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Brain Tissue Oxygen Monitoring in Severe Brain Injury, II

Implications for Critical Care Teams and Case Study

Linda R. Littlejohns has 20 years of experience as a neuroscience critical care nurse and 6 years of experience as a neuroscience clinical nurse specialist. She is currently vice president of clinical development at Integra NeuroSciences, San Diego, Calif.

Karen March has 29 years of experience as a neuroscience critical care nurse and 11 years of experience as a neuroscience clinical nurse specialist. She is currently the director of clinical development at Integra NeuroSciences, San Diego, Calif.

To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.

To receive CE credit for this article, visit the American Association of Critical-Care Nurses’ (AACN) Web site at http://www.aacn.org, click on "Education" and select "Continuing Education," or call AACN’s Fax On Demand at (800) 222-6329 and request item No. 1168.

	Putting It All Together

Top Putting It All Together Applying Brain Oxygen... Outcomes Associated With... Conclusion References

 
The Guidelines for the Management of Severe Brain Injury² describe evidence-based treatment that includes a discussion of appropriate management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP). An algorithm outlines a tiered approach to avoid secondary injury.² The literature review in the guidelines and a review of the Traumatic Coma Data Bank clearly indicate that the avoidance of early hypoxia and hypotension and a rapid resuscitation and evacuation of intracranial hematomas are necessary and could improve the chances for a good outcome.³

Data presented in the guidelines suggest that a CPP of 70 mm Hg or greater is sufficient for adequate perfusion of neuronal cells in the absence of other brain pathology.² The guidelines may enable patients to derive even greater benefit from a targeted approach to therapies that includes monitoring the partial pressure of oxygen in brain tissue (PbtO₂) because traumatic brain injury can be such a multifaceted problem.⁴

Meeting the Needs of the Injured Brain
Resuscitating patients with severe brain injury and stabilizing and maintaining their condition require an organized critical care team armed with protocols that define interventions to optimize cerebral oxygenation and reduce ICP. Targeting therapy to maintain ICP at less than 20 mm Hg has been the reference standard for years. With the introduction of methods for monitoring oxygen levels in brain tissue, interventions must take into account this important new variable. The goal of the critical care team is to balance ICP and PbtO₂ throughout the critical phases of patients’ hospitalization. In the following section, we present interventions that increase PbtO₂ and integrate them into the overall management of patients with severe traumatic brain injury.

Resuscitation Phase: Emergency Department Through Operating Room Procedures
The team’s focus on brain resuscitation begins in the emergency department and continues through diagnostic radiology and operating room procedures. During this time, invasive monitors for evaluating ICP and PbtO₂ are not in place. Establishing physiological goals for each phase will assist the team in targeting therapies to each patient’s situation until more definitive treatment can be delivered (Table 1).

Rapidly obtaining radiographic studies, including computed tomography (CT) scans of the brain and radiographs of the cervical spine, chest, and pelvis, assists in detecting injuries. Once severe brain injury has been diagnosed on the basis of findings on clinical examination and radiographic evidence, the patient is taken to the operating room for definitive intervention.

Once again, the goals of the operative phase must be understood by the entire team (Table 1). Placement of an ICP monitor and a brain tissue oxygen monitor as well as central venous monitoring assists the team in meeting the needs of the injured brain during this critical phase. Specific operative interventions, craniotomy for evacuation of acute hemorrhages or craniectomy, help reduce ICP and improve cerebral oxygenation.^7,8 Careful attention to coagulopathies that develop intraoperatively is important. Prompt attention to correcting the specific deficiency must occur, with administration of blood products, platelets, fresh-frozen plasma, and/or cryoprecipitate.

Because of the possibility of multiple operative procedures and a prolonged period in the operating room, it is helpful to have the intensive care unit (ICU)/trauma nurse present during this phase. This nurse works with the anesthesiologist by helping to intervene when ICP and PbtO₂ change rapidly. This nurse also assists with interventions and critical documentation so that an accurate record is kept of all of the interventions that occur during the operating room phase.

The hemodynamic status of many patients is unstable postoperatively. During transfer to the ICU, it is helpful to use a battery-operated ventilator. Doing so ensures that the ventilator mode remains stable. If a manual resuscitation bag is used, the person administering breaths may be inconsistent in delivering the correct number of breaths per minute, a situation that can lead to hypocapnia or hypercapnia.

