Han Suk Kim

Bio: Han Suk Kim is an academic researcher from New Generation University College. The author has contributed to research in topics: Bronchopulmonary dysplasia & Low birth weight. The author has an hindex of 35, co-authored 215 publications receiving 4128 citations. Previous affiliations of Han Suk Kim include Seoul National University & University of Pennsylvania.

Part 7: Neonatal resuscitation: 2015 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations

Abstract: ### Newborn Transition The transition from intrauterine to extrauterine life that occurs at the time of birth requires timely anatomic and physiologic adjustments to achieve the conversion from placental gas exchange to pulmonary respiration. This transition is brought about by initiation of air breathing and cessation of the placental circulation. Air breathing initiates marked relaxation of pulmonary vascular resistance, with considerable increase in pulmonary blood flow and increased return of now-well-oxygenated blood to the left atrium and left ventricle, as well as increased left ventricular output. Removal of the low-resistance placental circuit will increase systemic vascular resistance and blood pressure and reduce right-to-left shunting across the ductus arteriosus. The systemic organs must equally and quickly adjust to the dramatic increase in blood pressure and oxygen exposure. Similarly, intrauterine thermostability must be replaced by neonatal thermoregulation with its inherent increase in oxygen consumption. Approximately 85% of babies born at term will initiate spontaneous respirations within 10 to 30 seconds of birth, an additional 10% will respond during drying and stimulation, approximately 3% will initiate respirations after positive-pressure ventilation (PPV), 2% will be intubated to support respiratory function, and 0.1% will require chest compressions and/or epinephrine to achieve this transition.1–3 Although the vast majority of newborn infants do not require intervention to make these transitional changes, the large number of births worldwide means that many infants require some assistance to achieve cardiorespiratory stability each year. Newly born infants who are breathing or crying and have good tone immediately after birth must be dried and kept warm so as to avoid hypothermia. These actions can be provided with the baby lying on the mother’s chest and should not require separation of mother and baby. This does not preclude the need for clinical assessment of the baby. …

Pulmonary hypertension in preterm infants with bronchopulmonary dysplasia.

Abstract: Background and Objectives: With the increasing survival of preterm infants, pulmonary hypertension (PH) related to bronchopulmonary dysplasia (BPD) has become an important complication. The aim of this study was to investigate the characteristics and outcome of PH in preterm infants with BPD and to identify the risk factors for PH. Subjects and Methods: We reviewed the records of 116 preterm infants with BPD cared for at a single tertiary center between 2004 and 2008. Results: Twenty-nine (25%) infants had PH >2 months after birth. PH occurred initially at a median age of 65 days (range, 7-232 days). Severe BPD, a birth weight <800 g, long-term ventilator care and oxygen supplementation, a high ventilator setting, infection, and a patent ductus arteriosus (PDA) were related to PH based on univariate analysis (p<0.05). The infants who had longer oxygen supplementation were significantly more likely to have PH (odds ratio, 18.5; 95% confidence interval, 4.1-84.6; p<0.001). PH was improved in 76% of infants after a median of 85 days (range, 20-765 days). Four infants (14%) died. The death of 3 infants was attributed to PH. Conclusion: BPD was frequently complicated by PH. Although PH resolved in the majority of infants, PH in preterm infants with BPD can be fatal. Regular screening for PH and adequate management are required. (Korean Circ J 2010;40:131-136)

Part 7: Neonatal Resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations (Reprint).

