27(11):661-71.
6. Epidemiology
Incidence: 0.3-2.4 / 1000 live births
2-5 % of all NICU admissions
5-10 % of VLBW infants
Over 90 % of cases occur in preterm babies
About 10 % occur in term newborns: essentially
limited to those that have some underlying illness or
condition requiring NICU admission.2
2 Lambert DK et al. Necrotizing enterocolitis in term neonates: data from a multihospital health-care
system . J Perinatol. 2007 Jul;27(7):437-43 .
7. Epidemiology
Sporadic or epidemic clusters
Sex, race, geography, climate, season: No role
Holman et al.3:
o Male VLBW infants are at greater risk of death.
o Black infants: increased risk of NEC, and its
associated mortality
3 HolmanRC et al. The epidemiology of necrotizing enterocolitis infant mortality in the United States.
Am J Public Health 1997; 87: 2026–31.
8. Risk Factors: Prematurity
Prematurity is the single greatest risk
factor
The risk is inversely related to birth
weight and gestational age.4
4 LinPW, Stoll BJ. Necrotizing enterocolitis. Lancet. 2006 Oct 7;368(9543):1271-83.
5 Czyrko C et al. Maternal cocaine abuse and necrotizing enterocolitis: outcome and survival. J Pediatr
Surg. 1991 Apr;26(4):414-8; discussion 419-21.
9. Risk Factors: Genetics
Familial:
Fried and Vure (1974) reported a consanguineous Jewish
Ashkenazi family in which three of four children died
within a few weeks after birth from severe enterocolitis.5
Mégarbané and Sayad (2007) reported a Lebanese
consanguineous family where three term sibs presented
with severe early and lethal enterocolitis, all with delayed
meconium passage.6
5 FriedK, Vure E. A lethal autosomal recessive entero-colitis of early infancy. Clin Genet 1974 (6),
195-196.
6 Mégarbané A, Sayad R. Early lethal autosomal recessive enterocolitis: report of a second family. Clin
Genet. 2007 Jan;71(1):89-90.
10. Risk Factors: Genetics
Twins:
Bhandari et al, in a multicenter retrospective study of
450 twin pairs born at < or =32 weeks of gestation,
showed that intraventricular hemorrhage,
necrotizing enterocolitis, and bronchopulmonary
dysplasia are familial in origin.7
7 Bhandari et al. Familial and genetic susceptibility to major neonatal morbidities in preterm twins.
Pediatrics. 2006 Jun;117(6):1901-6.
11. Risk Factors: Gene Polymorphism
Vascular endothelial growth factor:
Bányász et al suggest that VEGF G+405C polymorphism might be
associated with a higher risk of preterm birth and that VEGF C-
2578A polymorphism may participate in the development of
perinatal complications such as NEC and ARF.8
Carbamoyl phosphate synthetase:
Moonen et al suggested that the CPS1 T1405N polymorphism may
be associated with the risk of NEC in preterm infants.9
8 Bányász et al. Genetic polymorphisms for vascular endothelial growth factor in perinatal
complications. Eur Cytokine Netw. 2006 Dec;17(4):266-70.
9 Moonen RM et al. Carbamoyl phosphate synthetase polymorphisms as a risk factor for necrotizing
enterocolitis. Pediatr Res. 2007 Aug;62(2):188-90.
12. Risk Factors: G-6-PD Deficiency
Schutzman and Porat, in a retrospective study10, found:
G6PD deficiency was significantly higher (27.8%) in
infants with NEC compared with the 5.3% prevalence
among NICU admissions (odds ratio = 6.9; 95%
confidence interval = 2 to 23.5).
G6PD deficiency also was found to be a marker for more
severe NEC.
G6PD deficiency should be considered a risk factor for
NEC.
10 Schutzman DL, Porat R. Glucose-6-phosphate dehydrogenase deficiency: another risk factor for
necrotizing enterocolitis?. J Pediatr. 2007 Oct;151(4):435-7.
13. Risk Factors: Cocaine
Maternal cocaine abuse increases the risk by
2.5 folds (95% CI = 1.17 to 5.32, P = 0.02) 11
11 CzyrkoC et al. Maternal cocaine abuse and necrotizing enterocolitis: outcome and survival. J
Pediatr Surg. 1991 Apr;26(4):414-8; discussion 419-21.
