Respiratory Distress in the Newborn
Yüklə 133,56 Kb. Pdf görüntüsü
|
| Respiratory Distress in the Newborn CHRISTIAN L. HERMANSEN, MD, and KEVIN N. LORAH, MD Lancaster General Hospital, Lancaster, Pennsylvania T he clinical presentation of respira- tory distress in the newborn includes apnea, cyanosis, grunting, inspira- tory stridor, nasal flaring, poor feed- ing, and tachypnea (more than 60 breaths per minute). There may also be retractions in the intercostal, subcostal, or supracostal spaces. Respiratory distress occurs in approximately 7 percent of infants, 1 and preparation is cru- cial for physicians providing neonatal care. Most cases are caused by transient tachypnea of the newborn, respiratory distress syndrome, or meconium aspiration syndrome, but vari- ous other causes are possible (Table 1).
Transient tachypnea of the newborn is the most common cause of neonatal respira- tory distress, constituting more than 40 per- cent of cases. 1 A benign condition, it occurs when residual pulmonary fluid remains in fetal lung tissue after delivery. Prostaglandins released after delivery dilate lymphatic vessels to remove lung fluid as pulmonary circula- tion increases with the first breath. When fluid persists despite these mechanisms, tran- sient tachypnea of the newborn can result. Risk factors include maternal asthma, 2 male
sex, macrosomia, maternal diabetes, 3 and cesarean delivery. 4 The clinical presentation includes tachypnea immediately after birth or within two hours, with other predictable signs of respiratory The most common etiology of neonatal respiratory distress is transient tachypnea of the newborn; this is triggered by excessive lung fluid, and symptoms usually resolve spontane- ously. Respiratory distress syndrome can occur in premature infants as a result of surfactant deficiency and underdeveloped lung anatomy. Intervention with oxygenation, ventilation, and surfactant replacement is often necessary. Prenatal administration of corticosteroids between 24 and 34 weeks’ gestation reduces the risk of respiratory distress syndrome of the newborn when the risk of preterm delivery is high. Meconium aspiration syndrome is thought to occur in utero as a result of fetal distress by hypoxia. The incidence is not reduced by use of amnio- infusion before delivery nor by suctioning of the infant during delivery. Treatment options are resuscitation, oxygenation, surfactant replacement, and ventilation. Other etiologies of respira- tory distress include pneumonia, sepsis, pneumothorax, persistent pulmonary hypertension, and congenital malformations; treatment is disease specific. Initial evaluation for persistent or severe respiratory distress may include complete blood count with differential, chest radiog- raphy, and pulse oximetry. (Am Fam Physician 2007;76:987-94. Copyright © 2007 American Academy of Family Physicians.) Table 1. Differential Diagnosis of Respiratory Distress in the Newborn Most common causes* Transient tachypnea of the newborn Respiratory distress syndrome (hyaline membrane disease)
Meconium aspiration syndrome Less common but significant causes Delayed transition Infection (e.g., pneumonia, sepsis) Nonpulmonary causes (e.g., anemia, congenital heart disease, congenital malformation, medications, neurologic or metabolic abnormalities, polycythemia, upper airway obstruction) Persistent pulmonary hypertension of the newborn
Pneumothorax *—Listed in order of incidence. Downloaded from the American Family Physician Web site at www.aafp.org/afp. Copyright © 2007 American Academy of Family Physicians. For the private, noncommercial use of one individual user of the Web site. All other rights reserved. Contact copyrights@aafp.org for copyright questions and/or permission requests.
988 American Family Physician www.aafp.org/afp Volume 76, Number 7
◆ October 1, 2007 distress. Symptoms can last from a few hours to two days. Chest radiography shows diffuse parenchymal infiltrates, a “wet silhouette” around the heart, or intralobar fluid accu- mulation
5 (Figure 1). Respiratory Distress Syndrome Respiratory distress syndrome of the newborn, also called hyaline membrane disease, is the most common cause of respiratory distress in premature infants, correlating with structural and functional lung immaturity. It occurs in 24,000 infants born in the United States annu- ally.