Abstract: Reprint: The American Heart Association requests that this document be cited as follows: Perlman JM, Wyllie J, Kattwinkel J, Wyckoff MH, Aziz K, Guinsburg R, Kim HS, Liley HG, Mildenhall L, Simon WM, Szyld E, Tamura M, Velaphi S; on behalf of the Neonatal Resuscitation Chapter Collaborators. Part 7: neonatal resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation . 2015;132(suppl 1):S204–S241. Reprinted with permission of the American Heart Association, Inc., European Resuscitation Council, and International Liaison Committee on Resuscitation. This article has been published in Circulation and Resuscitation . (Circulation. 2015;132[suppl 1]:S204–S241. DOI: 10.1161/CIR.0000000000000276.) ### Newborn Transition The transition from intrauterine to extrauterine life that occurs at the time of birth requires timely anatomic and physiologic adjustments to achieve the conversion from placental gas exchange to pulmonary respiration. This transition is brought about by initiation of air breathing and cessation of the placental circulation. Air breathing initiates marked relaxation of pulmonary vascular resistance, with considerable increase in pulmonary blood flow and increased return of now-well-oxygenated blood to the left atrium and left ventricle, as well as increased left ventricular output. Removal of the low-resistance placental circuit will increase systemic vascular resistance and blood pressure and reduce right-to-left shunting across the ductus arteriosus. The systemic organs must equally and quickly adjust to the dramatic increase in blood pressure and oxygen exposure. Similarly, intrauterine thermostability must be replaced by neonatal thermoregulation with its inherent increase in oxygen consumption. Approximately 85% of babies born at term will initiate spontaneous respirations within 10 to 30 seconds of birth, an additional 10% will respond during drying and stimulation, approximately 3% will initiate respirations after positive-pressure ventilation (PPV), 2% will be intubated to support respiratory function, and 0.1% will require chest compressions and/or epinephrine to achieve this transition.1–3 …

Blood transfusion increases radical promoting non-transferrin bound iron in preterm infants

Abstract: BACKGROUND—Blood transfusion has been recognised as a risk factor for the development of retinopathy of prematurity (ROP) or chronic lung disease (CLD) in preterm infants, but the precise mechanism involved is not understood. AIM—To investigate the level of non-transferrin bound "free" iron, which has the potential to promote the generation of reactive oxygen species, and its redox status in the plasma of preterm infants immediately before and after blood transfusion. METHODS—Twenty one preterm infants with a median gestational age and birth weight of 27 weeks and 1021 g respectively were prospectively enrolled in the study. Sixteen of the 21 infants developed ROP and/or CLD. The infants were transfused with concentrated red blood cells at a median age of 32 days. The plasma concentration of total bleomycin detectable iron (BDI) was measured and also the ferrous iron (Fe2+) activity by bleomycin-iron complex dependent degradation of DNA. RESULTS—Even before blood transfusion, BDI was detectable in one third of the blood samples, and all but one sample had ferrous iron activity. After transfusion, both BDI and ferrous iron activity were significantly increased, in contrast with the situation in full term infants. Plasma ascorbic acid (AA) concentration was significantly decreased after blood transfusion, whereas the level of its oxidation product, dehydroascorbic acid (DHAA), and the DHAA/AA ratio were significantly increased compared with before the transfusion. The activity of plasma ferroxidase, which converts iron from the ferrous to the ferric state, was appreciably decreased in preterm infants, as expected from their very low plasma caeruloplasmin concentration. CONCLUSIONS—Plasma non-transferrin bound iron was significantly increased in preterm infants after blood transfusion and existed partly in the ferrous form, because of the low ferroxidase activity and the reduction of ferric iron (Fe3+) by ascorbic acid. This finding was specific to preterm infants and was not observed in full term infants after blood transfusion. Non-transferrin bound "free" iron may catalyse the generation of reactive oxygen species, which may be responsible for the clinical association of blood transfusion with ROP and CLD.

Risk factors for pulmonary artery hypertension in preterm infants with moderate or severe bronchopulmonary dysplasia.

