Hyperacute measurement of brain-tissue oxygen, carbon dioxide, pH, and intracranial pressure before, during, and after cerebral angiography in patients with aneurysmatic subarachnoid hemorrhage in poor condition.

BACKGROUND The objective of this study was to examine early changes of intracranial pressure (ICP) and brain oxygenation before, during, and after cerebral angiography in patients with poor-grade subarachnoid hemorrhage (SAH). METHODS Fourteen patients with poor-grade SAH without intracerebral hematoma were studied. A significant change in monitored variables (arterial gases, ICP, brain-tissue oxygen pressure [Ptio(2)], brain-tissue carbon dioxide pressure, and pH) was defined as a register deviation of more than 20% compared with the baseline. Critical Ptio(2) values (<15 mm Hg) or significant Ptio(2) decreases were considered to be impaired brain oxygenation. These data were correlated with the angiography findings and the presence of massive brain edema and hypodense areas in follow-up computed tomography (CT) scan controls. RESULTS Neurotrend data were unavailable in 4 patients because of calibration failure. Impaired brain oxygenation during angiography was observed in 5 patients. Initial critical Ptio(2) values were found in 1 patient. Four patients developed a linear Ptio(2) and pH decrease after the angio-catheter canalized the examined vessels in the neck. Statistically significant correlation was found between brain pH and Ptio(2) changes in these patients (P < .001, Spearman rho). Arterial gases, ICP, and cerebral perfusion pressure did not show significant alterations at this time. Significant correlations existed between severe intracranial angiographic arterial caliber reduction and impaired Ptio(2) values (P < .01). Patients with impaired Ptio(2) values frequently showed lesions in CT scan controls (P < .05). CONCLUSIONS This study documented several fluctuations in the brain oxygenation of patients with poor-grade SAH during angiography. Patients with severe intracranial angiographic arterial caliber reduction at this time have an increased risk for impaired brain oxygenation.

[1]  W. Hoffman,et al.  Hypoxic Brain Tissue following Subarachnoid Hemorrhage , 2000, Anesthesiology.

[2]  W. Hoffman,et al.  Brain Tissue Oxygen, Carbon Dioxide, and pH in Neurosurgical Patients at Risk for Ischemia , 1996, Anesthesia and analgesia.

[3]  A. Kanat Brain oxygenation and energy metabolism: Part 1--Biological function and pathophysiology. , 2003, Neurosurgery.

[4]  A. Jödicke,et al.  Monitoring of brain tissue oxygenation during aneurysm surgery: prediction of procedure-related ischemic events. , 2003, Journal of neurosurgery.

[5]  F. Van Calenbergh,et al.  Early Endovascular Treatment of Ruptured Cerebral Aneurysms in Patients in Very Poor Neurological Condition , 2002, Neurosurgery.

[6]  J. Meixensberger,et al.  Effects of decompressive craniectomy on brain tissue oxygen in patients with intracranial hypertension , 2003, Journal of neurology, neurosurgery, and psychiatry.

[7]  M. Gelabert-González,et al.  Intra-Operative Monitoring of Brain Tissue O2 (PtiO2) During Aneurysm Surgery , 2002, Acta Neurochirurgica.

[8]  R. Bullock,et al.  Increased inspired oxygen concentration as a factor in improved brain tissue oxygenation and tissue lactate levels after severe human head injury. , 1999, Journal of neurosurgery.

[9]  J. Meixensberger,et al.  Brain tissue pO2 in relation to cerebral perfusion pressure, TCD findings and TCD-CO2-reactivity after severe head injury , 2005, Acta Neurochirurgica.

[10]  J. Pickard,et al.  Adverse Cerebral Events Detected after Subarachnoid Hemorrhage Using Brain Oxygen and Microdialysis Probes , 2002, Neurosurgery.

[11]  M. Bullock,et al.  Measurement of Nitric Oxide and Brain Tissue Oxygen Tension in Patients after Severe Subarachnoid Hemorrhage , 2001, Neurosurgery.

[12]  R. Behr,et al.  Transluminal Balloon Angioplasty Improves Brain Tissue Oxygenation and Metabolism in Severe Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Case Report , 2003, Neurosurgery.

[13]  M. Bullock,et al.  Brain Oxygenation and Energy Metabolism: Part I—Biological Function and Pathophysiology , 2002, Neurosurgery.

[14]  W. Hoffman,et al.  Cerebral interstitial tissue oxygen tension, pH, HCO3, CO2. , 1997, Surgical neurology.

[15]  C. Robertson,et al.  Brain tissue PO2: correlation with cerebral blood flow. , 2002, Acta neurochirurgica. Supplement.