Considerable advances have occurred in recent years in the scientific knowledge of the benefits of breastfeeding, the mechanisms underlying these benefits, and in the clinical management of breastfeeding. This policy statement on breastfeeding replaces the 1997 policy statement of the American Academy of Pediatrics and reflects this newer knowledge and the supporting publications. The benefits of breastfeeding for the infant, the mother, and the community are summarized, and recommendations to guide the pediatrician and other health care professionals in assisting mothers in the initiation and maintenance of breastfeeding for healthy term infants and high-risk infants are presented. The policy statement delineates various ways in which pediatricians can promote, protect, and support breastfeeding not only in their individual practices but also in the hospital, medical school, community, and nation.

/pdf/breastfeeding-and-the-use-of-human-milk-2m74a0njro.pdf

Breastfeeding and the Use of Human Milk

There is increasing recognition that systematic post–cardiac arrest care after return of spontaneous circulation (ROSC) can improve the likelihood of patient survival with good quality of life. This is based in part on the publication of results of randomized controlled clinical trials as well as a description of the post–cardiac arrest syndrome. 1–3 Post–cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury. 3,4 This section summarizes our evolving understanding of the hemodynamic, neurological, and metabolic abnormalities encountered in patients who are initially resuscitated from cardiac arrest. The initial objectives of post–cardiac arrest care are to ● Optimize cardiopulmonary function and vital organ perfusion. ● After out-of-hospital cardiac arrest, transport patient to an appropriate hospital with a comprehensive post–cardiac arrest treatment system of care that includes acute coronary interventions, neurological care, goal-directed critical care, and hypothermia. ● Transport the in-hospital post–cardiac arrest patient to an appropriate critical-care unit capable of providing comprehensive post–cardiac arrest care. ● Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest.

http://www.kardio.hu/feltoltott/dokumentumok/fajl_201148104747Cardiopulm_resuscit_Pt9_Post_cardiac.pdf

Part 9: Post-Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Many believe that informed consent makes clinical research ethical. However, informed consent is neither necessary nor sufficient for ethical clinical research. Drawing on the basic philosophies underlying major codes, declarations, and other documents relevant to research with human subjects, we propose 7 requirements that systematically elucidate a coherent framework for evaluating the ethics of clinical research studies: (1) value-enhancements of health or knowledge must be derived from the research; (2) scientific validity-the research must be methodologically rigorous; (3) fair subject selection-scientific objectives, not vulnerability or privilege, and the potential for and distribution of risks and benefits, should determine communities selected as study sites and the inclusion criteria for individual subjects; (4) favorable risk-benefit ratio-within the context of standard clinical practice and the research protocol, risks must be minimized, potential benefits enhanced, and the potential benefits to individuals and knowledge gained for society must outweigh the risks; (5) independent review-unaffiliated individuals must review the research and approve, amend, or terminate it; (6) informed consent-individuals should be informed about the research and provide their voluntary consent; and (7) respect for enrolled subjects-subjects should have their privacy protected, the opportunity to withdraw, and their well-being monitored. Fulfilling all 7 requirements is necessary and sufficient to make clinical research ethical. These requirements are universal, although they must be adapted to the health, economic, cultural, and technological conditions in which clinical research is conducted. JAMA. 2000;283:2701-2711.

/pdf/what-makes-clinical-research-ethical-1aaoil4fbl.pdf

What Makes Clinical Research Ethical

In contrast to adults, cardiac arrest in infants and children does not usually result from a primary cardiac cause. More often it is the terminal result of progressive respiratory failure or shock, also called an asphyxial arrest. Asphyxia begins with a variable period of systemic hypoxemia, hypercapnea, and acidosis, progresses to bradycardia and hypotension, and culminates with cardiac arrest.1

Another mechanism of cardiac arrest, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), is the initial cardiac rhythm in approximately 5% to 15% of pediatric in-hospital and out-of-hospital cardiac arrests;2,–,9 it is reported in up to 27% of pediatric in-hospital arrests at some point during the resuscitation.6 The incidence of VF/pulseless VT cardiac arrest rises with age.2,4 Increasing evidence suggests that sudden unexpected death in young people can be associated with genetic abnormalities in myocyte ion channels resulting in abnormalities in ion flow (see “Sudden Unexplained Deaths,” below).

Since 2010 marks the 50th anniversary of the introduction of cardiopulmonary resuscitation (CPR),10 it seems appropriate to review the progressive improvement in outcome of pediatric resuscitation from cardiac arrest. Survival from in-hospital cardiac arrest in infants and children in the 1980s was around 9%.11,12 Approximately 20 years later, that figure had increased to 17%,13,14 and by 2006, to 27%.15,–,17 In contrast to those favorable results from in-hospital cardiac arrest, overall survival to discharge from out-of-hospital cardiac arrest in infants and children has not changed substantially in 20 years and remains at about 6% (3% for infants and 9% for children and adolescents).7,9

It is unclear why the improvement in outcome from in-hospital cardiac arrest has occurred, although earlier recognition and management of at-risk patients on general inpatient units …