Abstract: Background: Despite the potential importance of pulmonary artery hypertension (PAH) in preterm infants with bronchopulmonary dysplasia (BPD), little is known about the risk factors for PAH. Objectives: To investigate the risk factors for PAH in preterm infants with BPD. Methods: Infants diagnosed with BPD were assigned to the PAH group or non-PAH group except for infants with mild BPD who had no PAH. PAH was diagnosed on the basis of echocardiograms demonstrating elevated right ventricle pressure beyond the postnatal age of 2 months. Logistic regression analysis was done for the multivariate assessment of the risk factors for PAH in preterm infants with moderate or severe BPD. Results: A total of 98 infants among 145 infants with BPD were divided into a PAH group (n = 25) or non-PAH group (n = 73), while the remaining 47 infants had mild BPD with no PAH. Among the study patients, survival rate of the PAH group was significantly lower than that of the non-PAH group. Infants with PAH had more severe cases of BPD and underwent longer durations of oxygen therapy, conventional or high-frequency ventilation, and hospitalization compared to those without PAH. Low 5-min Apgar scores (≤6; relative risk (RR) 6.2; 95% confidence interval (CI) 1.4–28.0; p = 0.017) and oligohydramnios (RR 7.7; 95% CI 2.0–29.6; p = 0.030) were found to be significant risk factors for PAH according to multivariate analysis. Conclusions: The present study shows that oligohydramnios is a specific risk factor for PAH in preterm infants with moderate or severe BPD.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Abstract: Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean?

Abstract: Free radicals and other reactive species (RS) are thought to play an important role in many human diseases. Establishing their precise role requires the ability to measure them and the oxidative damage that they cause. This article first reviews what is meant by the terms free radical, RS, antioxidant, oxidative damage and oxidative stress. It then critically examines methods used to trap RS, including spin trapping and aromatic hydroxylation, with a particular emphasis on those methods applicable to human studies. Methods used to measure oxidative damage to DNA, lipids and proteins and methods used to detect RS in cell culture, especially the various fluorescent ‘probes' of RS, are also critically reviewed. The emphasis throughout is on the caution that is needed in applying these methods in view of possible errors and artifacts in interpreting the results. Keywords: Cell culture, free radical, reactive species, antioxidant, oxidative stress, oxidative damage, fluorescent probe, lipid peroxidation, superoxide Introduction Free radicals and other ‘reactive oxygen (ROS)/nitrogen/chlorine species' (for an explanation of these terms see Table 1) are widely believed to contribute to the development of several age-related diseases, and perhaps, even to the aging process itself (Halliwell & Gutteridge, 1999; Sohal et al., 2002) by causing ‘oxidative stress' and ‘oxidative damage' (terms explained in Table 2). For example, many studies have shown increased oxidative damage to all the major classes of biomolecules in the brains of Alzheimer's patients (Halliwell, 2001; Butterfield, 2002; Liu et al., 2003). Other diseases in which oxidative damage has been implicated include cancer, atherosclerosis, other neurodegenerative diseases and diabetes (Hagen et al., 1994; Chowienczyk et al., 2000; Halliwell, 2000a, 2001, 2002a, 2002b; Parthasarathy et al., 2000). If oxidative damage contributes significantly to disease pathology (Table 3 lists the criteria needed to establish this), then actions that decrease it should be therapeutically beneficial (Halliwell, 2001; Lee et al., 2002a; Liu et al., 2003). If the oxidative damage is involved in the origin of a disease, then successful antioxidant treatment should delay or prevent the onset of that disease (Halliwell, 1991, 2002a, 2002b; Galli et al., 2002; Steinberg & Witztum, 2002). To establish the role of oxidative damage (Table 3), it is therefore essential to be able to measure it accurately. For example, the failure of interventions with antioxidants such as vitamin E, β-carotene or ascorbate to decrease disease incidence in several human intervention trials may have simply been due to the failure of these compounds to decrease oxidative damage in the subjects tested (Halliwell, 1999a, 2000c; Levine et al., 2001; Meagher et al., 2001). In this review, we will examine the methods available to measure reactive species (RS) and oxidative damage, with a particular emphasis on those applicable to human studies. Table 1 Nomenclature of reactive species Table 2 Some key definitions Table 3 Criteria for implicating RS as a significant mechanism of tissue injury in human disease Measuring RS in vivo: basic principles Some fascinating techniques such as L-band electron spin resonance (ESR) with nitroxyl probes and magnetic resonance imaging spin trapping are under development to measure RS directly in whole animals (e.g. Berliner et al., 2001; Han et al., 2001; Utsumi & Yamada, 2003), but no probes are currently suitable for human use. Most RS persist for only a short time in vivo and cannot be measured directly. There are a few exceptions: examples include H2O2 (discussed below), and perhaps, NO•, in the sense that serum levels of NO2− have been claimed to measure vascular endothelial NO• synthesis (Kelm et al., 1999), despite the fact that NO2− is quickly oxidized to NO3− in vivo (Kelm et al., 1999; Oldreive & Rice-Evans, 2001). Essentially, there are two approaches to detecting transient RS: attempting to trap these species and measure the levels of the trapped molecules and measuring the levels of the damage done by RS, that is, the amount of oxidative damage. Sometimes other approaches are used. They include measurements of erythrocyte antioxidant defences and of total antioxidant activity of body fluids; falls in these parameters are often taken as evidence of oxidative stress. Erythrocytes cannot synthesize proteins, however, and their antioxidant enzyme levels may drop as they ‘age' in the circulation (Denton et al., 1975). Thus changes in their levels are more likely to reflect changes in the rates of red blood cell turnover: if this slows down, the circulating erythrocytes will be older on average and so levels of antioxidant enzymes in them will appear to fall. Vice versa, if an intervention accelerates red cell removal or increases erythropoiesis, levels of antioxidants in red cells will seem to rise. Hence, such data should be interpreted with caution. Depending on the method that is used to measure it, the plasma or serum ‘total antioxidant capacity' (TAC) usually involves major contributions from urate, ascorbate and sometimes albumin −SH groups (Benzie & Strain, 1996; Halliwell & Gutteridge, 1999; Prior & Cao, 1999; Rice-Evans, 2000; Bartosz, 2003), although different methods measure different things (Schlesier et al., 2002; Bartosz, 2003). Thus, for example, if plasma albumin levels fall, TAC will fall. If urate levels rise, TAC will rise. The multiple changes in blood chemistry that occur in sick people mean that TAC changes should be interpreted with caution. TAC is also influenced by diet, often because consumption of certain foods may produce changes in plasma ascorbate and/or urate levels (Halliwell, 2003b).