14. Risk Factors: Indomethacin
Indomethacin for Tocolysis: Metaanalysis 2007
Recent exposure (within 48 hours of delivery) to
antenatal indomethacin was associated with
necrotizing enterocolitis (OR, 2.2; 95% CI; 1.1-4.2). 12
Some limitations.
12 AminSB et al. Metaanalysis of the effect of antenatal indomethacin on neonatal outcomes. Am J
Obstet Gynecol. 2007 Nov;197(5):486.e1-10.
15. Risk Factors: Indomethacin
Indomethacin in Early Life:
Associated with SIP 13
Prolonged versus Short Course of Indomethacin for the
treatment of PDA in preterm infants: Systematic Review 14
o The reduction of transient renal impairment does not outweigh the
increased risk of NEC associated with the prolonged course.
o Based on these results, a prolonged course of indomethacin cannot
be recommended for the routine treatment of PDA in preterm
infants.
13 Schmidt B et al. Long-term effects of indomethacin prophylaxis in extremely-low-birth-weight infants.
N Engl J Med 2001; 344: 1966–1972.
14 Herrera C et al. Prolonged versus short course of indomethacin for the treatment of patent ductus
arteriosus in preterm infants. Cochrane Database Syst Rev. 2007 Apr 18;(2):CD003480.
16. Risk Factors: Dexamethasone
Paquette et al showed that the combined use of
indomethacin and dexamethasone increases the
risk of SIP in VLBW neonates. 15
15 Paquette et al. Concurrent use of indomethacin and dexamethasone increases the risk of spontaneous
intestinal perforation in very low birth weight neonates. J Perinatol. 2006 Aug;26(8):486-92.
17. Risk Factors: H2-Blockers
Guillet et al, in large case control study using
NICHD Neonatal Research Network, showed
that “Antecedent H2-blocker use was associated
with an increased incidence of NEC.
(OR 1.71, 95% CI 1.34-2.19, P < .0001) 16
16 Guillet
R et al. Association of H2-blocker therapy and higher incidence of necrotizing enterocolitis in
very low birth weight infants. Pediatrics. 2006 Feb;117(2):e137-42.
18. Risk Factors: Co-amoxiclav
Kenyon et al. in a Systematic Review:
Co-amoxiclav should be avoided in women at
risk of preterm delivery because of the increased
risk of neonatal necrotising enterocolitis. 17
(RR 4.60, 95% CI 1.98 to 10.72)
17 KenyonS et al. Antibiotics for preterm rupture of membranes . Cochrane Database Syst Rev.
2003;(2):CD001058 .
19. Risk Factors: Acyclovir
Montjaux-Régis et al, case report: 18
Term baby, developed NEC after receiving
prophylactic acyclovir.
Mother had herpes genitalis and pROM at 32 wks of
GA, treated with acyclovir until vaginal delivery.
Acyclovir treatment in utero and after birth is
discussed as a possible cause of necrotizing
enterocolitis in the infant.
18 Montjaux-RégisN et al. Necrotizing enterocolitis in a full-term infant. Is acyclovir involved?. Arch
Pediatr. 2007 Oct 10.
20. Risk Factors: Kayexalate
Rugolotto et al., case report: 19
Necrotizing enterocolitis in a 850 gram infant
receiving sorbitol-free sodium polystyrene sulfonate
Their case report shows that Kayexalate per se, and
not necessarily suspended in sorbitol, can lead to
gastrointestinal tract complications and NEC in
preterm infants.
19 RugolottoS et al. Necrotizing enterocolitis in a 850 gram infant receiving sorbitol-free sodium
polystyrene sulfonate (Kayexalate): clinical and histopathologic findings. J Perinatol. 2007
Apr;27(4):247-9.
21. Risk Factors: UAC
Rand et al. suggested that UAC cause a decrease in mesenteric blood
flow. Therefore, their use in hemodynamically unstable neonates or
in those with gastrointestinal disease should be very carefully
considered. 20
High vs. low UAC: necrotising enterocolitis are not more frequent
with high compared to low catheters. 21
Havranek et al.: Preprandial SMA BFV and postprandial SMA BFV
responses to minimal enteral feedings were not affected by the
presence of a UAC. 22
20 Rand T et al. Effects of umbilical arterial catheterization on mesenteric hemodynamics. Pediatr
Radiol. 1996 Jul;26(7):435-8.