6 It is most common in infants born at fewer than 28 weeks’ gestation and affects one third of infants born at 28 to 34 weeks’ gesta- tion, but occurs in less than 5 percent of those born after 34 weeks’ gestation. 6 The condition is more common in boys, 7 and the incidence is approximately six times higher in infants whose mothers have diabetes, because of delayed pul- monary maturity despite macrosomia. 8 The pathophysiology is complex. Immature type II alveolar cells produce less surfactant, causing an increase in alveolar surface ten- sion and a decrease in compliance. The resul- tant atelectasis causes pulmonary vascular constriction, hypoperfusion, and lung tissue ischemia. Hyaline membranes form through the combination of sloughed epithelium, protein, and edema. Persistent respiratory distress syndrome leads to bronchopulmo- nary dysplasia, characterized by typical chest radiography findings and chronic oxygen dependence. The syndrome is associated with recurrent wheezing in children and a higher risk of hospital admission for asthma. 9 The diagnosis of respiratory distress syn- drome should be suspected when grunting, retractions, or other typical distress symp- toms occur in a premature infant immedi- ately after birth. Hypoxia and cyanosis often occur. Chest radiography shows homogenous opaque infiltrates and air bronchograms, indicating contrast in airless lung tissue seen against air-filled bronchi 5 (Figure 2); decreased lung volumes also can be detected. Meconium Aspiration Syndrome Meconium-stained amniotic fluid occurs in approximately 15 percent of deliveries, caus- ing meconium aspiration syndrome in the SORT: KEY RECOMMENDATIONS FOR PRACTICE Clinical recommendation Evidence rating References Prenatal administration of corticosteroids between 24 and 34 weeks’ gestation reduces the risk of respiratory distress syndrome of the newborn when the risk of preterm delivery is high. A 20
meconium aspiration syndrome. B 23 Use of selective serotonin reuptake inhibitors in late pregnancy may cause persistent pulmonary hypertension of the newborn. C 16
dence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, see page 922 or http://www.aafp.org/afpsort.xml. Figure 1. Chest radiograph of an infant with transient tachypnea of the newborn. Reprinted with permission from eMedicine.com, 2007. Available at: http://www.emedicine.com/radio/topic710.htm. Newborn Respiratory Distress October 1, 2007
◆ Volume 76, Number 7 www.aafp.org/afp American Family Physician 989 Newborn Respiratory Distress infant in 10 to 15 percent of those cases, typically in term and post-term infants. 10
Meconium is composed of desquamated cells, secretions, lanugo, water, bile pig- ments, pancreatic enzymes, and amniotic fluid. Although sterile, meconium is locally irritative, obstructive, and a medium for bacterial culture. Meconium passage may represent hypoxia or fetal distress in utero. Similar symptoms can occur after aspiration of blood or nonstained amniotic fluid. Meconium aspiration syndrome causes significant respiratory distress immedi- ately after delivery. Hypoxia occurs because aspiration takes place in utero. Chest radi- ography shows patchy atelectasis or consoli- dation 5
Infection Bacterial infection is another possible cause of neonatal respiratory distress. Common pathogens include group B streptococci (GBS), Staphylococcus aureus, Streptococcus