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.110.971101

Part 14: Pediatric Advanced Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Institutional Affiliations Chair Costanzo MR: Midwest Heart Foundation, Lombard Illinois, USA Task Force 1 Dipchand A: Hospital for Sick Children, Toronto Ontario, Canada; Starling R: Cleveland Clinic Foundation, Cleveland, Ohio, USA; Anderson A: University of Chicago, Chicago, Illinois, USA; Chan M: University of Alberta, Edmonton, Alberta, Canada; Desai S: Inova Fairfax Hospital, Fairfax, Virginia, USA; Fedson S: University of Chicago, Chicago, Illinois, USA; Fisher P: Ochsner Clinic, New Orleans, Louisiana, USA; Gonzales-Stawinski G: Cleveland Clinic Foundation, Cleveland, Ohio, USA; Martinelli L: Ospedale Niguarda, Milano, Italy; McGiffin D: University of Alabama, Birmingham, Alabama, USA; Parisi F: Ospedale Pediatrico Bambino Gesu, Rome, Italy; Smith J: Freeman Hospital, Newcastle upon Tyne, UK Task Force 2 Taylor D: Cleveland Clinic Foundation, Cleveland, Ohio, USA; Meiser B: University of Munich/Grosshaden, Munich, Germany; Baran D: Newark Beth Israel Medical Center, Newark, New Jersey, USA; Carboni M: Duke University Medical Center, Durham, North Carolina, USA; Dengler T: University of Hidelberg, Heidelberg, Germany; Feldman D: Minneapolis Heart Institute, Minneapolis, Minnesota, USA; Frigerio M: Ospedale Niguarda, Milano, Italy; Kfoury A: Intermountain Medical Center, Murray, Utah, USA; Kim D: University of Alberta, Edmonton, Alberta, Canada; Kobashigawa J: Cedar-Sinai Heart Institute, Los Angeles, California, USA; Shullo M: University of Pittsburgh, Pittsburgh, Pennsylvania, USA; Stehlik J: University of Utah, Salt Lake City, Utah, USA; Teuteberg J: University of Pittsburgh, Pittsburgh, Pennsylvania, USA; Uber P: University of Maryland, Baltimore, Maryland, USA; Zuckermann A: University of Vienna, Vienna, Austria. Task Force 3 Hunt S: Stanford University, Palo Alto, California, USA; Burch M: Great Ormond Street Hospital, London, UK; Bhat G: Advocate Christ Medical Center, Oak Lawn, Illinois, USA; Canter C: St. Louis Children Hospital, St. Louis, Missouri, USA; Chinnock R: Loma Linda University Children's Hospital, Loma Linda, California, USA; Crespo-Leiro M: Hospital Universitario A Coruna, La Coruna, Spain; Delgado R: Texas Heart Institute, Houston, Texas, USA; Dobbels F: Katholieke Universiteit Leuven, Leuven, Belgium; Grady K: Northwestern University, Chicago, Illlinois, USA; Kao W: University of Wisconsin, Madison Wisconsin, USA; Lamour J: Montefiore Medical Center, New York, New York, USA; Parry G: Freeman Hospital, Newcastle upon Tyne, UK; Patel J: Cedar-Sinai Heart Institute, Los Angeles, California, USA; Pini D: Istituto Clinico Humanitas, Rozzano, Italy; Pinney S: Mount Sinai Medical Center, New York, New York, USA; Towbin J: Cincinnati Children's Hospital, Cincinnati, Ohio, USA; Wolfel G: University of Colorado, Denver, Colorado, USA Independent Reviewers Delgado D: University of Toronto, Toronto, Ontario, Canada; Eisen H: Drexler University College of Medicine, Philadelphia, Pennsylvania, USA; Goldberg L: University of Pennsylvania, Philadelphia, Pennsylvania, USA; Hosenpud J: Mayo Clinic, Jacksonville, Florida, USA; Johnson M: University of Wisconsin, Madison, Wisconsin, USA; Keogh A: St Vincent Hospital, Sidney, New South Wales, Australia; Lewis C: Papworth Hospital Cambridge, UK; O'Connell J: St. Joseph Hospital, Atlanta, Georgia, USA; Rogers J: Duke University Medical Center, Durham, North Carolina, USA; Ross H: University of Toronto, Toronto, Ontario, Canada; Russell S: Johns Hopkins Hospital, Baltimore, Maryland, USA; Vanhaecke J: University Hospital Gasthuisberg, Leuven, Belgium.

http://www.jsht.jp/uploads/ISHLT_GL_TaskForce2_110810.pdf

The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients

The American Academy of Pediatrics places emphasis on increasing breastfeeding in the United States. A common reason for the cessation of breastfeeding is the use of medication by the nursing mother and advice by her physician to stop nursing. Such advice may not be warranted. This statement is intended to supply the pediatrician, obstetrician, and family physician with data, if known, concerning the excretion of drugs into human milk. Most drugs likely to be prescribed to the nursing mother should have no effect on milk supply or on infant well-being. This information is important not only to protect nursing infants from untoward effects of maternal medication but also to allow effective pharmacologic treatment of breastfeeding mothers. Nicotine, psychotropic drugs, and silicone implants are 3 important topics reviewed in this statement.

