Sakowitz Oliver W, Stover John F, Sarrafzadeh Asita S, Unterberg Andreas W, Kiening Karl L
Department of Neurosurgery, University of Heidelberg, Heidelberg, Germany.
J Trauma. 2007 Feb;62(2):292-8. doi: 10.1097/01.ta.0000203560.03937.2d.
Osmotic agents are widely used to lower elevated intracranial pressure (ICP). However, little data are available regarding cerebral oxygenation and metabolism in the traumatized brains studied under clinical conditions. The present prospective, open-labeled clinical study was designed to investigate whether administration of mannitol, with the aim of reducing moderate intracranial hypertension, improves cerebral metabolism and oxygenation in patients after severe traumatic brain injury (TBI).
Multimodal cerebral monitoring (MCM), consisting of intraparenchymal ICP, tissue oxygenation (ptiO2), and micro dialysis measurements was initiated in six male TBI patients (mean age 45 years; Glasgow Coma Scale score <9). A total of 14 mannitol boli (20%, 0.5g/kg, 20 minutes infusion time) were administered to treat ICP exceeding 20 mm Hg (2.7 kPa). Temporal alterations determined by MCM after mannitol infusions were recorded for 120 minutes. Microdialysates were assayed immediately for extracellular glucose, lactate, pyruvate, and glutamate concentrations.
Elevated ICP was successfully treated in all cases. This effect was maximal 40 minutes after start of infusion (25 +/- 6 mm Hg [3.3 +/- 0.8 kPa] to 17 +/- 3 mm Hg [2.3 +/- 0.4 kPa], p < 0.05) and lasted up to 100 minutes. Cerebral ptiO2 remained unaffected (21 +/- 5 mm Hg [2.8 +/- 0.7 kPa] to 23 +/- 6 mm Hg [3.1 +/- 0.8 kPa], n.s.). Microdialysate concentrations of all analytes rose unspecifically by 10% to 40% from baseline, reaching maximum concentrations 40 to 60 minutes after start of the infusion.
Mannitol efficiently reduces increased ICP. At an ICP of up to 30 mm Hg [4 kPa] it does not affect cerebral oxygenation. Unspecific increases of extracellular fluid metabolites can be explained by transient osmotic dehydration. Additional mechanisms, such as increased cerebral perfusion and blood volume, might explain an accelerated return to baseline.
渗透性药物被广泛用于降低升高的颅内压（ICP）。然而，关于在临床条件下研究的创伤性脑内脑氧合和代谢的数据很少。本前瞻性、开放标签的临床研究旨在调查以降低中度颅内高压为目的给予甘露醇是否能改善重度创伤性脑损伤（TBI）患者的脑代谢和氧合。
对6名男性TBI患者（平均年龄45岁；格拉斯哥昏迷量表评分<9）启动了多模态脑监测（MCM），包括脑实质内ICP、组织氧合（ptiO2）和微透析测量。总共给予14次甘露醇推注（20%，0.5g/kg，输注时间20分钟）以治疗超过20mmHg（2.7kPa）的ICP。在甘露醇输注后，通过MCM确定的时间变化记录120分钟。立即对微透析液进行细胞外葡萄糖、乳酸、丙酮酸和谷氨酸浓度的测定。
所有病例中升高的ICP均得到成功治疗。这种效果在输注开始后40分钟时最大（从25±6mmHg[3.3±0.8kPa]降至17±3mmHg[2.3±0.4kPa]，p<0.05），并持续长达100分钟。脑ptiO2保持未受影响（从21±5mmHg[2.8±0.7kPa]至23±6mmHg[3.1±0.8kPa]，无统计学意义）。所有分析物的微透析液浓度从基线非特异性地升高10%至40%，在输注开始后40至60分钟达到最大浓度。
甘露醇能有效降低升高的ICP。在ICP高达30mmHg[4kPa]时，它不影响脑氧合。细胞外液代谢物的非特异性增加可由短暂的渗透性脱水来解释。其他机制，如脑灌注和血容量增加，可能解释了更快恢复到基线的原因。
