A new technology—a brain-tissue oxygenation monitoring system—enables practitioners to assess level of brain oxygen associated with brain injury secondary to trauma.

Severe traumatic head injury—an injury to the head that disrupts normal function of the brain1—has challenged the medical team for decades. According to the Centers for Disease Control and Prevention, almost 1.5 million cases of traumatic brain injury, some mild, some severe, are reported annually in the United States.1 Approximately 50,000 of the patients diagnosed with traumatic brain injury die, and 80,000 are left with some form of permanent disability. The primary injury, which happens at the time of the event, causes a disruption of axons, cell bodies, and the integrity of the cell membrane, resulting in an accelerated disintegration of cell structure and function, eventually leading to cellular death.2

Secondary brain injury occurs in response to unchecked cerebral edema, ischemia, and the neurochemical changes associated with direct trauma to or systemic effects on the brain.

The brain cannot store oxygen. Therefore, to maintain adequate brain function, a constant supply of oxygen is required. Cerebral blood flow (CBF), among other factors, contributes to oxygen delivery to the brain. In the normal brain, CBF remains fairly constant despite fluctuations in the systemic blood pressure through autoregulation. In the injured brain, however, cerebral autoregulation is frequently impaired, which leads to change in CBF and oxygen delivery. Continuous brain tissue oxygen monitoring is a method to measure oxygen and identify cerebral hypoxia and ischemia in patients with brain injury, aneurismal subarachnoid hemorrhage, or malignant stroke, or other patients at risk for secondary brain injury.

Managing Trauma
Historically, the management of traumatic brain injury has focused on controlling intracranial pressure (ICP) and cerebral perfusion pressure (CPP) via a variety of methodologies. The concept of managing and treating only ICP in brain injury limits the ability to assess perhaps one of the most important parameters: brain tissue oxygenation. The delivery and use of oxygen at the cellular level, in addition to controlling excitatory amino acids, can directly affect tissue survival. Technology advances in brain tissue oxygenation monitoring provide information on the cellular dynamics of oxygenation and better understanding of the impact of low oxygen states in this patient population. New technology via a brain tissue oxygen monitoring system enables the bedside practitioners to assess levels of brain oxygen associated with secondary injury and treatment interventions.3

The system is a triple lumen catheter inserted through an intracranial bolt that displays cerebral tissue oxygen and temperature values. The technology includes a Clark cell polarographic probe that is a semipermeable membrane covering two electrodes, one silver and one gold. As dissolved oxygen crosses the membrane, an electrical current is generated and is transferred to the monitor for interpretation. The probe is inserted into the deep white matter of the brain because oxygen consumption is most stable in this region.4 To determine correct placement of the probe, the Fio2 is increased to 100% via the ventilator, and the brain tissue partial pressure (PbtO2) is observed for an increase. The goal is to maintain an acceptable PbtO2 in head-injured patients. If the PbtO2 cannot be maintained >20 torr after implementing brain-injury-protocol-driven interventions, such as cerebral spinal fluid drainage, increasing the arterial mean blood pressure, volume administration, and pharmacological interventions, the Fio2 is increased via the mechanical ventilator.5 A PbtO2 <5 torr is associated with serve brain injury and a low chance of brain survival. Palmer et al6 found that, in 22 patients with severe head injury, brain tissue oxygenation monitoring demonstrated that increasing the Fio2 led to an increase in PbtO2.

Influence of Carbon Dioxide
Hyperventilation continues to be the treatment for intracranial hypertension in some institutions even though it has deleterious effects in patients with severe brain injury when used injudiciously.7 Schneider found that, although hyperventilation dramatically decreased ICP and increased CPP, brain-tissue oxygenation could decrease to as low as 10 torr during hyperventilation.8 When researchers placed an oxygen probe in the cortex of patients undergoing craniotomy and observed both patients who had no secondary swelling and those who had pathological changes and swelling, both groups had an increase in PbtO2 when they were breathing 100% oxygen. There was no correlation between tissue PO2 and arterial PO2 in the group with no swelling, but there was a correlation in the group with pathological changes. In addition, low PbtO2 occurred in both groups after being hyperventilated, suggesting that some head-injured patients are at risk for brain hypoxia during this commonly practiced hyperventilation. Lowering the Paco2 produces vasoconstriction of the blood vessels, thus reducing blood flow and, ultimately, brain oxygen delivery. 9

A Fine Balance
Respiratory complications are common among severe traumatic brain injury patients, particularly those requiring mechanical ventilation. This can cause systemic hypoxia and inadequate brain tissue oxygenation. Hypoxia can result from pulmonary complications such as atelectasis, pulmonary edema, pneumonia, and acute lung injury. Often ventilatory interventions, such as increasing the mean airway pressure by raising the positive end expiratory pressure (PEEP), can be an effective means for optimizing alveolar recruitment and improving oxygenation10; but it may worsen or trigger intracranial hypertension. When managing a head-injured patient via mechanical ventilation, the clinician must balance between the positive and negative effect of their interventions. The goal is not only to improve arterial oxygenation but also to ensure an increase in the PbtO2. Brain oxygenation delivery can be optimized by observing how ventilatory adjustments affect the PbtO2.

Brain tissue oxygenation monitoring adds a new dimension to the care of patients with severe traumatic head injury. Research is demonstrating the basis for interventions and how they affect the critical oxygen levels in the brain. By understanding the causes of hypoxia and low oxygen states in the brain and the effects of clinical interventions on oxygen delivery to the brain, the critical care team can maximize the patient’s chance for recovery. As respiratory therapists, we are the gatekeepers of mechanical ventilation management. There has been great attention to providing adequate gas exchange without inducing ventilator-induced trauma. Now by utilizing this new technology, respiratory therapists can optimize gas exchange without negatively affecting brain oxygenation.

Kenneth Miller, MEd, RRT, is clinical educator, respiratory care, Lehigh Valley Hospital, Allentown, Pa.

References
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