21 Barrington KJ. Umbilical artery catheters in the newborn: effects of position of the catheter tip.
Cochrane Database Syst Rev. 2000;(2):CD000505.
22 Havranek T et al. Umbilical artery catheters do not affect intestinal blood flow responses to minimal
enteral feedings. J Perinatol. 2007 Jun;27(6):375-9.
22. Risk Factors: UVC
Butler-O'Hara et al. compared long-term (up to 28
days) and short-term (7-10 days) use of umbilical venous
catheters in premature infants with birth weights of less
than 1251 grams. 23
There were no differences in time to full feedings or to
regain birth weight or in the incidence of necrotizing
enterocolitis or death.
23 Butler-O'HaraM et al. A randomized trial comparing long-term and short-term use of umbilical
venous catheters in premature infants with birth weights of less than 1251 grams. Pediatrics. 2006
Jul;118(1):e25-35.
23. Risk Factors: PDA
Patole et al., in prospective observational study,
reported that: 24
No association between significant PDA and NEC.
The age at starting feed and full enteral feed was
significantly delayed in infants with significant PDA.
24 Patole
SK et al. Does patent ductus arteriosus affect feed tolerance in preterm neonates?. Arch Dis
Child Fetal Neonatal Ed. 2007 Jan;92(1):F53-5.
24. Risk Factors: in Term Babies
Limited to those that have some underlying
illness or condition requiring NICU admission.2
Congenital Heart Disease
Intrauterine growth restriction
Polycythemia
Hypoxic-ischemic events
2 Lambert DK et al. Necrotizing enterocolitis in term neonates: data from a multihospital health-care
system. J Perinatol. 2007 Jul;27(7):437-43.
25. Risk Factors: Exchange Transfusion
Dempsey and Barrington in a Systematic Review 25
showed:
There is no evidence of long term benefit from partial exchange
in polycythaemic infants.
The incidence of gastrointestinal injury is increased.
NEC (RR 8.68; 95% CI 1.06 to 71.1)
25 Dempsey EM, Barrington K. Short and long term outcomes following partial exchange transfusion in
the polycythaemic newborn: a systematic review. Arch Dis Child Fetal Neonatal Ed. 2006
Jan;91(1):F2-6.
28. Hypoxic-ischemic insult
Hypoxia-Reoxygenation.
Ischemia-Reperfusion.
Intramural microcirculation.
Balance between Endothelin-1 and Nitric Oxide.26
26 NowickiPT. Ischemia and necrotizing enterocolitis, Where, when, and how. Seminars in Pediatric
Surgery (2005) 14, 152-158.
29. Enteral Feeding
Formula vs. Donor Breast Milk: 27, 28
Formula is associated with higher risk of
NEC
27 Quigley M et al. Formula milk versus donor breast milk for feeding preterm or low birth weight
infants. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD002971.
28 Boyd CA et al. Donor breast milk versus infant formula for preterm infants: systematic review and
meta-analysis. Arch Dis Child Fetal Neonatal Ed. 2007 May;92(3):F169-75.
30. Enteral Feeding
Disadvantages of Formula:
Higher osmolality ±
Lack of immunoprotective factors
Lack of growth factors
Altering intestinal flora
31. Microbiologic Flora and Infection
Several organisms have been accused, but non has
been proven to be causative:
Enterobacteriaceae
Enterobacter sakazakii
Coagulase-negative staphylococci: SIP
Closrtidium perfringens
Candida species: SIP
Cytomegalovirus
Torovirus
HIV
Mucormycosis
32. Cytokines and Inflammatory Mediators
Platelet Activating Factor (PAF)
Tumor Necrosis Factor (TNF)
High-mobility group box 1 protein (HMGB 1)
Interferon-gamma (INF-gamma)
Interleukins (ILs)
Matrix metalloproteinases (MMPs)
33. Inflammatory cascade. The inflammatory cascade results in the secretion of multiple
proinflammatory and counterregulatory cytokines that eventually lead to the generation of
toxic metabolites and destruction of the intestinal mucosa.
29 Markel TA et al. Cytokines in necrotizing enterocolitis. Shock. 2006 Apr;25(4):329-37.
34. Pathophysiology, in summary
Ischemic or toxic mucosal Enteral feeding
damage
Loss of mucosal integrity Bacterial proliferation
Invasion of mucosa and submucosa
Intramural gas
Transmural necrosis
Perforation
Peritonitis
35. Pathology
Closeup of intestine of infant showing necrosis and
pneumatosis intestinalis. Autopsy
36. Pathology
Postmortem photograph of bowel involved with severe NEC. The arrows indicate areas of the bowel
wall where there has been so much necrosis and sloughing of the mucosa, submucosa, and muscularis
that only the serosa is intact.
