1. 2. 3. 4.

1. 2. 3. 4.

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Neonatal pneumonia is a pulmonary infection presenting with a clinical picture of respiratory distress, associated with chest radiological findings suggesting pneumonia and persisting for at least 48 hours. Infections may be transmitted via the placenta, by aspiration, or acquired postnatally. Neonatal pneumonia can be subdivided into 4 categories (with some overlap between them): Congenital pneumonia (transplacentally acquired), e.g. rubella, cytomegalovirus, toxoplasma, listeria, herpes simplex, Treponema pallidum. Intrauterine pneumonia (aspiration of infected amniotic fluid) Early-onset pneumonia (due to an ascending infection “vertically”) Late-onset pneumonia (due to organisms acquired nascomially (”horizontally”) or in the community. Early-onset pneumonia presents at birth or soon afterwards. Associated maternal risk factors are: spontaneous onset of preterm labour prolonged rupture of membranes (>18 maternal fever (> 37.5°C) chorioamnionitis offensive liquor Microbes involved are group B betahaemolytic streptococcus (GBS), pneumococcus and coliforms. Late-onset pneumonia occurs at least 48 hours after delivery and later. Presents more insidiously and may develop abdominal distension and feeding intolerance. Microbes involved are streptococci, staphylococci, E.coli, Klebsiella. Viral and chlamydial infections are also associated with pneumonia. Chlamydial pneumonia usually presents between 4 and 11 weeks of age (and earlier) with tachypnoea, apnoea, nasal congestion, paroxysmal and staccato cough and crepitations. ++++Neonatal pneumonia is lung infection in a neonate. Onset may be within hours of birth and part of a generalized sepsis syndrome, or after 7 days and confined to the lungs. Signs may be limited to respiratory distress or progress to shock and death. Diagnosis is by clinical and laboratory evaluation for sepsis. Treatment is initial broadspectrum antibiotics changed to organism-specific drugs as soon as possible. Early-onset pneumonia is part of generalized sepsis that presents at or within hours of birth. Late-onset pneumonia usually occurs after 7 days of age, most commonly in neonatal ICUs in infants who require prolonged endotracheal intubation because of lung disease. Etiology Organisms are acquired from the maternal genital tract or the nursery. These include gram-positive cocci (eg, groups A and B streptococci, Staphylococcus aureus) and gram-negative bacilli (eg, Escherichia coli , Klebsiella sp, and Proteus sp). In infants who have received broadspectrum antibiotics, many other pathogens may be found, including Pseudomonas, Citrobacter, Bacillus, and Serratia. Symptoms, Signs, and Diagnosis Late-onset hospital-acquired pneumonia may begin gradually, with more secretions being suctioned from the endotracheal tube and higher ventilator settings. Other infants may be acutely ill, with temperature instability and neutropenia. New infiltrates may be visible on chest x-ray but may be difficult to recognize if the infant has severe bronchopulmonary dysplasia. Evaluation includes cultures of blood and tracheal aspirate, chest xray, and pulse oximetry. CHLAMYDIAL PNEUMONIA Contamination with chlamydial organisms during delivery may result in development of chlamydial pneumonia at 2 to 12 wk. Infants are tachypneic but usually not critically ill and may also have conjunctivitis caused by the same organism. Eosinophilia may be present, and xrays show bilateral interstitial infiltrates. Treatment with erythromycin leads to rapid resolution. Clinical Presentation: Associated with premature rupture of the membranes (PROM) during labor. The disease may have an early onset with septicemia and fulminant progression to severe respiratory distress, shock and respiratory failure within 24 hours; or a late onset 1 to 12 weeks after birth with this more insidious onset frequently associated with meningitis. Neonatal pneumonia can closely mimic hyaline membrane disease clinically, and is the most frequent cause of septicemia in neonate.

