7.1 Introduction

Mitigation of secondary injury in the brain after a neurologic insult is one of the primary goals of neurocritical care. Dysfunctional oxygenation of brain tissue is an important cause of such secondary injury.

Cerebral oximetry encompasses a range of monitoring modalities to assess (directly or indirectly) the oxygenation status of the brain. These modalities include direct brain tissue oxygen (PbtO₂) monitoring (discussed in Chapter 6), microdialysis monitoring of extracellular glutamate and other molecules, nearinfrared spectroscopy (NIRS) measurement of regional brain tissue oxygen saturation, and jugular bulb oxygen saturation (SjO₂) monitoring.

Here, we discuss the technique for insertion of an SjO₂ monitor. Of the aforementioned cerebral oximetry modalities, only SjO₂ monitoring is recommended by current professional guidelines. ¹

Jugular venous oximetry provides an indirect assessment of oxygen use by the brain—it is used to determine the global balance of cerebral oxygen delivery and consumption.

Jugular venous oximetry can be performed intermittently or continuously. Intermittent SjO₂ monitoring entails the insertion of retrograde jugular catheter with subsequent periodic aspiration and laboratory analysis of blood samples from the jugular bulb. Here, we describe the technique for continuous SjO₂ monitoring which is accomplished by insertion of a fiber-optic catheter with an SjO₂ monitor situated within the jugular bulb. For this latter technique, aspiration and laboratory analysis of blood is only required for calibration.

Jugular venous oximetry is a relatively noninvasive, cost-effective, and reliable tool in the armamentarium of critical care physicians.

7.2 Relevant Anatomy and Physiology

Blood from the brain drains mainly through the sigmoid and inferior petrosal sinuses into the internal jugular veins, as seen in ▶ Fig. 7.1. The jugular bulb is the connection between these sinuses and the internal jugular vein, and drains about 70% of the blood from the ipsilateral hemisphere, and 30% from the contralateral hemisphere. To monitor SjO₂, the tip of the fiber-optic catheter is placed into the jugular bulb, conventionally on the side with dominant drainage. Dominance can be determined radiographically by measuring the jugular foramina on computed tomography (CT) scan or functionally, if an intracranial pressure (ICP) monitor is present, by alternatingly compressing both jugular veins and observing the extent of increase in ICP. The right jugular venous pathway is dominant 80% of the time.

The arteriovenous oxygen content difference of the brain (AVDO₂) is calculated according to the following formula:

AVDO₂ = Hgb × 1:34(SaO₂ – SjO₂ + 0:003(PaO₂ – PjO₂) ²

Cerebral oxygen extraction (CO₂E), a simplified representation of AVDO₂, is calculated according to the following formula:

CO₂E = SaO₂ – SjO₂

Saturation of arterial blood (SaO₂) is measured by continuous pulse oximetry, and saturation of jugular bulb blood (SjO₂) is measured continuously by the fiber-optic jugular bulb catheter.

Any disturbance that increases cerebral oxygen consumption or decreases oxygen delivery may decrease SjO₂. Current guidelines define SjO₂ < 50% as pathologic and harmful. ¹ SjO₂ > 75% is also correlated with adverse outcomes in head injury. ³ Thus, the brain tissue of a healthy person extracts between 25 and 50% of arterial oxyhemoglobin, yielding a normal SjO₂ of 50 to 75%.

One prospective study showed mortality benefit by maintaining CO₂E between 24 and 42%.

High CO₂E suggests low cerebral blood flow relative to metabolic demand. This could be caused by decreased oxygen supply due to anemia, hypotension, or hypoxemia, or due to increased demand due to agitation, fever, seizures, or pain. This state has been described as “oligemic cerebral hypoxia,” and can lead to ischemia.

Low CO₂E suggests that there is excess blood flow relative to metabolic demand, due to excessive cardiac output, or due to processes such as infarction, deep coma, or hypothermia causing decreased metabolism. This state of “luxury perfusion,” can cause intracranial hypertension or hemorrhage.

Limitations of SjO₂ monitoring include erroneous values due to the monitor coming into contact with the vessel wall, thrombosis on the catheter tip, and the fact that it is a global monitor and may not detect regional ischemia or hyperemia.