30 Epelman M et al. Necrotizing enterocolitis, review of state-of-the-art imaging findings with
pathologic correlation. RadioGraphics 2007; 27:285–305.
37. Pathology
NEC induced by an intravenous injection of
PAF in a rat model
38. Pathology
Microscopic images of (A) normal bowel and (B) characteristic findings of
NEC, which illustrates hemorrhagic necrosis, beginning in the mucosa and
extending to the muscular bowel wall, where the potential for perforation exists.
NEC frequently involves the terminal ileum. Reprinted with permission from
WebPath, courtesy of Edward C. Klatt, MD, Florida State University College of
Medicine, Tallahassee, FL (http://medlib.med.utah.edu/WebPath).
39. Pathology
Parietal ileal pneumatosis in neonatal necrotizing
enterocolitis
40. Clinical Presentation
Onset varies with gestational age
VLBW 14 – 20 days
Term first week
Course of the disease
Fulminant presentation
Slow, paroxysmal presentation
44. Diagnosis
A high index of suspicion is required
Sometimes cannot be differentiated from
sepsis
45. Diagnosis, Laboratory studies
No lab test is specific for NEC
The most common triad (!):
Thrombocytopenia
Persistent metabolic acidosis
Severe refractory hyponatremia
↑ WBC, ↓ WBC, ↓ PMN
Hyperkalemia
Stool: reducing substances, occult blood
46. Diagnosis, Radiologic studies
Abdominal X-ray:
Abnormal gas pattern, ileus
Bowel wall edema
Pneumatosis intestinalis
Fixed position loop
Intrahepatic portal venous gas ( in the absence of
UVC)
Pneumoperitonium, left lateral decubitus or cross-
table lateral views
47. Diagnosis, Radiologic studies
Supine radiograph of the
abdomen of a normal
neonate shows a normal
bowel gas pattern. Gas is
distributed throughout the
small and large bowel, and it
is difficult to differentiate the
small bowel from the large
bowel. Each loop causes
impressions on adjacent
loops, giving each loop a
multifaceted appearance; the
overall pattern resembles that
of a mosaic. The loops are
generally not rounded or
elongated.
30Epelman M et al. Necrotizing
enterocolitis, review of state-of-the-
art imaging findings with pathologic
correlation. RadioGraphics 2007;
27:285–305.
48. Diagnosis, Radiologic studies
Pneumatosis intestinalis.
Very obvious case.
Tremendous amount of
air in bowel walls
Reference:
Radiology Cases In Neonatology
Copyright 1996, Loren Yamamoto
49. Diagnosis, Radiologic studies
Pneumatosis intestinalis.
Note the air visible in
the bowel wall. The air
dissects the bowel wall
giving it a double lined
appearance (ie., railroad
tracks without the ties)
Reference:
Radiology Cases In Neonatology
Copyright 1996, Loren Yamamoto
51. Diagnosis, Radiologic studies
Supine AXR, The bowel is mildly dilated with gas, mainly on the left side. The bubbly pattern of
gas seen mainly in the right lower quadrant represents intramural gas.
30Epelman M et al. Necrotizing enterocolitis, review of state-of-the-art imaging findings with
pathologic correlation. RadioGraphics 2007; 27:285–305.
52. Diagnosis, Radiologic studies
Free intraperitoneal gas is present anteriorly (arrows)
30 Epelman M et al. Necrotizing enterocolitis, review of state-of-the-art imaging findings with
pathologic correlation. RadioGraphics 2007; 27:285–305.
54. Diagnosis, Radiologic studies
Left lateral decubitus radiograph shows free air
Ref: Necrotizing Enterocolitis, emidicine.com, Beverly P Wood, MD, MS, PhD
55. Diagnosis, Radiologic studies
Abdominal ultrasound:
Thick-walled loops of bowel with hypomotility.
Intraperitoneal fluid is often present.
Intramural gas can be identified in early-stage NEC 31
In the presence of pneumatosis intestinalis, gas is
identified in the portal venous circulation within the
liver.
