CEREBRAL-DAMAGE, FLUID BALANCE, INTRACRAN IAL-PRESSURE AND PRESSURE-VOLUME RELATIONSHIP IN SUBARACHNOID HEMORRHAGE

Citation
N. Stocchetti et al., CEREBRAL-DAMAGE, FLUID BALANCE, INTRACRAN IAL-PRESSURE AND PRESSURE-VOLUME RELATIONSHIP IN SUBARACHNOID HEMORRHAGE, Annales francaises d'anesthesie et de reanimation, 13(1), 1994, pp. 80-87
Citations number
NO
Categorie Soggetti
Anesthesiology
ISSN journal
07507658
Volume
13
Issue
1
Year of publication
1994
Pages
80 - 87
Database
ISI
SICI code
0750-7658(1994)13:1<80:CFBIIA>2.0.ZU;2-X
Abstract
Changes in osmolality and electrolyte concentrations are observed freq uently in patients with subarachnoid haemorrhage (SAH). Intracranial p ressure (ICP) plays a determinant role in the development of secondary brain damage following SAH and may be caused by haemorrhage itself, o edema formation and disturbance of cerebrospinal fluid (CSF) dynamics. The relationships among these factors are the aim of this investigati on. In 17 comatose SAH patients, ICP was monitored through a ventricul ar catheter ; serial of pressure-volume index (PVI) and CSF formation and reabsorption were performed. Arterio-jugular differences for oxyge n 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 P VI was 22.7 mL (SD = 7.4), ranging from 5 to 36. Eleven patients howev er, 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, treat ment was successful, even in case of reduced PVI. Mean C(a-vBAR)O2, co ffected for a Paco2 of 40 mmHg, was 3.7 mL . dL-1 (SD = 1.1) ranging f rom the extremely low value of 0.2 to 6.8 mL . L-1. Three patients wit h extremely low C(a-v)02 values showed a cerebral production of lactat e and developed areas of ischaemia on the CT scan. Hyponatraemia, cons idered as a sodium plasma concentration of less than 135 mmol . L-1, w as detected in seven patients. Hyponatraemia was treated by infusion o f hypertonic sodium solutions. Mannitol (I g . kg-1 . d-1 in four dose s) 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 v iscosity (Ht 30 %) and sustained arterial pressure. Correction of hypo natraemia was therefore achieved more through hypertonic fluids infusi on than by using diuretics.