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Etiology/Pathophysiology: There are three ways for the baby to acquire a neonatal pneumonia. First is infection acquired prior to birth by an ascending route or transplacental route. Classically this is Group B Streptococcus in the mother's vagina which passes to the infant during birth, particularly in cases with prolonged rupture of membranes and prolonged labor. Other normal inhabitants of the birth canal - staph, strep, diphtheroids, anaerobes, E. coli and Listeria - are other pathogens that may cause neonatal pneumonia. Second is infection acquired by aspiration during delivery, with the pathogens remaining the same. Third is via infection acquired after birth. Pathology: There is a less uniform distribution of hyaline membranes in collapsed alveoli than is seen in hyaline membrane disease. There are cocci in the alveolar membrane and in the interstitial inflammatory exudate. Imaging Findings: Ascending infection may resemble hyaline membrane disease very closely, especially in smaller infants. Most commonly seen are extensive granular confluent infiltrates whose distribution is often less uniform than that of hyaline membrane disease. There is less atelectasis than in hyaline membrane disease. May have pleural fluid and a normal lung volume, further distinguishing factors from hyaline membrane disease. Infection acquired perinatally often has a confluent miliary or nodular pattern that looks like meconium aspiration or transient tachypnea of the newborn while postnatally acquired infection often has a patchy more asymmetric pattern that looks like infection in older children. DDX: Hyaline Membrane Disease - usually has a uniform distribution of pulmonary opacities, never has pleural effusions, has a decreased lung volume. Meconium Aspiration - usually has nodular non homogeneous densities, may have pleural effusions, usually has an increased lung volume. Transient Tachypnea of the Newborn - usually has non homogeneous densities, may have pleural fluid. Etiology/Pathophysiology: Common pathogens include Staphylococcus, Pneumococcus (Streptococcus pneumonia), and Haemophilus influenza. Bacterial pneumonia usually has primarily alveolar involvement without airway involvement. Pneumatoceles may form during the recuperative phase and are transient accumulations of interstitial air that have escaped through necrotic bronchial foci and are usually of little significance, resolving over time. PATHOPHYSIOLOGY

BACKGROUND: The cause and mechanism of most cases of sudden unexpected death in infancy (SUDI) remain unknown, despite specialist autopsy examination. We reviewed autopsy results to determine whether infection was a cause of SUDI. METHODS: We did a systematic retrospective case review of autopsies, done at one specialist centre between 1996 and 2005, of 546 infants (aged 7-365 days) who died suddenly and unexpectedly. Cases of SUDI were categorised as unexplained, explained with histological evidence of bacterial infection, or explained by non-infective causes. Microbial isolates gathered at autopsy were classified as non-pathogens, group 1 pathogens (organisms usually associated with an identifiable focus of infection), or group 2 pathogens (organisms known to cause septicaemia without an obvious focus of infection). FINDINGS: Of 546 SUDI cases, 39 autopsies were excluded because of viral or pneumocystis infection or secondary bacterial infection after initial collapse and resuscitation. Bacteriological sampling was done in 470 (93%) of the remaining 507 autopsies. 2079 bacteriological samples were taken, of which 571 (27%) were sterile. Positive cultures yielded 2871 separate isolates, 484 (32%) of which showed pure growth and 1024 (68%) mixed growth. Significantly more isolates from infants whose deaths were explained by bacterial infection (78/322, 24%) and from those whose death was unexplained (440/2306, 19%) contained group 2 pathogens than did those from infants whose death was explained by a non-infective cause (27/243, 11%; difference 13.1%, 95% CI 6.9-19.2, p<0.0001 vs bacterial infection; and 8.0%, 3.2-11.8, p=0.001 vs unexplained). Significantly more cultures from infants whose deaths were unexplained contained Staphylococcus aureus (262/1628, 16%) or Escherichia coli (93/1628; 6%) than did those from infants whose deaths were of non-infective cause (S aureus: 19/211, 9%; difference 7.1%, 95% CI 2.2-10.8, p=0.005; E coli: 3/211, 1%, difference 4.3%, 1.5-5.9, p=0.003).

very-low-birth-weight infants are more likely than larger low-birthweight infants to be placed prone after discharge.21 There is strong evidence that whatever the benefits are of prone sleep in the NICU, the risk of prone sleep after discharge is great. So too is the risk for SIDS from sleeping laterally. Fleming and Blair note, “The evidence is clear that for the overwhelming majority of preterm infants approaching discharge from hospital there are no significant disadvantages, and many potential advantages to the supine sleeping position.”22(p162) This population is of particular concern because of the higher risk for SIDS deaths in premature infants 23 and the increasing number of births in this category.24 Lockridge et al 25 published one of the first articles on the need to develop NICU policies and procedures that met the simultaneous needs of developmentally appropriate care and SIDS risk reduction. In the appendix, we provide resources from which nurses may obtain model policies for NICUs and newborn nurseries as well as educational materials for parents. These materials suggest methods for integrating the newest SIDS risk reduction guidelines of the AAP with hospital policies and procedures, nursing protocols, and parent education. As with all policies, they are best achieved when nurses contribute to the development of their unit's policies and help design appropriate in-service programs to advance their knowledge of and confidence in these policies. Aris et al developed a survey for assessing the status of nursing opinions and practices with respect to discharge teaching related to sleep position and SIDS.26 They found that only 52% of neonatal nurses routinely provide instructions that are consistent with the promotion of supine sleep at home. The survey published in their article covers a wide range of issues related to sleep and thus can serve as a basis for identifying existing beliefs and practices upon which in-service education programs and policy reviews can be built.