Transfer of drugs and other chemicals into human milk

Guidelines for the ethical conduct of studies to evaluate drugs in pediatric populations

Publicity about the possible carcinogenicity of chloral hydrate along with the suggestion that alternative sedatives should be used in children has generated concern among physicians, dentists, and their patients.1,2 Replacement of chloral hydrate with other sedatives would represent a major change in practice because it is one of the drugs most widely employed to sedate young children undergoing dental and medical procedures and imaging studies. This statement will assist the practitioner in making an informed decision regarding the use of chloral hydrate by summarizing (1) information pertaining to the potential for carcinogenesis associated with use of chloral hydrate, (2) the risk/benefit considerations of available sedatives, and (3) risks associated with prolonged sedation with chloral hydrate.\n EVIDENCE FOR CARCINOGENESIS OF CHLORAL HYDRATE\n Some of the concern regarding potential carcinogenicity of chloral hydrate is based on the assumption that chloral hydrate is a reactive metabolite of trichloroethylene, an industrial solvent, and is responsible for the carcinogenicity of trichloroethylene.1,2 However, the validity of this assumption is open to question. Although chloral hydrate is a metabolite of trichloroethylene, there is evidence that the carcinogenicity of trichloroethylene is due to a reactive intermediate epoxide metabolite rather than chloral hydrate.3 As is the case for most chemical carcinogens, trichloroethylene is carcinogenic in some laboratory animal species but not in others.4 Multiple epidemiologic studies in humans have failed to document an increase in cancer incidence associated with trichloroethylene exposure,5-10 although the ability of these studies to detect small increases in risk of cancer is limited.\n There are no studies pertaining to chloral hydrate-associated carcinogenicity in humans.

Use of chloral hydrate for sedation in children

The recent introduction of an effective oral chelating agent for the reduction of a body burden of lead and the changing standards of care for children exposed to lead prompted the Committee on Drugs to review the therapy for lead intoxication. This statement reviews the pharmacology of available chelating agents. Screening standards and detailed discussions of environmental control and nutritional management have been previously published by the American Academy of Pediatrics.1\n Lead intoxication has been a problem throughout history. In the early 1940s it was recognized that the amount of lead in the urban industrial environment had increased to the point at which a striking number of children demonstrated hematologic effects and clinical signs of acute lead intoxication. Blood lead levels in children in the United States on average have decreased, and rarely are children seen with blood lead levels of greater than 70 µg/dL. Even in patients with levels of greater than 50 µg/dL, \"classic\" laboratory and clinical findings of lead toxicity, such as basophilic stippling and encephalopathy, are rarely seen.2 In the past, therapy was based on the ability of chelators to reverse the hematologic effects of lead and halt the progression of lead encephalopathy. The efficacy of chelation therapy for children without the hematologic or neurologic findings has yet to be demonstrated; a decrease in blood lead concentration is the only discernible goal for chelation therapy in this setting. Eliminating the source of lead exposure also can accomplish this result. A recent study of moderately lead-exposed children receiving chelation therapy failed to demonstrate any additional benefit of CaNa2-ethylenediaminetetraacetic acid (EDTA) compared with abatement at improving cognitive function.3

Treatment guidelines for lead exposure in children

The following addendum from the Committee on Drugs was prepared in response to numerous requests for reference material or rationale to support the dosage of naloxone for infants and children1 currently recommended by the Committee on Drugs. The currently recommended dose of naloxone is 0.1 mg/kg for infants and children from birth to 5 years of age or 20 kg of body weight. Children olden than 5 years of age or weighing more than 20 kg may be given 2.0 mg. These doses may be repeated as needed to maintain opiate reversal.’ The higher dose recommendation is based, in part, on a concern that 0.01 mg/kg, currently recommended in approved labeling, may not provide optimal opiate reversal in some infants.2 In addition, it is intended to simplify naloxone dosing and provide greater probability of optimal opiate reversal in most patients. Because doses as high as 0.4 mg/kg have been administered to newborns without ill effect,3 it is felt that the higher dose poses no increased risk. Naloxone doses ranging from 0.005 to 0.4 mg/kg have been reported in the pediatric literature.2’#{176} Individual doses up to 0.4 mg/kg and constant intravenous infusion of 0.16 mg/kg/h for 5 days4 have not been associated with naloxone-related adverse effects. The average half-life of naloxone in premature newborns is 70 minutes.5 The Committee’s naloxone dosing recommendation has been incorporated recently into the joint American Heart Association (AHA)/Amenican Academy of Pediatrics (AAP) textbook on neonatal resuscitation” and the accompanying test mate-

R. L. Gorman

Papers

Transfer of drugs and other chemicals into human milk

Guidelines for the ethical conduct of studies to evaluate drugs in pediatric populations

Use of chloral hydrate for sedation in children

Treatment guidelines for lead exposure in children

Naloxone dosage and route of administration for infants and children: Addendum to emergency drug doses for infants and children