Sheldon G F, Grzyb S
Ann Surg. 1975 Dec;182(6):683-9. doi: 10.1097/00000658-197512000-00004.
Phosphate depletion occurring during total parenteral nutrition has been frequently reported during the part 4 years. Hypophosphatemia may be associated with confusion, hyperventilation, and neuromuscular irritability, suggesting a total body phosphate deficiency. If inorganic phosphate levels fall below 1.0 mg %, diminished red cell glycolysis occurs with low erythrocyte levels of 2,3 diphosphoglycerate and adenosine triphosphate. Lowered red cell organic phosphates are associated with increased hemoglobin oxygen affinity. If severe hypophosphatemia occurs, hemolytic anemia, which is correctible by phosphate infusion, may result. In addition, leucocyte function is impaired by low levels of serum inorganic phosphate. While recognized as a needed additive, recommended phosphate supplements vary. Different infusion regimens have been suggested over the past 4 years, based primarily on assumed daily requirements. In the 19 trauma patients described who received hyperalimentation as part of their treatment, phosphate administration was calculated retrospectively and prospectively as a function of non-protein calories infused. Four different groups were studied. Group A received no phosphate additive and quickly became severely hypophosphatemic. Group B received from one to 15 meg of potassium acid phosphate per 1,000 K cal and developed a more gradual lowering of serum inorganic phosphate levels. Group C received 15 to 25 meg of potassium acid phosphate per 1,000 K cal and maintained normal phosphate levels throughout the course of treatment. Group D received greater than 25 meq of potassium acid phosphate per 1,000 K cal and gradually increased their serum inorganic phosphate levels. A significant positive correlation was found between serum inorganic phosphate levels, 2,3 diphosphoglycerate levels, adenosine triphosphate levels, and P50 of the oxy-hemoglobin dissociation curve. No patients developed hemolytic or neuromuscular syndromes which were attributable to hypophosphatemia. This study describes a simple method for the maintenance of adequate phosphate levels in patients whose dextrose-protein solutions may vary from day to day, by relating it to non-protein calories. Provision of 20 to 25 meq of potassium dihydrogen phosphate per 1,000 K cal will maintain normal serum levels of inorganic phosphate during total parenteral nutrition.
在过去4年中,全胃肠外营养期间发生的磷酸盐耗竭屡有报道。低磷血症可能与意识模糊、通气过度及神经肌肉应激性有关,提示全身磷酸盐缺乏。如果无机磷水平降至1.0mg%以下,红细胞糖酵解会减少,红细胞内2,3 -二磷酸甘油酸和三磷酸腺苷水平降低。红细胞有机磷酸盐水平降低与血红蛋白对氧的亲和力增加有关。如果发生严重低磷血症,可能会导致溶血性贫血,补充磷酸盐后可纠正。此外,血清无机磷水平低会损害白细胞功能。虽然磷酸盐被公认为是一种必需的添加剂,但推荐的补充剂量各不相同。在过去4年里,人们提出了不同的输注方案,主要是基于假定的每日需求量。在所描述的19例接受高营养治疗的创伤患者中,根据输注的非蛋白热量对磷酸盐的给药进行了回顾性和前瞻性计算。研究了4个不同的组。A组未添加磷酸盐添加剂,很快出现严重低磷血症。B组每1000千卡热量接受1至15毫克磷酸二氢钾,血清无机磷水平逐渐下降。C组每1000千卡热量接受15至25毫克磷酸二氢钾,在整个治疗过程中维持正常的磷酸盐水平。D组每1000千卡热量接受超过25毫克当量的磷酸二氢钾,血清无机磷水平逐渐升高。血清无机磷水平、2,3 -二磷酸甘油酸水平、三磷酸腺苷水平与氧合血红蛋白解离曲线的P50之间存在显著正相关。没有患者出现可归因于低磷血症的溶血性或神经肌肉综合征。本研究描述了一种简单的方法,通过将其与非蛋白热量相关联,来维持每天葡萄糖 - 蛋白质溶液可能不同的患者的适当磷酸盐水平。每1000千卡热量提供20至25毫克当量的磷酸二氢钾将在全胃肠外营养期间维持正常的血清无机磷水平。