Continuous monitoring of jugular venous oxygen saturation in head-injured patients

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✓ The continuous measurement of jugular venous oxygen saturation (SjvO2) with a fiberoptic catheter is evaluated as a method of detecting cerebral ischemia after head injury. Forty-five patients admitted to the hospital in coma after severe head injury had continuous and simultaneous monitoring of SjvO2, intracranial pressure, arterial oxygen saturation, and end-tidal CO2. Cerebral blood flow, cerebral metabolic rates of oxygen and lactate, arterial and jugular venous blood gas levels, and hemoglobin concentration were measured every 8 hours for 1 to 11 days. Whenever SjvO2 dropped to less than 50%, a standardized protocol was followed to confirm the validity of the desaturation and to establish its cause. Correlation of SjvO2 values obtained by catheter and with direct measurement of O2 saturation by a co-oximeter on venous blood withdrawn through the catheter was excellent after in vivo calibration when there was adequate light intensity at the catheter tip (176 measurements: r = 0.87, p < 0.01). A total of 60 episodes of jugular venous oxygen desaturation occurred in 45 patients. In 20 patients the desaturation value was confirmed by the co-oximeter. There were 33 episodes of desaturation in these 20 patients, due to the following causes: intracranial hypertension in 12 episodes, hypocarbia in 10, arterial hypoxia in six, combinations of the above in three, systemic hypotension in one, and cerebral vasospasm in one. The incidence of jugular venous oxygen desaturations found in this study suggests that continuous monitoring of SjvO2 may be of clinical value in patients with head injury.

Article Information

Address reprint requests to: Claudia S. Robertson, M.D., Department of Neurosurgery, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030.

© AANS, except where prohibited by US copyright law.

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    Algorithm for diagnosing the cause of jugular venous desaturations. SjvO2 = jugular venous oxygen saturation; R/O = rule out (exclude); SO2, SaO2 = venous, arterial oxygen saturation; CBF = cerebral blood flow.

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    Graph showing correlation of fiberoptic catheter values for jugular venous oxygen saturation (SjvO2) and oxygen saturation measured in a blood sample drawn through the catheter on those occasions when the catheter light intensity was adequate (176 measurements: r = 0.87, p < 0.01).

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    Graphs showing arterial oxygen saturation (SaO2) and jugular venous oxygen saturation (SjvO2) in a patient with jugular venous desaturation due to arterial hypoxia.

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    Graphs showing end-tidal CO2 (ETCO2) and jugular venous oxygen saturation (SjvO2) in a patient with jugular venous desaturation due to hypocarbia. The initial cerebral blood flow (CBF) was 0.19 ml/gm/min at a PaCO2 of 24 mm Hg. As the ventilator rate was reduced to allow PaCO2 to rise to 37 mm Hg, the SjvO2 gradually rose, and CBF increased to 0.38 ml/gm/min. CMRO2 = cerebral metabolic rate of oxygen.

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    Graphs showing mean arterial pressure (MAP) and jugular venous oxygen saturation (SjvO2) in a patient with jugular venous desaturation due to systemic hypotension.

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    Graphs showing cerebral perfusion pressure (CPP) and jugular venous oxygen saturation (SjvO2) in a patient with jugular venous desaturation during a transient decrease in CPP secondary to elevated intracranial pressure.

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    Graphs showing cerebral perfusion pressure (CPP) and jugular venous oxygen saturation (SjvO2) in a patient with jugular venous desaturation due to refractory intracranial hypertension following evacuation of a subdural hematoma. Cerebral blood flow (CBF) ranged from 0.67 to 0.75 ml/gm/min during the first 4 days after the injury. On Day 5, the intracranial pressure was unresponsive to maximum medical therapy including pentobarbital. As CPP fell to 25 mm Hg, both pupils became fixed and dilated. With further decreases in CPP, the SjvO2 fell to a low of 20%. CMRO2 = cerebral metabolic rate of oxygen; CMRL = cerebral metabolic rate of lactate; CT = computerized tomography.

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