N. Stocchetti

Effects of hyperoxia on brain tissue oxygen tension in cerebral focal lesions

We evaluated the systemic and cerebral effects induced by an increase to 100% of the inspired oxygen fraction (FiO2) on 20 comatose patients with head injury (9 patients) and SAH (11 patients). Brain tissue oxygen tension (PtiO2) was measured through a Clark electrode inserted in penumbra-like areas. We performed 55 hyperoxia tests by increasing FiO2 from 35 +/- 8% to 100% in one second and calculating the PtiO2 index as: PtiO2 variation from baseline at 1 minute/arterial oxygen tension (PaO2) variation from baseline at 1 minute x 100. One hundred percent FiO2 caused an increase of both arterial (from 139 +/- 28 to 396 +/- 77 mmHg) and cerebral (from 22.6 +/- 14 to 65.4 +/- 60 mmHg) oxygenation after 1 minute. The range of the PtiO2 response was not uniform and two groups were identified. The change was small, 0.8 mmHg/min/100 mmHg PaO2 (+/- 0.7; range 0-2) when mean PtiO2 was 19.7 +/- 13.1 mmHg, while a stronger response, 8 mmHg/min/100 mmHg PaO2 (+/- 5; range 3-18) (p < 0.01) was found when mean PtiO2 was 31.7 +/- 14.3 mmHg. Since O2 diffusion should follow the gas diffusion law, the increase in diffusion distance due to a reduction of capillary density in focal lesions may explain this relationship.

Brain oxygen tension during hyperoxia in a swine model of cerebral ischaemia.

UNLABELLEDnArterial hyperoxia improves oxygen tension measured into the cerebral tissue (ptiO2). The extent of this improvement in ameliorating O2 delivery to the cerebral tissue, when cerebral blood flow (CBF) is reduced, is still unclear. The present experiment was developed to investigate the effect of arterial hyperoxia at normal or reduced CBF (baseline, CBF = 50-60%, and CBF = 20-30% of the baseline). CBF reduction was achieved in 7 pigs by saline infusion in a lateral ventricle. PtiO2 was measured by Licox equipment. Arterovenous oxygen difference (AVDO2) was calculated as the difference between arterial oxygen content and superior sagittal sinus oxygen content. Hyperoxia was induced by increasing inspired oxygen fraction to 100%. PtiO2 moved respectively from 27.95 (+/- 10.15) to 45.98 (+/- 15.31), from 14.77 (+/- 3.58) to 30.71 (+/- 12.2), and from 3.45 (+/- 2.89) to 11.1 (+/- 12.6) mmHg at normal CBF, after the first reduction and after the second reduction. O2 supply showed only a negligible increase. AVDO2 decreased during the phases of intact and moderate CBF impairment, while it did not change during the phase of severe CBF impairment.nnnIN CONCLUSIONnan increase of ptiO2 does not necessarily correspond to an improvement of brain oxygen delivery. The small increase in oxygen delivery due to hyperoxia may cause a slight improvement in the balance between O2 delivery and consumption during mild CBF reduction, but such improvement is negligible when severe CBF reduction occurs.

Bispectral index during asleep-awake craniotomies.

