Kincaid E H, Miller P R, Meredith J W, Rahman N, Chang M C
Department of General Surgery, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
J Am Coll Surg. 1998 Oct;187(4):384-92. doi: 10.1016/s1072-7515(98)00202-6.
In trauma patients, the admission value of arterial base deficit stratifies injury severity, predicts complications, and is correlated with arterial lactate concentration. In theory, elevated base deficit and lactate concentrations after shock are related to oxygen transport imbalance at the cellular level. The purpose of this study was to test the hypothesis that an elevated base deficit in trauma patients is indicative of impaired systemic oxygen utilization and portends poor outcomes.
This study was a retrospective analysis of a prospectively collected database. The study population included all patients admitted to the trauma intensive care unit at a Level 1 trauma center during a 12-month period who were monitored with a pulmonary artery catheter and serial measurements of lactate and base deficit, and who achieved a normal arterial lactate concentration (< 2.2 mmol/L) with resuscitation. The patients were divided into those who maintained a persistently high base deficit (> or = 4 mmol/L) and those who achieved a low base deficit (< 4 mmol/L) during resuscitation.
One-hundred patients (mortality 20%) were monitored with a pulmonary artery catheter and achieved a normal arterial lactate concentration. The mean age+/-SD (SEM) of the group was 37+/-17 years and the Injury Severity Score was 25+/-11. Subgroup analysis revealed that patients with a persistently high base deficit (n=26) had higher rates of multiple organ failure (35% versus 5%, p < 0.001) and death (50% versus 9%, p < 0.00001) compared with patients who achieved a low base deficit. Patients with a persistently high base deficit also had lower oxygen consumption (126+/-40 mL/m2 versus 156+/-30 mL/m2, p=0.01 at 48 hours) and a lower oxygen utilization coefficient (0.20+/-0.05 versus 0.24+/-0.03, p=0.01 at 48 hours) compared with patients with a low base deficit. At 48 hours, both oxygen consumption (r=-0.44, [r, correlation coefficient] p=0.002) and oxygen utilization (r=-0.46, p=0.001) had a significant negative correlation with base deficit.
In trauma patients, a persistently high arterial base deficit is associated with altered oxygen utilization and an increased risk of multiple organ failure and mortality. Serial monitoring of base deficit may be useful in assessing the adequacy of oxygen transport and resuscitation.
在创伤患者中，动脉碱缺失的入院值可对损伤严重程度进行分层、预测并发症，且与动脉血乳酸浓度相关。理论上，休克后碱缺失和乳酸浓度升高与细胞水平的氧输送失衡有关。本研究的目的是检验以下假设：创伤患者碱缺失升高表明全身氧利用受损，并预示预后不良。
本研究是对前瞻性收集的数据库进行的回顾性分析。研究人群包括在12个月期间入住一级创伤中心创伤重症监护病房的所有患者，这些患者接受了肺动脉导管监测以及乳酸和碱缺失的系列测量，并且复苏后动脉血乳酸浓度恢复正常（<2.2 mmol/L）。将患者分为复苏期间碱缺失持续较高（≥4 mmol/L）的患者和碱缺失较低（<4 mmol/L）的患者。
100例患者（死亡率20%）接受了肺动脉导管监测，且动脉血乳酸浓度恢复正常。该组患者的平均年龄±标准差（标准误）为37±17岁，损伤严重程度评分为25±11。亚组分析显示，与碱缺失较低的患者相比，碱缺失持续较高的患者（n = 26）发生多器官功能衰竭的比例更高（35%对5%，p<0.001），死亡比例更高（50%对9%，p<0.00001）。与碱缺失较低的患者相比，碱缺失持续较高的患者在48小时时氧耗也更低（126±40 mL/m²对156±30 mL/m²，p = 0.01），氧利用系数也更低（0.20±0.05对0.24±0.03，48小时时p = 0.01）。在48小时时，氧耗（r = -0.44，[r，相关系数] p = 0.002）和氧利用（r = -0.46，p = 0.001）均与碱缺失呈显著负相关。
在创伤患者中，动脉碱缺失持续较高与氧利用改变以及多器官功能衰竭和死亡风险增加相关。连续监测碱缺失可能有助于评估氧输送和复苏的充分性。
