gms | German Medical Science

Objective: Aneurysmal subarachnoid hemorrhage (aSAH) initiates a deleterious cascade activating multiple inflammatory agents contributing to the development of delayed cerebral ischemia (DCI). Procalcitonin (PCT) has gained its credentials in sepsis diagnosis and treatment monitoring. The course of this inflammation marker during DCI and its potential as a biomarker for DCI, however, remains unclear. The goal of this analysis is to characterize the time course of PCT around the occurrence of DCI and to assess its potential as a predictive or confirmative biomarker.

Methods: A prospective series of 169 patients after aSAH were routinely monitored for PCT level as part of an observational trial. Only patients with daily measurements were eventually included (n=132), culminating in a total of 1.848 data points. The time course of levels before and after the development of DCI are plotted after exclusion of patients with SIRS or sepsis. Patients were further dichotomized according to the presence or absence of DCI (DCI, noDCI) and with and without DCI related infarction (DCIinf, noDCIinf).

Results: Baseline levels of PCT were not predicative for eventual DCI development. However, once DCI developed, it induced a spike in PCT levels around day 2 after the first DCI event. In cases without progression into cerebral infarction, PCT values normalized, but peaking again around day 10. In patients developing DCI related infarction, PCT levels steadily increased after the first DCI event reaching a plateau phase around day 14.

Conclusion: PCT is not able to predict DCI but significantly increases with DCI occurrence and secondary deterioration. The value of PCT in treatment monitoring beyond natural disease progression is still unclear. Frequent complications of ICU treatment such as SIRS or sepsis preclude a routine utilization of PCT.