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.