Color Doppler US is more accurate than abdominal
radiography in depicting bowel necrosis in NEC. 32
31 Kim WY et al. Sonographic evaluation of neonates with early-stage necrotizing enterocolitis. Pediatr
Radiol. 2005 Nov;35(11):1056-61.
32 Faingold R et al. Necrotizing Enterocolitis: Assessment of Bowel Viability with Color Doppler US,
Radiology 2005;235:587-594.
56. Diagnosis, Radiologic studies
Sonogram of a bowel loop shows differentiation of intraluminal gas from intramural gas.
The intraluminal gas (L) is surrounded by a thickened bowel wall. Within the bowel wall
are multiple hyperechoic foci (arrows), which represent intramural gas.
30Epelman M et al. Necrotizing enterocolitis, review of state-of-the-art imaging findings with
pathologic correlation. RadioGraphics 2007; 27:285–305.
57. Diagnosis, Radiologic studies
Sonogram shows a bowel loop with a large amount of intramural gas (arrows) in the more
dependent and vertically oriented parts of the loop. This gives the bowel wall a typical
granular appearance and causes a posterior artifact.
30Epelman M et al. Necrotizing enterocolitis, review of state-of-the-art imaging findings with
pathologic correlation. RadioGraphics 2007; 27:285–305.
58. Diagnosis, Radiologic studies
Abdominal Doppler ultrasound:
Murdoch et al., in a prospective cohort study,
concluded that neonates with high resistance patterns
of blood flow velocity in the superior mesenteric
artery on the first day of life are at increased risk of
developing necrotizing enterocolitis. 33
33 Murdoch EM et al. Doppler flow velocimetry in the superior mesenteric artery on the first day of life
in preterm infants and the risk of neonatal necrotizing enterocolitis. Pediatrics. 2006
Nov;118(5):1999-2003.
59. Modified Bell’s Staging Criteria
Stage I : Suspected NEC
Clinical signs and symptoms
No diagnostic radiograph
60. Modified Bell’s Staging Criteria
Stage II : Definite (confirmed) NEC
A: Mild NEC
• Sign & symptoms, absent B/S, gross blood in stool
• AXR: ileus, focal areas of pneumatosis intestinalis
B: Moderate NEC
• Systemically ill
• AXR: extensive pneumatosis intestinalis, early
ascites, possible intrahepatic portal venous gas
61. Modified Bell’s Staging Criteria
Stage III: Advanced NEC
A: Severe NEC without perforation
• Critically ill
• Abdominal wall induration, extensive erythema
• AXR: prominent ascites, paucity of bowel gas,
persistent fixed loop
B: Severe NEC with perforation
63. Management
The main principle of management of
confirmed NEC is to treat it as an acute
abdomen with impending or septic
peritonitis
Isolation: cohort isolation in case of
epidemic clusters
64. Management, Medical
Basic NEC protocol: for all stages
NPO
NGT with low pressure suction
Close monitoring of vital signs & abdominal girth
Remove UAC and UVC
Septic workup: blood, urine, and stool cultures
LP and CSF culture: controversial
Antibiotics: ampicillin + gentemicin or cefotaxime
add metronidazole or clindamycin if peritonitis or
perforation is suspected
65. Management, Medical
Basic NEC protocol …..continued
Monitor for GI bleeding
Fluid balance: maintain urine output 1-3 ml/kg/hr
Lab.: CBC, PLT, electrolytes q 8-12 hrs
PT, PTT, LFT’s as indicated
CRP 34
Radiology: serial AXR q 6-8 hrs in the first 2-3 days
Family support
34 Pourcyrous M et al. C-reactive protein in the diagnosis, management, and prognosis of neonatal
necrotizing enterocolitis. Pediatrics. 2005 Nov;116(5):1064-9.
66. Management, Medical
Stage I
Basic NEC protocol
If all cultures are negative, the infant improved
clinically, and AXR is normal, antibiotics can
be stopped after 2-3 days and feeding can be
resumed.
67. Management, Medical
Stage II
Basic NEC protocol
NPO for 14 days
TPN, 90-110 kcal/kg/day
Antibiotics for 14 days
Respiratory support
± Inotropic support
Surgical consultation
68. Management, Medical
Stage III
As stage II
Inotropic support
Treat anemia, thrombocytopenia,
coagulopathy
Surgical intervention
69. Management, Surgical
Early Surgical Consultation
Indications for surgery:
Perforation: 20-30 % of cases
12-48 hrs after onset
Full-thickness necrosis
Deterioration despite aggressive medical treatment
71. Management, Surgical
Exploratory laparotomy:
The most commonly used approach.