INTERPRETATION: Although many post-mortem bacteriological cultures in SUDI yield organisms, most seem to be unrelated to the cause of death. The high rate of detection of group 2 pathogens, particularly S aureus and E coli, in otherwise unexplained cases of SUDI suggests that these bacteria could be associated with this condition.

ADDRESSING NURSING CONCERNS ABOUT COMPONENTS OF THE RISK REDUCTION GUIDELINES To serve as role models and educators who promote SIDS risk reduction guidelines, nurses need to feel knowledgeable about the information they are presenting to families before discharge, reassured that any potential adverse consequences have been identified and addressed, and confident that the guidance is evidence-based and that the benefits outweigh any possible risks.27 Yet, historically, the research and review articles and policy statements on SIDS are disproportionately found in medical rather than nursing journals. Without access to this information, nurses' concerns about the guidelines will remain a challenge to the provision of a consistent and evidence-based message to parents.28,29 Nurses are therefore encouraged to participate in continuing education, to collaborate in multidisciplinary committees that share and update relevant information, and to develop evidence-based policies.25,30 One of the more commonly voiced concerns by nurses has been whether the supine position increases the risk of death from aspiration. This issue has been studied, and although there has been a welcome rise in the use of a supine sleep position for infants, there is no evidence of an increased risk of death from aspiration.31,32 Another concern relates to an increased incidence of positional plagiocephaly without stenosis. Without a population-based study of the incidence of any flattening at the back of the head, it is unclear if and by what degree plagiocephaly without stenosis is increasing or if a possible rise may reflect an increase in awareness as well as in true incidence.2 However, even with the possibility of an increase in true diagnosis, the sections on Plastic Surgery and Neurological Surgery of the American Academy of Pediatrics Committee on Practice and Ambulatory Medicine continue to support the benefits of supine sleep.33 The AAP policies also offer several suggestions for reducing the risk for developing positional flattening, including the use of tummy time for infants when they are awake and under supervision, the avoidance of too much time in such devices as car-seat carriers and bouncers, the use of upright “cuddle time,” and shifts in the direction the infant faces while asleep. An additional benefit of tummy time is the promotion of motor development, especially upper body muscle development. Finally, general health in the infant appears to benefit from the supine sleep position. There were no increases in symptoms or illnesses in the first 6 months.34 There were fewer cases of fever at 1 month, fewer stuffy noses at 6 months, and fewer outpatient visits for ear infections at both 3 and 6 months.

The Back to Sleep initiative reflects policy statements issued by the American Academy of Pediatrics (AAP), commencing in 1992, that are derived from a review of scientific evidence. These policy statements are periodically revised to reflect advancements in knowledge and are published in Pediatrics, the official journal of the AAP.2 The current AAP SIDS policy recommendations, issued in 2005, including references for the underlying research, can be accessed on-line at www.aap.org/healthtopics/Sleep.cfm . Education to reduce modifiable risk factors such as nonsupine sleep is the most effective intervention currently available. Moreover, even as genetic predispositions for SIDS are identified, it appears that a geneenvironment interaction must occur for the infant's vulnerability to be realized. For example, in a study of a cardiac sodium channel variant that may raise susceptibility to acidosis-induced arrhythmias in infants, the authors noted, “It is imperative to continue to support effective public health efforts to decrease known environmental risk factors (e.g., prone sleeping position). SIDS is argued … to result, like many common disorders, from a genetic predisposition that yields poor tolerance of common challenges to physiological homeostasis.”5(p434) NURSING IMPACT ON PARENTAL KNOWLEDGE AND COMPLIANCE Overall, infants are more likely to be placed to sleep in the supine position if this recommendation had been provided by a healthcare professional.15 For mothers of very-low-birth-weight infants, nursery practices were the most important factor in choice of position.16 The recommendations of both the physician and nurse mattered.17 However, compliance was greatest when parents not only heard advice before discharge but also observed it in practice in the nursery.18 Unfortunately, discrepancies exist between nursing knowledge and practice, with those in practice longer found to be less likely to believe in the association between SIDS and sleep position.19 However, teaching programs can be effective in providing an understanding of the basis for the Back to Sleep policies. Such programs can help nurses recognize the impact of their discussions and role modeling on parental practices.20 The NICU poses a particularly challenging environment in which to teach parents about SIDS risk reduction. For much of their stay, infants may have been kept in the prone position. Prolonged exposure of parents to this model has been hypothesized to be one reason why

