- Meeting abstract
- Open Access
Sepsis: cause of late deterioration of intracranial pressure in patients with severe traumatic brain injury?
© Current Science Ltd 1998
Published: 1 March 1998
Increased intracranial pressure (ICP) in patients with severe traumatic brain injury without findings of CT scan deterioration is frequently observed late during the course of treatment. The aim of this study was to evaluate the possible relationship between the late increase of ICP in head injured patients and the development of sepsis during their course on ICU.
22 consecutive patients (median age 18) admitted to the ICU with severe traumatic brain injury (GCS < 8) and maintained according to a standard treatment protocol were retrospectively studied and divided into three groups. Group I (n = 6) were patients who developed no intracranial hypertension during their ICU stay, group II (n = 9) were patients with early intracranial hypertension and group III (n = 7) were patients who developed ICP deterioration on the 5th day or later after admission. Age, sex, initial GCS, incidence of secondary insults during first 24 hours after the injury, CT finding on admission, incidence of sepsis during the ICU stay, coincidence of sepsis with ICP deterioration, modified SOFA score (without neurological component) on the 2nd and 7th day of ICU stay, day of ICP deterioration and mortality in the groups were recorded. Fisher's exact test, t-test, and one way ANOVA test were used for statistical analysis (SigmaStat Statistical Software, Jandel Co.,USA), P < 0.05 was considered statistically significant.
No differences in age, sex, initial GCS, modified SOFA score on the 2nd day and incidence of secondary insults during first 24 h after the injury among groups were observed The overall incidence of sepsis was 33% (7/22 patients) and mortality rate was 22.2% (5/22 patients). The late intracranial hypertension was more frequently associated with the development of sepsis in group III (coincidence of sepsis and ICP deterioration in 1/9 patients in group II and 5/7 patients in group III, P = 0.035). Subsequent analysis in group III showed tendency to ICP deterioration in patients with sepsis compared to patients without sepsis (5/6 septic patients developed ICP deterioration compared to 2/5 nonseptic patients with ICP deterioration) but the difference did not reach statistical significance (P = 0.165).
Frequent coincidence of late ICP deterioration and sepsis in patients with severe traumatic brain injury was observed. Late ICP deterioration could be in some cases the result of sepsis induced changes in vascular reactivity due to overproduction of NO and other vasodilatatory mediators.
Partially supported by grant IGA MZ CR 3672-3.