Hyperosmolar Solutions Effects on Cerebral Oxygenation and Metabolism

Abstract

Purpose: To estimate the dynamics of cerebral oxygenation and metabolism during intracranial pressure (ICP) correction with 15% Mannitol and 7,2% saline in 6% HES 200/0,5. Methods: We analyzed 39 episodes of ICP correction with 15% Mannitol or 7,2% NaCl in 6% HES 200/0,5 ("Hyper-HAES") in 9 patients with intracranial hemorrhage (GCS 4-8). Monitoring of ICP, systemic hemodynamics, SvjO 2 and cerebral microdialysis was used in all patients. Brain temperature (Tbr) and brain oxygen tension (PbrO 2) were investigated in 5 patients. ICP > 20 mmHg was the indication for treatment. Results: The duration of ICP reduction below 20 mmHg was 121 ± 58 min for 15% Mannitol and 258 ± 122 min for "Hy-perHAES" (p<0,001). Administration of the investigated solutions was associated with slight PbrO 2 increase. 15% Manni-tol infusion did not change brain metabolism in "intact" and "lesioned" tissue. HyperHAES administration was accompanied with significant increase of glucose and pyruvate concentration in "intact" and "lesioned" brain tissue. We observed the same dynamics of cerebral oxygenation and metabolism in patients with traumatic and nontraumatic intracerebral hemorrhage. Infusion of investigated solutions was not accompanied by significant dynamics of cardiac preload and function. Conclusions: "HyperHAES" infusion results in prolong ICP reduction than 15% Mannitol and is accompanied with slight increase of PbrO 2 and significant improvement of cerebral metabolism. 15% Mannitol administration does not influence cerebral oxygenation and metabolism. 15% Mannitol and "HyperHAES" infusion does not influence systemic hemody-namics in normovolemic patients. Brain lesion, caused by intracranial hemorrhage may be accompanied by mitochondrial dysfunction, characterized by reduction and even enlargement of lactate/pyruvate ratio in condition of sufficient oxygen and glucose delivery to the brain. Brain edema is the main cause of intracranial hyperten-sion in patients with intracranial hemorrhage. In turn, intrac-ranial hypertension aggravates brain edema by altering cere-bral perfusion and cerebral venous blood outflow [1-3]. Therefore intracranial pressure (ICP) correction is one of the main goals of intensive care in patients with intracranial hemorrhage. Infusion of hyperosmolar solutions is common therapy of intracranial hypertension [4, 5]. Hyperosmolar solutions increase the osmolar gradient between plasma and cerebral interstitium, and lead to fluid moving from the brain to intravascular space. Infusion of hyperosmolar solutions is accompanied by hypervolemia and reduces blood viscosity, that cause transient increase of cerebral blood flow and reflex vasoconstriction. The most popular hyperosmolar agents used for intracra-nial hypertension correction are mannitol (15% and 20%) and hypertonic saline (3%, 7.5%, 10%). To increase the duration of their action hyperosmolar solutions are combined with colloids. In spite of a large amount of investigations, data about hyperosmolar solutions influence on the ICP, systemic hemodynamics and mortality are controversial. There are only few studies, in which effects of mannitol were compared with hypertonic saline [6]. R. Vialet et al., 2003 found that in patients with severe traumatic brain injury (TBI) 7,5% saline was more effective in intracranial hypertension treatment than 20% mannitol [7]. C. Battison et al., 2005 investigated the effects of equimolar doses of 20% mannitol and 7,5% saline in 6% dextran-70 in patients with TBI and an-eurismal subarachnoid hemorrhage (SAH). Authors mentioned that hypertonic saline combined with colloid solution reduced ICP more effectively than mannitol [8]. Information about effects of hyperosmolar solutions on cerebral oxygenation and metabolism is very small. P.G. Al-Rawi et al., 2005 showed increase of brain oxygen tension and decrease of lactate/pyruvate ratio at 60 min after reducing the intracranial hypertension with hypertonic saline in patients with poor grade SAH [9]. O.W. Sakowitz et al., 2007 didn't find changes in brain oxygen tension after ICP correction with 20% mannitol, but showed 10-40% increase of intracerebral glucose, lactate, pyruvate and glutamate levels in patients with severe TBI [10].