Lucey J F, Dangman B
Pediatrics. 1984 Jan;73(1):82-96.
A critical review of the literature of retrolental fibroplasia indicates that the cause of this disease is not yet known. Oxygen is certainly a critical factor but it is still not possible to make precise recommendations as to the amount or the duration of therapy that is safe. We have overemphasized the role of oxygen in the past, and as a result of this the false impression has been created that RLF is a disease that can be prevented. This gross oversimplification of a complex disease with multiple causes has resulted in many unjustified malpractice claims. A study of the present epidemic indicates that excessive oxygen administration probably plays a minor role, in contrast to the first epidemic in which prolonged oxygen administration was clearly a major factor. A reasonable working hypothesis is that the developing retina is highly sensitive to any disturbance in its oxygen supply, either hyperoxemic or hypoxemic. The retinal circulation is subject to the same wide fluctuations as the cerebral circulation in newborn infants. The very low-birth-weight, sick premature infant suffers from a number of conditions, many of which can seriously disturb the retinal circulation, resulting in hypoperfusion and ischemia. These factors (immaturity, hyperoxia, hypoxia, blood transfusions, intraventricular hemorrhage, apnea, infection, hypercarbia, hypocarbia, patent ductus arteriosus, prostaglandin synthetase inhibitors, vitamin E deficiency, lactic acidosis, prenatal complications, genetic factors) may all be present in an infant. They may interact to produce various degrees of retinal damage. Nearly all of these factors cannot be prevented or controlled by our present methods of care. Unfortunately, this means that RLF is an extremely difficult disease to prevent, treat, or investigate. A disease of this complexity with multiple causes will require very large numbers of infants in any controlled study of a therapy. Retrolental fibroplasia should not be considered an avoidable iatrogenic disease in very low-birth-weight infants. Its cause in these infants is not known.
对晶状体后纤维增生症文献的批判性综述表明，这种疾病的病因尚不清楚。氧气无疑是一个关键因素，但对于安全治疗的剂量或持续时间仍无法给出精确的建议。过去我们过度强调了氧气的作用，结果造成了一种错误的印象，即认为晶状体后纤维增生症是一种可以预防的疾病。对这种具有多种病因的复杂疾病的严重过度简化，导致了许多毫无根据的医疗事故索赔。对当前这一流行病的研究表明，与第一次流行病中长时间吸氧显然是主要因素形成对比的是，过度吸氧可能只起了较小的作用。一个合理的可行假设是，发育中的视网膜对其氧气供应的任何干扰（高氧或低氧）都高度敏感。新生儿的视网膜循环与脑循环一样，会出现大幅度波动。极低体重的患病早产儿患有多种病症，其中许多病症会严重干扰视网膜循环，导致灌注不足和局部缺血。这些因素（不成熟、高氧、低氧、输血、脑室内出血、呼吸暂停、感染、高碳酸血症、低碳酸血症、动脉导管未闭、前列腺素合成酶抑制剂、维生素E缺乏、乳酸酸中毒、产前并发症、遗传因素）可能在一个婴儿身上都存在。它们可能相互作用，造成不同程度的视网膜损伤。几乎所有这些因素目前都无法通过我们的护理方法来预防或控制。不幸的是，这意味着晶状体后纤维增生症是一种极难预防、治疗或研究的疾病。对于这样一种病因复杂的疾病，在任何治疗对照研究中都需要大量的婴儿。对于极低体重婴儿，不应将晶状体后纤维增生症视为一种可避免的医源性疾病。其在这些婴儿中的病因尚不清楚。
