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Ebook A manual of neonatal intensive care (5/E): Part 2

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Ebook A manual of neonatal intensive care (5/E): Part 2

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Ebook A manual of neonatal intensive care (5/E): Part 2ins an important cause of morbidity and mortality at all birth weights and gestations, but is particularly important in very preterm babies.■Perinatal

infection is an important contributor to neuronal damage and adverse outcome in preterm babies, even without meningitis ('cytokine'-mediated damage). Ebook A manual of neonatal intensive care (5/E): Part 2

■The bacterial organisms that most commonly infect babies are group B beta-haemolytic Streptococcus and Escherichia coli, with coagulase-negative stap

Ebook A manual of neonatal intensive care (5/E): Part 2

hylococci a frequent cause of late-onset sepsis in very low birth weight babies.■Any baby suspected of sepsis must have investigations, including a bl

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Ebook A manual of neonatal intensive care (5/E): Part 2are, it is important to think of the diagnosis and start intravenous aciclovir; one clue is the absence of bacterial organisms on a gram Stain of cere

brospinal fluid (CSF) when the CSF also contains a high number of white cells in a baby who has not been previously treated with antibiotics.■Neonatal Ebook A manual of neonatal intensive care (5/E): Part 2

bacterial meningitis has a high risk of adverse outcome. All cases should be managed in large centres with appropriate expertise.M Infection control

Ebook A manual of neonatal intensive care (5/E): Part 2

in neonatal unitsBabies usually emerge from a sterile intra-utcrinc environment, and it follows from this that most infections in babies admitted to n

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Ebook A manual of neonatal intensive care (5/E): Part 2wding of babies in the unit, the number of infections in those babies, and the number of people (visitors and staff) going in and our of the unit. Sta

ff who are overworked have less rime for hand w ashing. XXUs should be spacious and designed so that only those who need to enter them pass through, a Ebook A manual of neonatal intensive care (5/E): Part 2

nd w ith plenty of sinks. Babies should be admitted to the NNƯ only if absolutely necessary, and staffing levels should be maintained.Scrupulous atten

Ebook A manual of neonatal intensive care (5/E): Part 2

tion to hand washing is the single most important factor in the prevention of cross-infection. Hands and forearms should always be washed with a suita

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Ebook A manual of neonatal intensive care (5/E): Part 2. Watches and jewellery must be removed so that staff arc ‘bare below the elbows’. There is no evidence that the use of gowns, masks and overshoes by

staff or parents makes any difference to the level of cross-infection in an XXL’. Gowns and masks should be used only when it is necessary to protect Ebook A manual of neonatal intensive care (5/E): Part 2

the staff during outbreaks of serious infection.1 orInfectionStaff with a current infectious disease such as a respiratory illness, boils, gastroenter

Ebook A manual of neonatal intensive care (5/E): Part 2

itis or weeping dermatitis should lie excluded from the unit. Staff with cold sores or herpetic whitlows should cover them, treat with aciclovir and c

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Ebook A manual of neonatal intensive care (5/E): Part 2their high vaginal swab (HVS) should be allowed in, but any exposed lesions should be covered and their hand washing should be supervised and particul

arly fastidious. Topical aciclovir should be applied to any cold sores. Mothers of babies with Listeria arc inevitably faecal carriers and should be i Ebook A manual of neonatal intensive care (5/E): Part 2

solated themselves, as should their affected baby.Communal equipment such as stethoscopes and thermometers is a major source of cross-infection. Indiv

Ebook A manual of neonatal intensive care (5/E): Part 2

idual pieces of equipment must be provided. Disposable equipment should be used where possible, for example blood pressure cuffs.Neonates with infecti

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Ebook A manual of neonatal intensive care (5/E): Part 2 for most infected neonates if the hand washing technique is rigorous, and is adequate for asymptomatic carriers of pathogenic organisms.When confront

ed by epidemic infectious disease (c.g. recurrent Scrratia septicaemia or enterovirus infections), there is no alternative but to close rhe unit to ne Ebook A manual of neonatal intensive care (5/E): Part 2

w admissions. Occasionally outbreaks of particular organisms require investigation to locate them, or a change in practice to eradicate them c.g. Pseu

Ebook A manual of neonatal intensive care (5/E): Part 2

domonas can contaminate taps, and gentamicin resistance can spread rapidly between different gram negative organisms requiring a change of first line