Pneumonia and sepsis have various manifes- tations, including the typical signs of distress as well as temperature instability. Unlike transient tachypnea, respiratory distress syn- drome, and meconium aspiration syndrome, bacterial infection takes time to develop, with respiratory consequences occurring hours to days after birth. Risk factors for pneumonia include pro- longed rupture of membranes, prematu- rity, and maternal fever. Prevention of GBS infection through universal screening and antepartum treatment reduces rates of early-onset disease, including pneumonia and sepsis, by 80 percent. 11 Current U.S. protocol mandates screening for GBS in all pregnant patients late in pregnancy and treating those who have positive results with intrapartum antibiotics at least four hours before delivery. 12 Chest radiography helps in the diagnosis, with bilateral infiltrates suggesting in utero infection. Pleural effusions are present in two thirds of cases. 13 Serial blood cultures may be obtained to later identify an infect- ing organism. Less Common Causes Pneumothorax, defined as air in the pleural space, can be a cause of neonatal respiratory distress when pressure within the pulmonary space exceeds extrapleural pressure. It can occur spontaneously or as a result of infec- tion, meconium aspiration, lung deformity, or ventilation barotrauma. The incidence of spontaneous pneumothorax is 1 to 2 percent
respiratory distress syndrome of the newborn. Reprinted from Auckland District Health Board. Accessed June 28, 2007, at: http://www.adhb.govt.nz/newborn/ TeachingResources/Radiology/LungParenchyma.htm#RDS. Figure 3. Chest radiograph of an infant with meconium aspiration syndrome. Reprinted from © Auckland District Health Board. Accessed June 28, 2007, at: http://www.adhb.govt.nz/newborn/ TeachingResources/Radiology/LungParenchyma.htm#RDS. 990 American Family Physician www.aafp.org/afp Volume 76, Number 7
◆ October 1, 2007 Newborn Respiratory Distress in term births, 14 but it increases to about 6 percent in premature births. 15 Persistent pulmonary hypertension of the newborn occurs when pulmonary vas- cular resistance fails to decrease soon after birth as with normal transition. The eti- ology may be idiopathic or secondary to meconium aspiration syndrome, pneumo- nia or sepsis, respiratory distress syndrome, or transient tachypnea of the newborn. Maternal use of selective serotonin reup- take inhibitors in the third trimester also has been implicated. 16 Certain congenital malformations can lead to respiratory distress; these include pulmonary hypoplasia, congenital emphy- sema, esophageal atresia, and diaphragmatic hernia. Upper airway obstructions from cho- anal atresia or vascular rings may cause similar results. Obstructive lesions include choanal atresia, macroglossia, Pierre Robin syndrome, lymphangioma, teratoma, medi- astinal masses, cysts, subglottic stenosis, and laryngotracheo- malacia. Congenital heart dis- ease also may be implicated. Cyanotic heart disease includes transposition of the great arteries and tetralogy of Fal- lot. Noncyanotic heart lesions may cause a pulmonary over- flow state leading to congestive heart failure. These lesions include large septal defects, patent ductus arteriosus, and coarctation of the aorta. Malformations can sometimes be found on antepartum imaging. Neurologic disorders such as hydrocepha- lus and intracranial hemorrhage can cause respiratory distress. Central respiratory depression can occur after maternal expo- sure to medications, including labor analge- sia and illicit drugs. Metabolic and hematologic derangements (e.g., hypoglycemia, hypocalcemia, polycy- themia, anemia) can also cause respiratory symptoms. Inborn errors of metabolism should also be considered. Finally, a small but significant number of infants do not fit previously described pat- terns. Delayed transition is diagnosed retro- spectively when symptoms resolve within the first few hours of life instead of progressing as respiratory distress syndrome, transient tachypnea of the newborn, or meconium aspiration syndrome. The etiology is most likely a combination of retained fluid and incompletely expanded alveoli. Treatment is supportive until the distress resolves in a few hours as the transition completes.