Intestinal resection with enterostomy.
Primary anastomosis. 35, 36
35 Hall NJ et al. Resection and primary anastomosis is a valid surgical option for infants with
necrotizing enterocolitis who weigh less than 1000 g. Arch Surg. 2005 Dec;140(12):1149-51.
36 Singh m et al. Surgery for intestinal perforation in preterm neonates: anastomosis vs stoma. J Pediatr
Surg. 2006 Apr;41(4):725-9.
72. Management, Surgical
Peritoneal drainage:
More conservative approach, Started in 1977
Insertion of a peritoneal draine local anaesthesia
Initially, used for very sick premature babies, with
weight ≤ 1000 g
Now, it is used more commonly with larger and more
stable babies
It is used as a definite treatment in some centers
73. Management, Surgical
Algorithm for the treatment of necrotizing enterocolitis
37 Xavier
Demestre et al Peritoneal drainage as primary management in necrotizing enterocolitis: A
prospective study, J Pediatr Surg. 2002 Nov • Volume 37 • Number 11 • p1534 to p1539.
74. Management, Surgical
Laparoscopy:
Clarck and Mackinaly reported the use of laparoscopy on day 30 of
life in the treatment of a VLBW infant (900 g) with perforated NEC.38
Tan et al.: 4 babies (500-1000 g)
Needlescopic diagnosis is feasible and appears to be safe, even in
critically ill micropremmies less than 1000 g. The technique can
provide useful information for surgical decision-making and allows
for precise placement of a microlaparotomy incision over the site of
perforation, thus minimizing the trauma from open surgery in this
special group of patients. 39
38 Clark C, Mackinlay GA. Laparoscopy as an adjunct to peritoneal drainage in perforated necrotizing
enterocolitis. J Laparoendosc Adv Surg Tech A. 2006 Aug;16(4):411-3.
39 Tan HL et al. The role of diagnostic laparoscopy in micropremmies with suspected necrotizing
enterocolitis. Surg Endosc. 2007 Mar;21(3):485-7.
75. Prognosis and Outcome
NEC with perforation: mortality 20-40 %
Recurrent NEC : rare complication, 4%
Subacute or intermittent symptoms of bowel obstruction:
strictures, 10-35 %
Short-gut syndrome: FTT, high mortality.
The type of operation (peritoneal drain vs. laparotomy)
performed for perforated NEC does not influence survival
or other clinically important early outcomes in preterm
infants. 40
40 Moss
RL et al. Laparotomy versus Peritoneal Drainage for Necrotizing Enterocolitis and Perforation.
N Engl J Med. 2006 May 25;354(21):2225-34.
76. Neurodevelopmental Outcome
Soraisham et al.: Preterm infants who develop
NEC are at a significantly higher risk for
developing neurodevelopmental disability. 41
41 SoraishamAS et al. Does necrotising enterocolitis impact the neurodevelopmental and growth
outcomes in preterm infants with birthweight < or =1250 g?. J Paediatr Child Health. 2006
Sep;42(9):499-504.
77. Neurodevelopmental Outcome
Rees et al. Systematic Review (UK):
NEC is associated with significantly worse
neurodevelopmental outcome than prematurity alone.
Presence of advanced NEC and need for surgery increase
the risk of neurological impairment. 42
Schulzke et al. Systematic Review (Australia):
Survivors of stage II or higher NEC are at risk for long-
term neurodevelopmental impairment, especially if they
require surgery for the illness. 43
42 Rees CM et al. Neurodevelopmental outcomes of neonates with medically and surgically treated
necrotizing enterocolitis. Arch Dis Child Fetal Neonatal Ed. 2007 May;92(3):F193-8.
43 Schulzke SM et al. Neurodevelopmental outcomes of very low-birth-weight infants with necrotizing
enterocolitis: a systematic review of observational studies. Arch Pediatr Adolesc Med. 2007
Jun;161(6):583-90.