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Ebook A manual of neonatal intensive care (5/E): Part 2h infants in incubators pending surface swabs ami cultures. Babies who require readmission and who have symptoms of viral infections such as respirato

ry syncytial virus (RSV) must not be readmitted to NN Us unless they can be isolated, as epidemics can follow. Viral infections can be life threatenin Ebook A manual of neonatal intensive care (5/E): Part 2

g to babies with chronic lung disease (CLD).■ Host defences in the newborn and the inflammatory responserhe newborn baby has a ‘good enough’ immune sy

Ebook A manual of neonatal intensive care (5/E): Part 2

stem for his needs, which are usually limited. Tic depends on his mother for ‘immune protection’ via transplacental antibody transmission and rhe prot

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Ebook A manual of neonatal intensive care (5/E): Part 2m is ‘downrcgulatcd’ in rhe newborn, bur rhe baby is srill capable of mounting a robust, even an exaggerated, pro-inflammatory response to infection i

n some circumstances. Il is this inflammatory response, involving interleukins and other cytokines, which is thought to be potentially damaging to neu Ebook A manual of neonatal intensive care (5/E): Part 2

ronal development, particularly rhe prc-oligodcndrocytcs. These arc rhe cells which will make myelin when fully mature. Both rhe feral and neonatal in

Ebook A manual of neonatal intensive care (5/E): Part 2

flammatory response have been linked to brain injury in preterm babies, and babies who have mounted an inflammatory response ar term may be ‘precondit

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Ebook A manual of neonatal intensive care (5/E): Part 2ry rhin, easily damaged and infected. The umbilical stump becomes necrotic after birth and acts as a locus for infections which can then disseminate.

The passage ofan endotracheal tube, a nasogastric tube or an intravascular catheter provides a route for pathogenic organisms to enter the body.Table Ebook A manual of neonatal intensive care (5/E): Part 2

16.1 Comparison of innate and adaptive immune systemsInnateAdaptiveCharacteristicsNon-specific responseHighly specific responseResponse is fast (minut

Ebook A manual of neonatal intensive care (5/E): Part 2

es)Response is slow IdayslHas no memoryHas memoryComponentsNatural barriers, e.g. skin Complement Neutrophils and macrophages Pattern-recognition mole

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Ebook A manual of neonatal intensive care (5/E): Part 2moleculesThe newborn bain is virtually germ-free ar birth, apart from organisms that become smeared over him as he passes through the vagina. lie ther

efore lacks rhe protection afforded b\ having a resident flora of non-pathogenic organisms. A normal neonate is colonized by generally non pathogenic Ebook A manual of neonatal intensive care (5/E): Part 2

organisms acquired from his mother, including those in her vagina and rectum, to which he was exposed during delivery. However, particularly if he is

Ebook A manual of neonatal intensive care (5/E): Part 2

in an NNU, he may also be colonized by, and subsequently infected with, potentially pathogenic organisms acquired from the hospital environment. The g

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Ebook A manual of neonatal intensive care (5/E): Part 2 a very important way of establishing a colony of‘friendly’ bacteria. Approximately 80% of the body's entire immune system is in the intestine, and nu

trition and immune function arc closely linked in the newborn period (and remain so throughout life). Much current research is directed at evaluating Ebook A manual of neonatal intensive care (5/E): Part 2

the role of probiotics in preventing gut associated lymphoid tissue (necrotizing enterocolitis (NEC)). Probiotics arc strains of ‘friendly’ bacteria s

Ebook A manual of neonatal intensive care (5/E): Part 2

uch as lactobacillus CG or ĩìifid (/bacterium given by mouth, which multiply in the gut and colonize it. However, concerns remain about the emergence

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Ebook A manual of neonatal intensive care (5/E): Part 2nityCells involved in the immune system arc macrophages, neutrophils, eosinophils and mast cells. Lymphocyte function is well developed even in the 28

-wcck fetus. The absolute number of T-cells present is similar to adult values. T-cells arc able to mount a response from the third trimester, and ant Ebook A manual of neonatal intensive care (5/E): Part 2

igen-specific T-cells arc found in cord blood.A full complement of B lymphocyte types is present by the end of the second trimester, and these cells c

Ebook A manual of neonatal intensive care (5/E): Part 2

an respond by synthesizing antibodies, although their function is still suboptimal (De Vries ft al. 1999). A swift antibody synthetic response by the

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