Treatment for neonatal respiratory distress can be both generalized and disease-specific. Physicians should be aware of current neo- natal resuscitation protocols. Oxygenation can be enhanced with blow-by oxygen, nasal cannula, or mechanical ventilation in severe cases. Surfactant administration may be required. Antibiotics are often administered if bacterial infection is suspected clinically or because of leukocytosis, neutropenia, or hypoxemia. Ampicillin and gentami- cin are often used together based on their effectiveness and synergy. 12 Extracorporeal membrane oxygenation, similar to an arti- ficial external lung, is used as a last resort in critical circumstances. Oral feedings are often withheld if the respiratory rate exceeds 80 breaths per minute. If pneumothorax occurs, needle decom- pression or chest tube drainage may be required. Small pneumothoraces can be treated in term infants without invasive management through nitrogen washout. Administration of 100% oxygen can accel- erate the resolution of the pneumothorax as readily absorbed oxygen replaces nitrogen in the extrapulmonary space. This technique can reduce pneumothorax duration from two days to eight hours. 17 Because evidence in the specific treatment of neonatal respiratory distress continues to evolve, family physicians should work con- jointly with neonatal intensivists. If services required for the neonate are unavailable at the family physician’s facility, care should be transferred to a higher acuity hospital. TRANSIENT TAChYPNEA OF ThE NEwbORN Treatment for transient tachypnea of the newborn is supportive because the condi- tion is usually self-limited. Oral furosemide Amnioinfusion for meco- nium does not decrease the incidence of meconium aspiration syndrome or perinatal death. October 1, 2007
◆ Volume 76, Number 7 www.aafp.org/afp American Family Physician 991 Newborn Respiratory Distress (Lasix) has not been shown to significantly improve status and should not be given. 18
Data suggest that prenatal administration of corticosteroids 48 hours before elective cesarean delivery at 37 to 39 weeks’ gestation reduces the incidence of transient tachy- pnea of the newborn; however, this has not become common practice. 19
Treatment for respiratory distress syndrome often requires some of the general inter- ventions mentioned. In addition, prenatal administration of corticosteroids between 24 and 34 weeks’ gestation reduces the risk of respiratory distress syndrome when the risk of preterm delivery is high, with an odds ratio of 0.53. 20 Postnatal corticosteroid administra- tion for respiratory distress syndrome may decrease mortality risk, but it may increase the risk of cerebral palsy. 21 Inhaled nitric oxide may alleviate concomitant persistent pulmonary hypertension of the newborn, but its use in preterm infants is experimental. 22
General treatment practices are often used for meconium aspiration syndrome. Stan- dard prevention and treatment for meco- nium aspiration syndrome previously included suctioning the mouth and nares upon head delivery before body delivery. However, recent evidence suggests that aspi- ration occurs in utero, not at delivery; there- fore, infant delivery should not be impeded for suctioning. 23 After full delivery, the infant should be handed to a neonatal team for evaluation and treatment. Although infants previously have been given intubation and airway suctioning, current evidence favors expectant management unless certain crite- ria (i.e., spontaneous respiration, heart rate greater than 100 beats per minute, and rea- sonable tone) are absent (Figure 4). 24 Meta-analyses have suggested that amnio- infusion reduces aspiration for thick meconium. 25,26 A recent well-designed, randomized, multicenter trial with 1,998 women found that amnioinfusion for meconium (even thick meconium) does not decrease the incidence of meconium aspiration syndrome or perinatal death. 27
There is insufficient evidence to recom- mend steroid administration. 28
A detailed history is critical to proper evalua- tion. The differential diagnosis changes with gestational age: respiratory distress syndrome typically affects preterm infants, whereas meconium aspiration syndrome affects term or post-term neonates. Antepartum infection status is important, especially regarding GBS infection status and prophylaxis. Information about the duration of rupture, color of amni- otic fluid, maternal temperature, maternal tachycardia, and fetal heart tracing status is vital to detect meconium aspiration and cho- rioamnionitis. Family history assists in iden- tifying inheritable congenital defects. The onset and duration of respiratory symptoms also provide clues. Transient tachypnea of the newborn begins early and improves with time. Conversely, sepsis and pneumonia may have no early signs but may develop hours to days later. Respiratory distress syndrome
Expectant management Intubation and suctioning Presence of meconium-stained amniotic fluid Use minimal stimulation and keep head down to prevent breathing in meconium Hand infant to neonatal evaluation team Yes
No Is infant vigorous by these criteria? Heart rate > 100 beats per minute Spontaneous respiration Reasonable tone
deliveries with meconium-stained amniotic fluid.
