Decompressive craniectomy and brain death prevalence and mortality: 8-year retrospective review.

Decompressive craniectomy (DC) is a surgical practice that has been used since the late 19th century. The cerebral blood flow increase after the performance of a DC can delay and even prevent the development of cerebral circulatory arrest and brain death (BD). We aimed to determine the prevalence of BD, the use of DC, and the evolution to BD with versus without DC. This retrospective, observational, cross-sectional study was performed in a single high-intensity center in Argentina from January 2003 to December 2010. Inclusion criteria were all patients with Glasgow Coma Score of at most 7 on admission or during their stay in the intensive care units. Exclusion criteria were patients with incomplete data. In cases of death, we assessed whether they fulfilled BD criteria or if the cause of death was a cardiac arrest (CA). The 698 patients considered for analysis showed a 60% (n = 418) global mortality rate. The causes were: CA (n = 270); BD (n = 108) and others considered to be "undefined," namely not assessed completely for the diagnosis of BD (n = 40). According to diagnosis category, traumatic brain injury (TBI) was largest (nearly 50%). The DC group (n = 206) showed significant differences regarding sex and diagnosis category versus no DC group. Mortality was significantly lower in this group (48% versus 65%, P < .001). No significant differences were observed comparing causes of death (CA, BD, or undefined). The use of DC did not influence the frequency of BD development (24% versus 26%, P = .72). The average DC rate was 30% and of BD 16%. The prevalence of DC and better survival were recorded compared with subjects without DC. The prevalence of BD was lower than expected in accordance with national registries; however, among our group, DC did not seem to modify the evolution to BD.

Incidence of intracranial hypertension related to jugular bulb oxygen saturation disturbances in severe traumatic brain injury patients.

OBJECTIVE: To analyze the Intracranial Hypertension (IH) development related to jugular bulb oxygen saturation (SjO2) disturbances in severe traumatic brain injury patients (sTBI). MATERIALS AND METHODS: One hundred and thirty-five sTBI patients were reviewed. Those without IH at admission (n = 116) were included. All patients underwent ICP and SjO2 continuous monitoring. Two groups were distinguished according to the SjO2 values during the first 24 hours. Group A: those with abnormal SjO2 (SjO2 more than 75% or less than 55%) and Group B: those with normal SjO2 (55-75%). Differences in IH development and outcome between groups were analyzed. Causes of abnormally low SjO2 were identified. RESULTS: IH developed in 56.9% of patients, between 12 and 48 hours from admission. Group A had a significantly higher incidence of IH than Group B (p < 0.001) and it also had a worse outcome than Group B (GOS 1-2) (p < 0.005). Patients from Group A had a risk of IH 4.5 fold higher than Group B. Considering only patients who developed IH, an abnormal SjO2 value increased 2.3 fold the risk of death compared to those without SjO2 disturbances. Main causes of SjO2 desaturation were hyperventilation (40.7%), hypovolemia (28.4%) and anemia (21%). CONCLUSIONS: Early detection of disturbances in oxygen supply-demand relationship and prevention or resolution of the secondary insults which produce these disturbances, might lead to a reduction in the incidence of intracranial hypertension.