HEALTH BEHAVIOR CHANGE THEORY AS A TOOL FOR NURSES

An important element in changing health behavior is developing a relationship of trust with the parent and family. Nurses have a unique opportunity to achieve an effective patient-provider relationship with new parents and caregivers and thus educate and influence the family. By communicating conversationally with families, nurses can elicit and address any fears and concerns that may serve as barriers to compliance. Behavior change is more likely to occur if providers use nonjudgmental responses to beliefs associated with culture-based infant care practices. Once cultural and personal beliefs are shared, correct information regarding SIDS risk reduction practices can be discussed in this context and potential concerns elicited and addressed. By asking specific questions during hospitalization and at discharge, the nurse will be able to tailor and thus personalize SIDS risk reduction education. Who will provide care to the baby? What bedding will be used? Does anyone in the home smoke? Where and in what position will the infant sleep? Baseline awareness of SIDS risk factors can thus be determined, and the nurse and family can work collaboratively to improve safety. Thus, if a grandparent will serve as caregiver, it will be important to work with the family to discuss risk reduction with this essential family role model.43

died of known causes, many infants who died of SIDS have toxigenic bacteria, such as Escherichia coli, Staphylococcus aureus, and Clostridium difficile, as well as influenza and respiratory syncytial virus (RSV). Most strongly implicated is RSV, which is well known for its association with central apnea.

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Start prenatal care early. Schedule frequent well-baby checkups, and ensure that immunizations are current.

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Avoid cigarettes, alcohol, and other drugs while pregnant. Avoid exposing the baby to cigarette smoke. If possible, breastfeed the baby. Burp the baby during and after feedings, especially before putting the baby to sleep.

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Place the baby on a firm, flat mattress in a safety-approved crib; avoid pillows, blankets, sheepskins, foam pads, or waterbeds.

Nurses can also guide families by pointing out the reasons for any temporary discrepancies between hospital-based practices related to care and what will be recommended for SIDS risk reduction as the hospitalization ensues and discharge occurs. In the context of the trusting relationship, nurses can thus eliminate confusion about what parents are being advised to do at home. Black infants are more likely than infants from other racial groups to be placed in the prone position after discharge.42,43 The greater use of prone sleep is but one of many factors which may contribute to the racial disparity in SIDS.5,36,44–46 Given the value families place on nursing guidance, nurses have a unique opportunity to use their role to promote awareness of the modifiable risk factors for SIDS by all racial and ethnic groups. Nurses in newborn nurseries and neonatal intensive care units are instrumental in educating parents about reducing the risk for SIDS. Nurse participation is acknowledged and encouraged in the current policy statement on SIDS Risk Reduction put forth by the American Academy of Pediatrics. Despite the decline in SIDS, it remains the leading cause of postneonatal infant mortality, and despite greater public compliance with the risk reduction guidelines there is room for improvement in how effectively and consistently they are disseminated. To facilitate nursing participation as educators, role models, and collaborators in the development of relevant hospital policies and procedures, we review the current recommendations, addressing issues that may serve as barriers to participation, describing the biological plausibility underlying risk-reducing practices, and presenting resources from which nurses may obtain teaching materials and model policies. The sudden death of an infant younger than 1 year of age that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and a review of the clinical history. The sudden demise of an infant, thankfully, is not a common occurrence. While the unexpected death of an infant may result from a number of processes, the leading postneonatal cause is a syndrome with an etiology that has not been fully elucidated. The peak incidence of SIDS coincides with critical periods in the development of the immune system; at such a time, the infant might be transiently vulnerable to lethal infection. SIDS incidence increases in the winter, during viral epidemics in a community, and 2 weeks after viral infection. Compared with healthy control infants and infants who

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Do not restrain the baby during sleep. Use of a fan in the infant's room was associated with a 72% reduction in the risk of SIDS.32 It is thought that inadequate ventilation may result in pooling of carbon dioxide around the dead air space around an infant's mouth and nose, increasing the likelihood of rebreathing. The fan functions to dispense this accumulated carbon dioxide.

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The supine sleeping position