ICU Phase
The stabilization period, the first few hours in the ICU, is a critical period during which the patient must be quickly brought into the zone of control. Members of the critical care team must understand the effect that each intervention has on PbtO₂ and ICP. Use of a standardized protocol with team interventions provided via standardized physician orders will help the team prioritize and orchestrate interventions while continuing to stabilize the patient’s condition (Table 3). PbtO₂ is influenced by multiple factors^8–18 (Table 4). Critical care nurses must understand how to manipulate each factor and the appropriate sequence in which to initiate changes in order to balance oxygen delivery to the brain and ICP. Maintaining these therapies until brain swelling is reduced and brain oxygenation stays within the normal range is the primary focus of critical care nurses.

If the PbtO₂ is less than 15 mm Hg, the team should ensure that the FIO₂ administered via the mechanical ventilator is 100%, even if the oxygen saturation is 100%, because the driving force that moves oxygen into tissue is the gradient between the dissolved oxygen in the blood and brain tissue oxygen levels. Supranormal levels of oxygen may be needed for the first few hours during stabilization in the ICU.¹⁰ The FIO₂ can be slowly decreased once the PbtO₂ is greater than 20 mm Hg and stable. Next, ICP and PaCO₂ are assessed. These 2 variables must be considered together when their effect on PbtO₂ is evaluated.^13,19 If the ICP is less than 20 mm Hg and PbtO₂ is less than 20 mm Hg, the PaCO₂ is allowed to increase up to 45 mm Hg so long as the ICP remains less than 20 mm Hg. If ICP is greater than 20 mm Hg and PbtO₂ is less than 20 mm Hg, cerebrospinal fluid is drained if a ventriculostomy was done. Increasing the PaCO₂ might worsen the ICP, but it will increase the PbtO₂.13,19 In efforts to increase PbtO₂, ICP is considered in relation to mean arterial pressure and CPP. If the CPP is less than 70 mm Hg, efforts should be made to increase the mean arterial pressure.¹⁷ If the pulmonary capillary wedge pressure is less than 8 mm Hg, a bolus of isotonic sodium chloride solution or 250 mL of 5% albumin should be given. If the hematocrit is less than 0.33, packed red blood cells are administered. Then, the patient’s fluid volume status should be reassessed. Fluids should be given until the pulmonary capillary wedge pressure is greater than 8 but less than 12 mm Hg. If the patient is euvolemic and the CPP is still low, a vasopressor may be given.

Next, the PbtO₂, CPP, and ICP are reevaluated. If PbtO₂ is greater than 20 mm Hg and ICP is less than 20 mm Hg, the CPP should be maintained at that level. The minimal CPP requirement of patients with severe traumatic brain injury will change and must be evaluated frequently. Once CPP is optimized, the ICP and PbtO₂ are reevaluated. If the ICP is still greater than 20 mm Hg, 0.25 to 1.0 g/kg mannitol may be given as an intravenous bolus and/or propofol may be infused intravenously at a rate of 10 to 100 µg/kg per minute. During this time, administration of analgesic and sedative agents should be started and then maintained continuously. Cooling measures should be used to maintain the patient’s body temperature at 36°C to 37°C.

If PbtO₂ is greater than 20 mm Hg on admission to the ICU, assessment of ICP and the other factors will provide information for planning strategies for care. If PbtO₂ and ICP are normal, then the patient’s condition can be stabilized by using an FIO₂ of 30% to 40% and a PaCO₂ of 35 to 40 mm Hg, and efforts can be made to determine the optimal CPP. A CPP of 55 to 60 mm Hg may be acceptable if the PbtO₂ is greater than 20 mm Hg without supplemental increased oxygen support.^8,14 The fluid volume status should be assessed, and euvolemia should be maintained. Administration of analgesic and sedative agents should begin. The patient’s condition should be evaluated frequently.

If ICP is elevated but PbtO₂ is normal, then efforts should be made to reduce ICP. These efforts include draining cerebrospinal fluid, decreasing PaCO₂ so long as the PbtO₂ is greater than 20 mm Hg, optimizing the mean arterial pressure with fluids and vasopressors, and administering sedatives, analgesic agents, and/or an osmotic diuretic. If the ICP remains greater than 20 mm Hg, consultation with the physician team may lead to an emergent CT scan, orders for propofol and/or barbiturates, and, possibly, a craniectomy. The optimal CPP for a patient with an elevated ICP and normal PbtO₂ must be determined and may exceed the "recommended" CPP of 70 mm Hg. In some instances, patients might require a CPP of 90 to 110 mm Hg to decrease the ICP.