992 American Family Physician www.aafp.org/afp Volume 76, Number 7
◆ October 1, 2007 Newborn Respiratory Distress begins early in premature infants without signs of spontaneous improvement. Physical examination also is helpful. In the general assessment, physicians should look for apnea, tachypnea, or cyanosis. Car- diac auscultation detects murmurs sugges- tive of congenital heart anomalies. Lung auscultation may show asymmetrical chest movement in pneumothorax or crackles in pneumonia, or be completely clear in tran- sient tachypnea or persistent pulmonary hypertension of the newborn. The severity of distress should be estimated with an initial assessment. Mild distress may warrant observation and pulse oximetry. Severe distress, especially with a complicated birth history, requires immediate resuscita- tion, chest radiography, and laboratory tests. Newborns commonly demonstrate signs of respiratory compromise much earlier than cardiovascular collapse. The variation of neonatal distress makes application of a gen- eral algorithm difficult, although a “rule of two hours” for continuous reassessment has
ratory distress syndrome; MAS = meconium aspiration syndrome; NICU = neonatal intensive care unit; TTN = transient tachypnea of the newborn.)
Infant presents with respiratory distress Apply “rule of two hours”: NICU consult/transfer (and consider laboratory tests or antibiotics) if any of following is present: (1) Abnormality on chest radiograph (2) > 40% oxygen needed to oxygenate (3) Condition deteriorates (4) Condition does not improve within two hours Endotracheal intubation Ventilation NICU consult/transfer Consider antibiotics Consider laboratory tests (Table 2) Routine newborn care Chest radiography Pulse oximetry Supplemental oxygen Suggests TTN or delayed transition Resolves spontaneously? Clinical improvement? Observe for 10 to 20 minutes Yes No
Yes Resuscitation Pulse oximetry Supplemental oxygen Chest radiography Suggests RDS or MAS Severe (severe grunting/flaring, apnea, cyanosis) Mild (Mild tachypnea/grunting) October 1, 2007
◆ Volume 76, Number 7 www.aafp.org/afp American Family Physician 993 been suggested (Figure 5). 29 During this time, chest radiography and blood tests can be per- formed (Table 2), and possible consultation or patient transfer can be implemented. This reassessment allows physicians to reevaluate symptom severity as well as to update and educate the parents. The distinguishing features of tran- sient tachypnea of the newborn, respira- tory distress syndrome, and meconium aspiration syndrome are summarized in Table 3. 2-8,19,20,23,27 The Authors Christian L. hermansen, mD, is associate director of the Lancaster (Pa.) General hospital Family medicine residency Program. he received his medical degree from Jefferson medical College in Philadelphia, Pa., and completed a residency in family medicine at Lancaster General hospital. Kevin n. Lorah, mD, is medical director of the neo- natal intensive care unit and the newborn nursery at the Lancaster (Pa.) General Women & Babies hospital. he received his medical degree from Jefferson medical College. Dr. Lorah completed a residency in pediatrics at Geisinger medical Center in Danville, Pa., and a fellowship