Background: Asleep-awake craniotomy presents challenges for the anesthetist who has to provide adequate sedation and analgesia but also requires an awake and cooperative patient for neurological testing. In this setting, we hypothesized that Bispectral Index (BIS) monitoring might be helpful in shortening the patient’s awakening and in predicting recovery of consciousness in order to initiate reliable intraoperative brain mapping. Methods: An observational prospective study was performed on 27 consecutive asleep-awake craniotomies, in which BIS was monitored and BIS data collected offline. Nine critical intraoperative time points were defined and analyzed [preinduction, start of surgery, termination of hypnotic drug, eye opening, obeying simple commands, laryngeal mask airway (LMA) removal, initiation of brain mapping, initiation of closure, and end of surgery]. Results: A shorter time to LMA removal was associated with a higher BIS at the termination of the hypnotic drug (P=0.016, Mann-Whitney U test). From the initiation of surgery to the time of LMA removal, BIS was significantly lower than the preinduction values, whereas at the initiation of brain mapping, BIS returned to the preinduction values (Friedman test P<0.0001, Dunns multiple comparisons test). Compared with LMA removal, BIS values >85 predicted the initiation of brain mapping with a sensitivity of 44% (95% confidence interval, 25.5%-64.7%) and a specificity of 74% (95% confidence interval, 53.7%-89%). Conclusions: During asleep-awake craniotomies, higher BIS values at the end of the asleep phase are associated with shorter time to LMA removal, suggesting that BIS monitoring may be beneficial in shortening recovery from anesthesia. During the awake phase, the return of BIS to the preinduction values appeared to indicate full recovery of consciousness, thereby allowing a reliable language testing.

Cerebral veno-arterial pCO2 difference as an estimator of uncompensated cerebral hypoperfusion.

The aim of the present study was to assess the veno-arterial difference in pCO2 (delta pCO2) as an indicator of ischemia compared to the arteriovenous O2 difference (AVDO2). Staircase cerebral blood flow (CBF) reductions were obtained in seven domestic pigs by inducing intracranial hypertension: CBF 100%, 50-60% of baseline, 20-30% of baseline. ICP, MAP, CPP and CBF (Laser-Doppler method) were continuously recorded. The superior sagittal sinus was punctured to determine AVDO2 and delta pCO2. AVDO2 was 5.9 (+/- 1.78, range 3.3-7.4), 7.01 (+/- 1.31, range 5-8.9) and 8.17 (+/- 1.51, range 6.0-11.3) ml/100 ml in the three CBF steps (p = 0.001). CBF impairment was accompanied by the following increases in delta pCO2: from 10 (+/- 4, range 4-15) mmHg to 14.5 (+/- 4.11, range 10-27) mmHg, and to 31.2 (+/- 9.0, range 17-39) mmHg (p < 0.001). When CBF declines AVDO2 increases, indicating greater extraction of O2 to satisfy the aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. delta pCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is impressive during marked CBF impairment when anaerobic metabolism takes place with proton buffering in CO2 and H2O. Therefore, when the brains ability to compensate for low blood flow is exceeded, CO2 production outweighs O2 extraction.

Vascular issues in neurodegeneration and injury

Traumatic brain injury (TBI) is one of the leading causes of injury-related deaths in the Western hemisphere. Traumatic brain damage is a result of direct (immediate mechanical disruption of brain tissue, or primary injury) and indirect (delayed or secondary) mechanisms. Secondary injuries, because of their delayed onset and progression over minutes to months after the initial trauma, are potentially amenable to postinjury therapeutic intervention. Vascular pathology and alterations in cerebral blood flow are major contributors to mortality and morbidity following TBI. This article summarizes the pathology of vascular disruptions following TBI, the time course and major mechanisms of posttraumatic cerebral blood flow alterations, and the influence of genetic susceptibility to vascular changes after TBI.

Pathophysiology of Brain Temperature

The brain is more sensitive than other organs to abnormal temperature. A rise of four or five degrees above normal deeply disturbs brain functions. Indeed it may be that the temperature of the brain is the single most important factor limiting the survival of man and other animals in hot environments. This can be desumed by the sophisticated control of the brain temperature present in mammalian.

Integrated Monitoring in Intensive Care Head Injured Patients

Multimodality monitoring is becoming very popular in intensive care notwithstanding its high cost. The increasing amount of knowledge provided by sophisticated monitoring is worthless if it does not translate into clinical or scientific benefits. In some instance the clinical benefit is directly transferred to the patient studied, in other cases information gathered from many cases drives new insight into the understanding of an illness, and may benefit other patients in the future. In this era of boosting technology the quantity of data obtainable is rapidly increasing. As a side-effect, state of the art critical care is severely threatened by data overload.