Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Neurocrit Care. 2009 Dec;11(3):322-9. doi: 10.1007/s12028-009-9265-1.
To describe the risk factors of early and delayed increases in pancreatic enzymes (PE) in children after severe traumatic brain injury (TBI) and to determine if cerebral events (such as intracranial hemorrhage or intracranial hypertension) are associated with increases in PE.
Retrospective analysis of prospectively collected Pediatric Neurotrauma Registry for children with severe TBI (GCS ≤ 8). We assessed the association of clinical characteristics with the development of increases in PE using regression analyses.
Fifty-one children with severe TBI were classified into three groups [normal PE; early PE (PE increases within first 24 h); delayed PE (PE increases after 24 h)].
Increases in PE were observed in 29/51 children [57% total; n = 9 (18%) early; n = 20 (39%) delayed]. Multisystem trauma was more prevalent in patients with early increases in PE compared to those without increases in PE (70 vs. 30%, RR = 2.8, 95% CI 1.1-7) but not different between delayed PE and normal PE groups. In the bivariate analyses, increasing age (odds ratios, [95% CI]; 1.2, [1.05-1.4]), intracranial hypertension (14.6, [2.6-80.5]), intracranial hemorrhage (6.2, [1.15-33.7]), receipt of pentobarbital (9.3, [2.1-39.9]), mannitol (13.2, [2.7-62.2]), and vasoactive medications (6.9, [1.5-31.3]) were associated with the development of delayed increases in PE, whereas sex, initial Glasgow Coma Scale, severity of injury (PRISM, Injury Severity Score), therapeutic hypothermia, morphine and furosemide were not associated. Both intracranial hypertension and intracranial hemorrhage independently predicted the development of increases in PE (14.6, [2.6-80.5], and 9.1, [1.31-63.3], respectively).
Increases in PE, often used as the only measures of pancreatitis in children with other severe injuries, are common in children after severe TBI and delayed presentation appears related to intracranial events. This suggests a possible interaction between the brain and the gastrointestinal system, implying that disturbances in cerebral hemodynamics may lead to pancreatic dysfunction.
描述儿童严重创伤性脑损伤（TBI）后胰酶（PE）早期和延迟升高的危险因素，并确定颅内事件（如颅内出血或颅内高压）是否与 PE 升高有关。
对严重 TBI（GCS≤8）儿童的前瞻性收集的儿科神经创伤登记处进行回顾性分析。我们使用回归分析评估了临床特征与 PE 升高发展的相关性。
51 例严重 TBI 患儿分为三组[正常 PE；早期 PE（PE 在 24 小时内升高）；延迟性 PE（PE 在 24 小时后升高）]。
29/51 例患儿出现 PE 升高[57%总发生率；n=9（18%）早期；n=20（39%）延迟]。与无 PE 升高的患儿相比，早期 PE 升高的患儿更常发生多系统创伤（70%比 30%，RR=2.8，95%CI 1.1-7），但在延迟性 PE 与正常 PE 组之间无差异。在单变量分析中，年龄增长（优势比，[95%CI]；1.2，[1.05-1.4]）、颅内高压（14.6，[2.6-80.5]）、颅内出血（6.2，[1.15-33.7]）、戊巴比妥（9.3，[2.1-39.9]）、甘露醇（13.2，[2.7-62.2]）和血管活性药物（6.9，[1.5-31.3]）与延迟性 PE 升高的发展相关，而性别、初始格拉斯哥昏迷量表、损伤严重程度（PRISM、损伤严重程度评分）、亚低温治疗、吗啡和呋塞米则无关联。颅内高压和颅内出血均独立预测 PE 升高的发生（14.6，[2.6-80.5]和 9.1，[1.31-63.3]）。
在患有其他严重损伤的儿童中，PE 升高常作为胰腺炎的唯一指标，但在严重 TBI 后儿童中很常见，且延迟表现似乎与颅内事件有关。这表明大脑和胃肠道系统之间可能存在相互作用，提示脑血流动力学紊乱可能导致胰腺功能障碍。