78. Neurodevelopmental Outcome
Adesanya et al. Retrospective Study:
Intestinal perforation caused by NEC, as compared to
SIP, is associated with worse neurodevelopmental
outcome at 1 year. 44
Blakely et al. Retrospective Study:
the risk-adjusted odds ratio favoring laparotomy for death
or impairment, indicate the need for a large, multicenter
clinical trial to assess the effect of the initial surgical
therapy on outcome at > or =18 months. 45
44 Adesanya OA et al. Intestinal perforation in very low birth weight infants: growth and
neurodevelopment at 1 year of age. J Perinatol. 2005 Sep;25(9):583-9.
45 Blakely ML et al. Laparotomy versus peritoneal drainage for necrotizing enterocolitis or isolated
intestinal perforation in extremely low birth weight infants: outcomes through 18 months adjusted
age. 2006 Apr;117(4):e680-7.
80. Prevention: Breast Milk
Formula vs. Donor Breast Milk: 27, 28
Breast milk is associated with
lower risk of NEC
slower growth in the early postnatal period
27 Quigley M et al. Formula milk versus donor breast milk for feeding preterm or low birth weight
infants. Cochrane Database Syst Rev. 2007 Oct 17;(4):CD002971.
28 Boyd CA et al. Donor breast milk versus infant formula for preterm infants: systematic review and
meta-analysis. Arch Dis Child Fetal Neonatal Ed. 2007 May;92(3):F169-75.
81. Prevention: Antenatal Steroids
Antenatal corticosteroids for women at risk of
preterm birth: Systematic Review 46
Decreased risk of NEC
RR 0.46, 95% CI 0.29 to 0.74, eight studies, 1675 infants
46 Roberts D, Dalziel S. Antenatal corticosteroids for accelerating fetal lung maturation for women at
risk of preterm birth. Cochrane Database Syst Rev. 2006 Jul 19;3:CD004454.
82. Prevention: Oral Immunoglobulin
The evidence does not support the administration
of oral immunoglobulin for the prevention of
NEC. There are no randomised controlled trials
of oral IgA alone for the prevention of NEC. 47
47 Foster
J et al, Oral immunoglobulin for preventing necrotizing enterocolitis in preterm and low birth-
weight neonates. Cochrane Database Syst Rev. 2004;(1):CD001816.
83. Prevention: Probiotics
Probiotics might reduce the risk of necrotising
enterocolitis in preterm neonates with less than 33 weeks'
gestation (relative risk 0.36, 95% CI 0.20-0.65)
the short-term and long-term safety of probiotics needs to
be assessed in large trials
Unanswered questions include the dose, duration, and
type of probiotic agents (species, strain, single or
combined, live or killed) used for supplementation. 48
48 Deshpande G et al. Probiotics for prevention of necrotising enterocolitis in preterm neonates with
very low birthweight: a systematic review of randomised controlled trials. Lancet. 2007 May
12;369(9573):1614-20 .
84. Prevention: Feeding Strategies
Pietz et al. reported 20-year experience, in
Fairview Hospital, Cleveland, Ohio, with 1239
very low birth weight infants suggests strongly
that the late-onset, slow, continuous drip feeding
protocol and avoidance of indomethacin and
early dexamethasone treatment contribute to the
prevention of necrotizing enterocolitis. 49
49 Pietz
J et al. Prevention of necrotizing enterocolitis in preterm infants: a 20-year experience.
Pediatrics. 2007 Jan;119(1):e164-70 .
85. Prevention: Glutamine
The available data from good quality randomised
controlled trials suggest that glutamine
supplementation does not confer clinically
significant benefits for preterm infants. The
narrow confidence intervals for the effect size
estimates suggest that a further trial of this
intervention is not a research priority. 50
50 Tubman TR et al, Dalziel S. Glutamine supplementation to prevent morbidity and mortality in preterm
infants. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD001457.
86. Prevention: Arginine
The data are insufficient at present to support a
practice recommendation. A multicentre
randomized controlled study of arginine
supplementation in preterm neonates is needed,
focusing on the incidence of NEC, particularly
the more severe stages (2 or 3). 51
51 ShahP, Shah V., Arginine supplementation for prevention of necrotising enterocolitis in preterm
infants. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD004339 .
87. References
Manual of Neonatal Care, Cloherty, 5th ed, 2004,
Lippincott Williams & Wilkins
Neonatology, Tricia Gomella, 5th ed, 2004,
McGraw Hill
A Manual of Neonatal Intensive Care, Rennie &
Roberton, 4th ed, 2002, Arnold