Enteral nutrient supply for preterm infants: commentary from the European Society of Paediatric Gastroenterology, Hepatology and Nutrition Committee on Nutrition

Abstract: The number of surviving children born prematurely has increased substantially during the last 2 decades. The major goal of enteral nutrient supply to these infants is to achieve growth similar to foetal growth coupled with satisfactory functional development. The accumulation of knowledge since the previous guideline on nutrition of preterm infants from the Committee on Nutrition of the European Society of Paediatric Gastroenterology and Nutrition in 1987 has made a new guideline necessary. Thus, an ad hoc expert panel was convened by the Committee on Nutrition of the European Society of Paediatric Gastroenterology, Hepatology, and Nutrition in 2007 to make appropriate recommendations. The present guideline, of which the major recommendations are summarised here (for the full report, see http://links.lww.com/A1480), is consistent with, but not identical to, recent guidelines from the Life Sciences Research Office of the American Society for Nutritional Sciences published in 2002 and recommendations from the handbook Nutrition of the Preterm Infant. Scientific Basis and Practical Guidelines, 2nd ed, edited by Tsang et al, and published in 2005. The preferred food for premature infants is fortified human milk from the infant's own mother, or, alternatively, formula designed for premature infants. This guideline aims to provide proposed advisable ranges for nutrient intakes for stable-growing preterm infants up to a weight of approximately 1800 g, because most data are available for these infants. These recommendations are based on a considered review of available scientific reports on the subject, and on expert consensus for which the available scientific data are considered inadequate.