Cerebral venous oxygen saturation studied with bilateral samples in the internal jugular veins.

The current literature reports many measurements (arteriovenous oxygen content difference and cerebral metabolic rate of oxygen, etc.) with samples from the internal jugular veins (IJs), obtained from either side of the neck, based on the assumption that a reliable sample of mixed venous blood can be drawn. We compared oxygen saturation in both IJs in 32 patients with head injuries to establish the similarities or discrepancies in the two veins. Both IJs were cannulated with 20-G catheters; in five patients, a fiberoptic catheter was used to obtain a continuous recording of the hemoglobin saturation. Blood samples were taken simultaneously from the two IJs and immediately processed; the total number of samples processed was 342, with an average of 5.34 paired samples from each patient. The mean and the standard deviation of the differences between the saturation of the two IJs were, respectively, 5.32 and 5.15. Fifteen patients showed differences greater than 15% in hemoglobin saturation; three more patients showed differences greater than 10% at some point during the investigation. Ultimately, only eight patients had differences of less than 5%. No relationship was found among the computed tomographic scan data and the pattern of hemoglobin saturation detected. Therefore, we were not able to identify the side more appropriate for monitoring in patients with bilateral, predominantly monolateral, cortical, or deeply located lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

[Subarachnoid hemorrhage: cerebral damage, fluid balance, intracranial pressure and pressure-volume relation]. / Hémorragie sous-arachnoïdienne: lésion cérébrale, équilibre hydrique, pression intracrânienne et relation pression-volume.

Changes in osmolality and electrolyte concentrations are observed frequently in patients with subarachnoid haemorrhage (SAH). Intracranial pressure (ICP) plays a determinant role in the development of secondary brain damage following SAH and may be caused by haemorrhage itself, oedema formation and disturbance of cerebrospinal fluid (CSF) dynamics. The relationships among these factors are the aim of this investigation. In 17 comatose SAH patients, ICP was monitored through a ventricular catheter; serial of pressure-volume index (PVI) and CSF formation and reabsorption were performed. Arterio-jugular differences for oxygen and lactate were measured. The average ICP recorded for each 12 hour interval was 18.9 mmHg (SD = 5.9); mean cerebral perfusion pressure (CPP) was 75 mmHg (SD = 13); the lowest CPP value was 30 mmHg. Mean PVI was 22.7 mL (SD = 7.4), ranging from 5 to 36. Eleven patients however, showed a PVI less than 15 mL at some point during testing. Values of CSF dynamics indicated disturbances of CSF reabsorption in 11 cases. When the cause of ICP rise was identified in CSF disturbances, treatment was successful, even in case of reduced PVI. Mean C(a-v)O2, corrected for a PaCO2 of 40 mmHg, was 3.7 mL.dL-1 (SD = 1.1) ranging from the extremely low value of 0.2 to 6.8 mL.L-1. Three patients with extremely low C(a-v)O2 values showed a cerebral production of lactate and developed areas of ischaemia on the CT scan. Hyponatraemia, considered as a sodium plasma concentration of less than 135 mmol.L-1, was detected in seven patients. Hyponatraemia was treated by infusion of hypertonic sodium solutions. Mannitol (1 g.kg-1.d-1 in four doses) was infused if the sodium plasma concentration was not corrected by the former treatment or if ICP exceeded 20 mmHg. Treatment was aimed at preserving cerebral perfusion by providing adequate pre-load, low viscosity (Ht 30%) and sustained arterial pressure. Correction of hyponatraemia was therefore achieved more through hypertonic fluids infusion than by using diuretics.