Blood culture May indicate bacteremia Not helpful initially because results may take 48 hours Blood gas Used to assess degree of hypoxemia if arterial sampling, or acid/base status if capillary sampling (capillary sample usually used unless high oxygen requirement) Blood glucose Hypoglycemia can cause or aggravate tachypnea Chest radiography Used to differentiate various types of respiratory distress Complete blood count with differential Leukocytosis or bandemia indicates stress or infection Neutropenia correlates with bacterial infection Low hemoglobin level shows anemia High hemoglobin level occurs in polycythemia Low platelet level occurs in sepsis Lumbar puncture If meningitis is suspected Pulse oximetry Used to detect hypoxia and need for oxygen supplementation
TTN
Persistent lung fluid
Any Cesarean delivery 4 Macrosomia Male sex Maternal asthma 2 Maternal diabetes 3 Tachypnea Often no hypoxia
or cyanosis
Parenchymal infiltrates 5 “Wet silhouette” around the heart
5 Intralobar fluid accumulation 5 Supportive, oxygen if hypoxic
Prenatal corticosteroids before cesarean delivery if 37 to 39 weeks’ estimated gestation (not accepted U.S. practice) 19 RDS
Surfactant deficiency Lung under- development Preterm Male sex
7 Maternal diabetes 8 Preterm delivery 6 Tachypnea Hypoxia Cyanosis
Homogenous infiltrates 5 Air bronchograms 5 Decreased lung volumes Resuscitation, oxygen, ventilation, surfactant Prenatal corticosteroids if risk of preterm delivery (24 to 34 weeks’ estimated gestation) 20
(accepted U.S. practice) MAS
Lung irritation and
obstruction Term or
post- term
Meconium- stained
amniotic fluid Post-term delivery Tachypnea Hypoxia
Patchy atelectasis 5 Consolidation 5 Resuscitation, oxygen, ventilation, surfactant Do not impede delivery for suctioning 23 ; amnioinfusion of no benefit
27 TTN = transient tachypnea of the newborn; RDS = respiratory distress syndrome; MAS = meconium aspiration syndrome. Information from references 2 through 8, 19, 20, 23, and 27. 994 American Family Physician www.aafp.org/afp Volume 76, Number 7
◆ October 1, 2007 Newborn Respiratory Distress in neonatal and perinatal medicine at the state University of new York health science Center in syracuse. author disclosure: nothing to disclose. Address correspondence to Christian L. Hermansen, MD, Lancaster General Hospital Family Medicine Residency Program, 555 N. Duke St., Lancaster, PA 17604 (e-mail: clherman@lancastergeneral.org). Reprints are not avail- able from the authors. REFERENCES 1. Kumar A, Bhat BV. Epidemiology of respiratory distress of newborns. Indian J Pediatr 1996;63:93-8. 2. Demissie K, Marcella SW, Breckenridge MB, Rhoads GG. Maternal asthma and transient tachypnea of the newborn. Pediatrics 1998;102(1 pt 1):84-90. 3. Persson B, Hanson U. Neonatal morbidities in gesta- tional diabetes mellitus. Diabetes Care 1998;21(suppl 2):B79-84. 4. Levine EM, Ghai V, Barton JJ, Strom CM. Mode of deliv- ery and risk of respiratory diseases in newborns. Obstet Gynecol 2001;97:439-42. 5. Kurl S, Heinonen KM, Kiekara O. The first chest radio- graph in neonates exhibiting respiratory distress at birth. Clin Pediatr (Phila) 1997:285-9. 6. Respiratory distress syndrome of the newborn fact sheet. American Lung Association, 2006. Accessed May 7, 2007, at: http://www.lungusa.org/site/pp.asp? c=dvLUK9O0E&b=35693. 7. Ingemarrson I. Gender aspects of preterm birth. BJOG 2003;110(suppl 20):34-8. 8. Cowett RM. The infant of the diabetic mother. Neo- reviews 2002;3:e173-89. 9. Koivisto M, Marttila R, Saarela T, Pokela ML, Valkama AM, Hallman M. Wheezing illness and re-hospitaliza- tion in the first two years of life after neonatal respira- tory distress syndrome. J Pediatr 2005;147:486-92. 10. Cleary GM, Wiswell TE. Meconium-stained amniotic fluid and the meconium aspiration syndrome. An update. Pediatr Clin North Am 1998;45:511-29. 11. Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A. Pre- vention of perinatal group B streptococcal disease. Revised guidelines from CDC. MMWR Recomm Rep 2002;51(RR-11):1-22. 12. Edwards MS. Antibacterial therapy in pregnancy and neonates. Clin Perinatol 1997;24:251-66. 13. Cleveland RH. A radiologic update on medical diseases of the newborn chest. Pediatr Radiol 1995;25:631-7. 14. Davis C, Stevens G. Value of routine radiographic examination of the newborn, based on a study of 702 consecutive babies. Am J Obstet Gynecol 1930;20:73. 15. Horbar JD, Badger GJ, Carpenter JH, Fanaroff AA, Kilpatrick S, LaCorte M, et al., and Members of the Vermont Oxford Network. Trends in mortality and morbidity for very low birth weight infants, 1991-1999. Pediatrics 2002;110(1 pt 1):143-51. 16. Chambers CD, Hernandez-Diaz S, Van Marter LJ, Werler MM, Louik C, Jones KL, et al. Selective serotonin-reuptake inhibitors and risk of persistent pulmonary hypertension of the newborn. N Engl J Med 2006;354:579-87. 17. Al Tawil K, Abu-Ekteish FM, Tamimi O, Al Hathal MM, Al Hathlol K, Abu Laimun B. Symptomatic spontaneous pneumothorax in term newborn infants. Pediatr Pulm- onol 2004;37:443-6. 18. Lewis V, Whitelaw A. Furosemide for transient tachy- pnea of the newborn. Cochrane Database Syst Rev 2002;(1):CD003064. 19. Stutchfield P, Whitaker R, Russel I, for the Antenatal Steroids for Term Elective Cesarean Section (ASTECS) Research Team. Antenatal betamethasone and inci- dence of neonatal respiratory distress after elective cesarean section: pragmatic randomized trial. BMJ 2005;331:662-4. 20. Roberts D, Dalziel S. Antenatal corticosteroids for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev 2006;(3): CD004454. 21. Doyle LW, Halliday HL, Ehrenkranz RA, Davis PG, Sin- clair JC. Impact of postnatal systemic corticosteroids on mortality and cerebral palsy in preterm infants: effect modification by risk for chronic lung disease. Pediatrics 2005;115:655-61. 22. Barrington KJ, Finer NN. Inhaled nitric oxide for respira- tory failure in preterm infants. Cochrane Database Syst Rev 2006;(1):CD000509. 23. Vain NE, Szyld EG, Prudent LM, Wiswell TE, Aguilar AM, Vivas NI. Oropharyngeal and nasopharyngeal suction- ing of meconium-stained neonates before delivery of their shoulders: multicentre, randomised controlled trial. Lancet 2004;364:597-602. 24. Wiswell TE, Gannon CM, Jacob J, Goldsmith L, Szyld E, Weiss K, et al. Delivery room management of the apparently vigorous meconium-stained neonate: results of the multicenter, international collaborative trial. Pediatrics 2000;105:1-7. 25. Hofmeyr GJ, Gulmezoglu AM, Buchmann E, How- arth GR, Shaw A, Nikodem VC, et al. The Col- laborative Randomised Amnioinfusion for Meconium Project (CRAMP): 1. South Africa. Br J Obstet Gynaecol 1998;105:304-8. 26. Hofmeyr GJ. Amnioinfusion for meconium-stained liquor in labour. Cochrane Database Syst Rev 2000;(1): CD000014. 27. Fraser WD, Hofmeyr J, Lede R, Faron G, Alexander S, Goffinet F, et al., for the Amnioinfusion Trial Group. Amnioinfusion for the prevention of the meconium aspiration syndrome. N Engl J Med 2005;353:909-17. 28. Ward M, Sinn J. Steroid therapy for meconium aspira- tion syndrome in newborn infants. Cochrane Database Syst Rev 2003;(4):CD003485. 29. Hein HH, Ely JW, Lofgren MA. Neonatal respiratory distress in the community hospital: when to transport, when to keep. J Fam Pract 1998;46:284-9. Yüklə 133,56 Kb. Dostları ilə paylaş:
|