Roberts Joan S, Vavilala Monica S, Schenkman Kenneth A, Shaw Dennis, Martin Lynn D, Lam Arthur M
Division of Pediatric Critical Care Medicine, Children's Hospital and Regional Medical Center and University of Washington, Seattle, WA, USA.
Crit Care Med. 2006 Aug;34(8):2217-23. doi: 10.1097/01.CCM.0000227182.51591.21.
Cerebral edema associated with diabetic ketoacidosis is an uncommon but severe complication of insulin-dependent diabetes mellitus with unclear pathophysiology. We sought to determine whether cerebral edema in patients with diabetic ketoacidosis was related to changes in cerebral blood flow, autoregulation, regional cerebral saturation, or S100B.
Prospective case series.
Pediatric intensive care unit of a tertiary children's hospital.
Six patients with diabetic ketoacidosis and altered mental status, requiring computed tomographic scan of the head.
Study evaluations included: 1) transcranial Doppler evaluations to determine middle cerebral artery flow velocities and cerebral autoregulation, defined by the autoregulatory index, at 6 and 36 hrs; 2) continuous monitoring of regional cerebral oxygenation on the left lateral forehead using near-infrared spectroscopy for the first 24 hrs of admission; 3) serial measurement of S100B as a marker of central nervous system injury; and 4) follow-up head computed tomographic scan.
Serial computed tomographic scans showed that four of six patients had changes in brain volume without overt cerebral edema. Initial scans showed narrowing of the third and lateral ventricles when compared with follow-up. There was no difference in middle cerebral artery flow velocities between admission and recovery at 36 hrs, despite Paco2 increasing during treatment. Cerebral flow was normal to increased, despite hypocapnia. Cerebral autoregulation was impaired in five of six patients at 6 hrs and normalized by 36 hrs. Mean regional cerebral oxygenation was measured in five of six patients and decreased linearly with time. Two patients showed maximal regional cerebral oxygenation before returning to baseline. There were no periods of low regional cerebral oxygenation in any patient at any time. No elevation in S100B was found.
We found normal to increased cerebral blood flow, elevated regional cerebral oxygenation, impaired autoregulation, and changes in brain volume in clinically ill pediatric patients with diabetic ketoacidosis. We found no evidence of cerebral ischemia. These findings suggest that the pathophysiology of cerebral edema in diabetic ketoacidosis may involve a transient loss of cerebral autoregulation, allowing a paradoxic increase in cerebral blood flow and the development of vasogenic cerebral edema.
糖尿病酮症酸中毒相关的脑水肿是胰岛素依赖型糖尿病一种罕见但严重的并发症,其病理生理学尚不清楚。我们试图确定糖尿病酮症酸中毒患者的脑水肿是否与脑血流量、自动调节、局部脑血氧饱和度或S100B的变化有关。
前瞻性病例系列研究。
一家三级儿童医院的儿科重症监护病房。
6例糖尿病酮症酸中毒且精神状态改变、需要进行头部计算机断层扫描的患者。
研究评估包括:1)经颅多普勒评估,以确定6小时和36小时时大脑中动脉血流速度及由自动调节指数定义的脑自动调节功能;2)入院后头24小时使用近红外光谱法持续监测左侧前额的局部脑氧合情况;3)连续测量S100B作为中枢神经系统损伤的标志物;4)随访头部计算机断层扫描。
系列计算机断层扫描显示,6例患者中有4例脑容量有变化但无明显脑水肿。初始扫描显示与随访相比第三脑室和侧脑室变窄。尽管治疗期间动脉血二氧化碳分压升高,但入院时和36小时恢复时大脑中动脉血流速度无差异。尽管存在低碳酸血症,但脑血流量正常或增加。6例患者中有5例在6小时时脑自动调节功能受损,至36小时时恢复正常。6例患者中有5例测量了平均局部脑氧合情况,且其随时间呈线性下降。2例患者在恢复至基线前局部脑氧合达到最大值。任何患者在任何时间均未出现局部脑氧合降低的情况。未发现S100B升高。
我们发现临床患病的糖尿病酮症酸中毒儿科患者脑血流量正常或增加、局部脑氧合升高、自动调节功能受损及脑容量改变。未发现脑缺血的证据。这些发现表明,糖尿病酮症酸中毒脑水肿的病理生理学可能涉及脑自动调节功能的短暂丧失,从而导致脑血流量反常增加及血管源性脑水肿的发生。