OBJECTIVE: This study investigated the relationship among intracranial pressure (ICP), the development of acute lung injury (ALI) and systemic inflammatory response syndrome (SIRS) following a severe traumatic brain injury (TBI). METHODS: Post-traumatic ICP was continuously monitored for the first week following injury in a series of consecutive patients with isolated severe TBI. The initial ICP and the duration of intracranial hypertension (ICH) were calculated. The risk factors associated with the development of ALI and SIRS were evaluated. RESULTS: Of the 86 patients enrolled, 22 patients developed ALI and 52 patients developed SIRS during the observation period. The patients with ALI presented with a significantly higher initial ICP (31.3±7.8 mmHg vs. 23.0±8.8 mmHg, p<0.001) and a longer duration of ICH (16.8±6.5 h vs. 11.9±6.0 h, p=0.002) than those without ALI. The incidence of both ALI and SIRS increased with increasing initial ICP, and the presence of SIRS was associated with a fourfold increase in the risk of developing ALI (odds ratio [OR], 4.0; 95% confidence interval [CI], 1.2-13.0). CONCLUSIONS: Increased ICP is associated with increased risks of developing ALI and SIRS following severe TBI. Future studies designed to verify the causative relationship between increased ICP and the systemic responses are warranted.
OBJECTIVE: This study investigated the relationship among intracranial pressure (ICP), the development of acute lung injury (ALI) and systemic inflammatory response syndrome (SIRS) following a severe traumatic brain injury (TBI). METHODS: Post-traumatic ICP was continuously monitored for the first week following injury in a series of consecutive patients with isolated severe TBI. The initial ICP and the duration of intracranial hypertension (ICH) were calculated. The risk factors associated with the development of ALI and SIRS were evaluated. RESULTS: Of the 86 patients enrolled, 22 patients developed ALI and 52 patients developed SIRS during the observation period. The patients with ALI presented with a significantly higher initial ICP (31.3±7.8 mmHg vs. 23.0±8.8 mmHg, p<0.001) and a longer duration of ICH (16.8±6.5 h vs. 11.9±6.0 h, p=0.002) than those without ALI. The incidence of both ALI and SIRS increased with increasing initial ICP, and the presence of SIRS was associated with a fourfold increase in the risk of developing ALI (odds ratio [OR], 4.0; 95% confidence interval [CI], 1.2-13.0). CONCLUSIONS: Increased ICP is associated with increased risks of developing ALI and SIRS following severe TBI. Future studies designed to verify the causative relationship between increased ICP and the systemic responses are warranted.
Authors: Lynne C Weaver; Feng Bao; Gregory A Dekaban; Todd Hryciw; Sandy R Shultz; Donald P Cain; Arthur Brown Journal: Exp Neurol Date: 2015-07-11 Impact factor: 5.330
Authors: Patricia E Molina; Paige S Katz; Flavia Souza-Smith; Stephen M Ford; Sophie X Teng; Tracy Y Dodd; John K Maxi; Jacques P Mayeux Journal: Alcohol Res Date: 2015