Analysis of abnormal jugular bulb oxygen saturation data in patients with severe head injury

Abstract

Jugular bulb oximetry provides the first bedside, continuously available information on cerebral perfusion adequacy. An extensive analysis was made of all jugular bulb oxygen saturation (SjO2) data obtained in 50 patients suffering from severe head injury. A total of 176 periods (more than 30 minutes) with reliable, abnormal SjO2-values was observed, with 62 desaturation periods (SjO2 < 55%) and 114 high SjO2-periods (SjO2 > 80%). Jugular desaturation periods were predominantly observed in the first 2 days of monitoring and seemed the most closely correlated to lowered cerebral perfusion pressure and lowered arterial carbon dioxide tension. The high SjO2-values were more equally distributed over the first 5 days of monitoring and seemed mostly correlated to increased arterial carbon dioxide tension. Highlights of the general management of severely head injured patients is discussed, focussing attention on the importance of cerebral perfusion pressure and normoventilation.

The effect of pneumoperitoneum and Trendelenburg position on acute cerebral blood flow–carbon dioxide reactivity under sevoflurane anaesthesia

“…SjvO 2 is a useful indicator of CBF provided that the cerebral metabolic rate is constant, since it theoretically reflects the relationship between global cerebral oxygen supply and demand [9][10][11][12][13] and it can be used to calculate CBF-CO 2 reactivity [14,15]. In contrast, other methods for measuring the cerebrovascular reactivity such as transcranial Doppler ultrasonography or near-infrared spectroscopy may not represent the changes of whole CBF, and become unreliable with changes in body position [16].…”

Monitoring of Brain and Systemic Oxygenation in Neurocritical Care Patients

“…Increased ICP also is associated with reduced SjvO 2 [192,201,202] but the response of SjvO 2 to ICP treatment including hyperventilation, osmotherapy, surgery, or hypothermia is variable [202][203][204][205][206]. A decrease in SjvO 2 associated with hyperventilation can be used to deescalate therapy i.e., guide hyperventilation during ICP treatment [195,196,[207][208][209][210][211][212]. A failure of AVDO 2 to improve once ICP is normalized is associated with a greater likelihood of cerebral infarction [213].…”

Metabolic Crisis without Brain Ischemia is Common after Traumatic Brain Injury: A Combined Microdialysis and Positron Emission Tomography Study

“…Numerous clinical studies have documented ischemia early after TBI. The evidence of brain ischemia occurring after TBI comes from pathological autopsy series of fatal cases of brain injury and from hyperacute studies of cerebral blood flow and jugular venous oximetry (Bouma et al, 1991;De Deyne et al, 1996;Vigue et al, 1999). Early pathological studies of fatal brain injuries such as those by Graham and Adams (1971), Graham et al (1989) documented ischemic damage in 91% of cases.…”