Strategies for feeding the preterm infant.
Strategies for feeding the preterm infant.
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作者：
Hay WW Jr
根据许多新生儿营养专家的说法，早产儿营养的目标应该是达到与同胎龄正常胎儿接近的出生后生长速度。不幸的是，大多数早产儿，特别是那些出生体重极低的早产儿，没有得到足够的营养来产生正常的胎儿生长速度，因此，在出生后的住院期间，最终生长受到限制。生长受限是一个重要的问题，因为许多研究已经明确表明，在发育的关键阶段，营养不足，特别是蛋白质不足，会导致长期身材矮小，器官生长失败，神经元数量和树突连接不足，以及后来的行为和认知结果。此外，临床随访研究表明，在喂养配方奶粉的婴儿中，配方奶粉的营养成分与日后的精神和运动结果直接呈正相关。营养需求不会在出生时停止。因此，出生后延迟营养“直到婴儿稳定”忽略了一个基本点，即出生后没有立即开始营养，婴儿进入分解代谢状态，而分解代谢无助于正常发育和生长。氧气是所有代谢过程所必需的。最近限制氧供应以防止氧中毒的趋势具有发展生长障碍的潜力，特别是当血液血红蛋白浓度福尔斯降至低于8 g/dl时。出生后应尽快提供6-8 mg/min/kg的葡萄糖，并根据频繁的血糖测量进行调整，以达到并维持浓度> 45 mg/dl但< 120 mg/dl，以避免高血糖和低血糖的频繁问题。同样，需要提供至少0.5 g/kg/天的脂质，以预防必需脂肪酸缺乏症。然而，早产儿经常获得的高碳水化合物和脂质供应，基于促进蛋白质生长所必需的不完整假设，往往会在肝脏和心脏等器官以及脂肪组织中产生增加的脂肪。更多和更好的必需脂肪酸营养是有价值的，但更多的器官和脂肪没有已知的好处和许多问题。氨基酸和蛋白质不仅对身体生长至关重要，而且对代谢信号、蛋白质合成和蛋白质增长也至关重要。3.5-4.0 g/kg/天是非常早产儿产生正常蛋白质平衡和生长所必需的。用胰岛素促进蛋白质生长的尝试有许多问题-它是无效的，同时有助于进一步的器官和脂肪组织脂肪沉积。肠内喂养总是有指征的，迄今为止，几乎所有的研究都表明，最低限度的肠内喂养方法（例如，“营养饲料”）促进肠内进食的能力。牛奶在避免坏死性小肠结肠炎（NEC）方面具有明显的优势，而喂养与NEC相关，最小肠内喂养方案产生的NEC比那些更积极引入肠内喂养的方案少。最后，过度喂养有可能产生脂肪组织或肥胖，从而导致胰岛素抵抗、葡萄糖耐受不良和糖尿病。这种情况更常见，因为婴儿在出生后喂养更多，体重增加更快，无论他们的出生体重如何。胎儿宫内发育迟缓和出生后生长障碍的婴儿可能是这种结果的唯一“设定”，而子宫内肥胖的婴儿，如糖尿病母亲的婴儿，已经沿着这种不利的结果途径
According to many experts in neonatal nutrition, the goal for nutrition of the preterm infant should be to achieve a postnatal growth rate approximating that of the normal fetus of the same gestational age. Unfortunately, most preterm infants, especially those born very preterm with extremely low birth weight, are not fed sufficient amounts of nutrients to produce normal fetal rates of growth and, as a result, end up growth-restricted during their hospital period after birth. Growth restriction is a significant problem, as numerous studies have shown definitively that under nutrition, especially of protein, at critical stages of development produces long-term short stature, organ growth failure, and both neuronal deficits of number and dendritic connections as well as later behavioral and cognitive outcomes. Furthermore, clinical follow-up studies have shown that among infants fed formulas, the nutrient content of the formula is directly and positively related to mental and motor outcomes later in life. Nutritional requirements do not stop at birth. Thus, delaying nutrition after birth ‘until the infant is stable’ ignores the fundamental point that without nutrition starting immediately after birth, the infant enters a catabolic condition, and catabolism does not contribute to normal development and growth. Oxygen is necessary for all metabolic processes. Recent trends to limit oxygen supply to prevent oxygen toxicity have the potential, particularly when the blood hemoglobin concentration falls to less than 8 g/dl, to develop growth failure. Glucose should be provided at 6–8 mg/min/kg as soon after birth as possible and adjusted according to frequent measurements of plasma glucose to achieve and maintain concentrations > 45 mg/dl but < 120 mg/dl to avoid the frequent problems of hyperglycemia and hypoglycemia. Similarly, lipid is required to provide at least 0.5 g/kg/day to prevent essential fatty acid deficiency. However, the high rate of carbohydrate and lipid supply that preterm infants often get, based on the incomplete assumption that this is necessary to promote protein growth, tends to produce increased fat in organs like the liver and heart as well as adipose tissue. More and better essential fatty acid nutrition is valuable, but more organ and adipose fat has no known benefit and many problems. Amino acids and protein are essential not only for body growth but for metabolic signaling, protein synthesis, and protein accretion. 3.5–4.0 g/kg/day are necessary to produce normal protein balance and growth in very preterm infants. Attempts to promote protein growth with insulin has many problems – it is ineffective while contributing to even further organ and adipose tissue fat deposition. Enteral feeding always is indicated and to date nearly all studies have shown that minimal enteral feeding approaches (e.g., ‘trophic feeds’) promote the capacity to feed enterally. Milk has distinct advantages over formulas in avoiding necrotizing enterocolitis (NEC), and while feeding is associated with NEC, minimal enteral feeding regimens produce less NEC than those geared towards more aggressive introduction of enteral feeding. Finally, overfeeding has the definite potential to produce adipose tissue, or obesity, which then leads to insulin resistance, glucose intolerance, and diabetes. This scenario occurs more commonly as infants are fed more and gain weight more rapidly after birth, regardless of their birth weight. Infants with IUGR and postnatal growth failure may be uniquely ‘set up’ for this outcome, while infants with in utero obesity, such as infants of diabetic mothers, already are well along this adverse outcome pathway
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DOI：
10.1097/01.mpg.0000302965.93546.b8
发表时间：
2007-12-01
影响因子：
2.9
作者：
Hay, William W., Jr.
通讯作者：
Hay, William W., Jr.
DOI：
10.1080/07315724.2004.10719428
发表时间：
2004-12-01
影响因子：
3.5
作者：
Barker, DJP
通讯作者：
Barker, DJP
影响因子：
5.1
作者：
DANCIS, J;OCONNELL, JR;HOLT, LE
通讯作者：
HOLT, LE
DOI：
10.1152/ajpregu.1999.276.3.r809
发表时间：
1999-03-01
影响因子：
2.8
作者：
Das, UG;Schroeder, RE;Devaskar, SU
通讯作者：
Devaskar, SU
DOI：
10.1053/siny.2001.0093
发表时间：
2001-10-01
期刊：
Seminars in neonatology : SN
影响因子：
--
作者：
Carlson, S E
通讯作者：
Carlson, S E