Palmese S, Pezza M, De Robertis E
Intensive Care Unit, University of Naples Federico II, Naples, Italy.
Minerva Anestesiol. 2005 May;71(5):237-42.
The aim of the paper was to describe an unusual case of non lactic metabolic acidosis connected to hypophosphatemia and refractory to infusion of bicarbonate. A 37 year old man was admitted to Intensive Care Unit with a severe metabolic acidosis. On admission the arterial gas analysis showed non lactic metabolic acidosis (pH 7.17; base excess [BE] -20.3; lactic acid 0.8 mMol/L), with hypoxemia and critical hypocapnia. Despite therapy with bicarbonate the acidosis persisted. After 4 hours glucose phosphate was administered, although the phosphoremia was unknown. After phosphate supplementation an improvement of acidosis was observed. Our hypothesis is that in the kidney phosphate depletion caused impaired tubular reabsorption of bicarbonate, which led to a non lactic metabolic acidosis.
本文旨在描述一例与低磷血症相关且对输注碳酸氢盐治疗无效的非乳酸代谢性酸中毒的罕见病例。一名37岁男性因严重代谢性酸中毒入住重症监护病房。入院时动脉血气分析显示为非乳酸代谢性酸中毒(pH 7.17;碱剩余[BE] -20.3;乳酸0.8毫摩尔/升),伴有低氧血症和严重低碳酸血症。尽管使用碳酸氢盐进行治疗,但酸中毒仍持续存在。4小时后给予磷酸葡萄糖,尽管当时血磷情况未知。补充磷后酸中毒有所改善。我们的假设是,肾脏中磷缺乏导致肾小管对碳酸氢盐的重吸收受损,从而引发非乳酸代谢性酸中毒。