Mégarbane Bruno, Guerrier Gilles, Blancher Anne, Meas Taly, Guillausseau Pierre-Jean, Baud Frederic J
Medical Critical Care Department, Lariboisière Hospital, Paris, France.
Am J Med Sci. 2007 Jun;333(6):384-6. doi: 10.1097/MAJ.0b013e318065adc4.
Hypophosphatemia, a common metabolic disorder, is usually silent and diagnosed by blood tests. However, misdiagnosis may result in delayed phosphate repletion, responsible for significant morbidity and potential mortality. We report an exceptional case of hypophosphatemia-related, life-threatening encephalopathy. A 49-year-old type-1 diabetic woman was admitted to our intensive care unit with coma and severe ketoacidosis. Initial neurologic impairment worsened despite improvement in acid-base disturbances and glucose levels. The electroencephalogram showed bilateral spikes with a background theta wave rhythm. Profound hypophosphatemia <0.20 mmol/L (<0.6 mg/dL) was diagnosed. No other cause of encephalopathy was found. Prompt phosphate repletion resulted in progressive and complete recovery. This observation allowed us to study the relations between the coma depth, the electroencephalographic findings, and the serum phosphate concentrations. Our data strongly suggest that phosphate depletion-induced encephalopathy probably originates from direct impairment of cerebral electrophysiological activity rather than from cardiac flow alteration.
低磷血症是一种常见的代谢紊乱疾病，通常无明显症状，通过血液检查确诊。然而，误诊可能导致磷酸盐补充延迟，从而引发严重的发病率和潜在的死亡率。我们报告了一例与低磷血症相关的、危及生命的脑病罕见病例。一名49岁的1型糖尿病女性因昏迷和严重酮症酸中毒入住我们的重症监护病房。尽管酸碱平衡紊乱和血糖水平有所改善，但最初的神经功能损害仍在恶化。脑电图显示双侧尖波，背景为θ波节律。诊断为严重低磷血症<0.20 mmol/L（<0.6 mg/dL）。未发现其他脑病病因。及时补充磷酸盐后患者逐渐完全康复。这一观察结果使我们能够研究昏迷深度、脑电图结果和血清磷酸盐浓度之间的关系。我们的数据强烈表明，磷酸盐缺乏引起的脑病可能源于脑电生理活动的直接损害，而非心脏血流改变。
