Blanc P L, Bedock B, Jay S, Martin A, Marc J M
Service de Réanimation polyvalente, Centre hospitalier, Annonay.
Presse Med. 1994 Nov 19;23(36):1655-8.
We observed two cases of severe diabetic ketoacidosis with coma and shock. In one case, coma was present at admission and in the second occurred within 15 hours. In both cases, intracranial hypertension was confirmed with an extradural captor. These findings are in agreement with observations of brain oedema in diabetic ketoacidosis with coma. Clinical data suggest that brain oedema may occur after a latency period but that clinical expression is much more rare, perhaps favoured by treatment (excessive rehydratation, alkalinization, too sharp drop in blood glucose level). In our cases, despite major fluid infusion, shock persisted requiring norepinephrine. This shock could have been the expression of the severe ketoacidosis or have resulted from an underlying infection. In case of sudden onset coma, a regularly encountered manifestation of brain oedema, respiratory assistance and mannitol infusion must be instituted rapidly. With this type of management, it should be possible to improve the severe prognosis of brain oedema in diabetic ketoacidosis.
我们观察到两例伴有昏迷和休克的严重糖尿病酮症酸中毒病例。一例入院时即处于昏迷状态,另一例在15小时内出现昏迷。两例均通过硬膜外传感器证实存在颅内高压。这些发现与伴有昏迷的糖尿病酮症酸中毒患者脑水肿的观察结果一致。临床数据表明,脑水肿可能在一段潜伏期后发生,但临床表现更为罕见,可能与治疗(过度补液、碱化、血糖水平急剧下降)有关。在我们的病例中,尽管大量补液,休克仍持续存在,需要使用去甲肾上腺素。这种休克可能是严重酮症酸中毒的表现,也可能是由潜在感染引起的。对于突然发生的昏迷这种脑水肿常见的表现,必须迅速给予呼吸支持和输注甘露醇。采用这种治疗方法,应该有可能改善糖尿病酮症酸中毒患者脑水肿的严重预后。