Once the patient’s condition is stabilized and the parameters have reached the recommended goals for therapy, then the actions of the critical care team must be organized to keep the situation under control. Rarely does a patient continue without elevations of ICP or decreases in PbtO₂. Therefore, the ICU nurse must continually reassess the patient and reprioritize the interventions with other team members. The ICU team usually develops a sense of where the patient’s various parameters should be in order to maintain all parameters within the goal established for the patient. Using the interventions listed in Table 3 ensures an organized approach to patients’ management.

Critical-thinking algorithms are extremely helpful in guiding team members in decision making (Table 5). The interventions are prioritized and allow the team to think through the situation in a standardized manner, ensuring that primary interventions are done before more complex interventions. The patient’s status will change. Sometimes the changes are minute to minute in the early phases of care and day to day in the later phases.

After peak edema has passed, the patient’s intensity of care will diminish. Once the patient has achieved a consistently normal ICP and PbtO₂ with little need for interventions, then the team can begin to wean the patient off therapy (Figure 1). The more complex interventions are discontinued first, and the patient is slowly brought out of the coma state.

View larger version (26K): [in this window] [in a new window]   Figure 1 Weaning patients with severe traumatic brain injuries off therapies.

	Applying Brain Oxygen Monitoring: Case Study

Top Putting It All Together Applying Brain Oxygen... Outcomes Associated With... Conclusion References

A.P., a 29-year-old woman, was driving home from work at 6:10 PM when she crossed the center line and hit an oncoming car. A.P. was not wearing a seat belt, and her car did not have an air bag. Witnesses called 911. Paramedics arrived at 6:20 PM and described A.P.’s condition as critical. After a prolonged extrication, A.P.’s clinical examination revealed the following: airway open, breathing shallow; weak pulses/unable to obtain a palpable blood pressure; GCS score 1 for eye opening, 1 for motor response, and 1 for verbal response elicited with painful stimuli; obvious facial, pelvic, and left leg deformities. Initial interventions at the scene were completed. After the base station was contacted, A.P. was designated a critical trauma patient and was sent to the nearest trauma center.

Emergency Department to Radiology Department
At 7:01 PM, A.P. arrived in the emergency department in critical condition. Paramedics were supporting her airway by using a manual resuscitation bag and 100% oxygen. Because of her depressed respirations, inability to maintain a patent airway, and a GCS score of 3, A.P. was emergently intubated by using a rapid-sequence intubation. She was supported with 100% FIO₂, and the end-tidal carbon dioxide level (PetCO₂) was maintained at 35 mm Hg. Circulation assessment revealed weak pulses of 140/min and a systolic blood pressure of 70 mm Hg. Paramedics had started 1 intravenous catheter. A large-bore intravenous catheter was started by using a rapid-infusion kit and was attached to a rapid-infuser pump to allow intravenous administration of fluids and blood products. A.P.’s neurological status included a GCS score of 3; both pupils were 5 mm in diameter and nonreactive. An oral gastric tube to decompress stomach contents, a Foley catheter for urinary drainage, and an arterial catheter for monitoring blood pressure were inserted. Her hematocrit was 0.25. Diagnostic radiographs revealed fractures of the pelvis, left femur, and left tibia/fibula. By the completion of the 20-minute emergency department phase, she had received 1 L of isotonic sodium chloride solution and 4 units of O-negative packed red blood cells.

A.P. was transported by the trauma team to the radiology department for an emergent CT scan at 7:20 PM. A battery-operated ventilator was used during transport to maintain consistent PetCO₂ levels. The unenhanced CT scan of the brain revealed cerebral edema, a small right-sided subdural hematoma, right-to-left shifting of intracranial contents, and multiple facial fractures (Figure 2). Fluid resuscitation continued because of her low blood pressure (80–90 mm Hg systolic). The goal was to achieve a mean arterial pressure of at least 90 mm Hg. A.P. received an additional 5 units of packed red blood cells and 4 units of fresh-frozen plasma. Neuro-surgical consultation resulted in a decision to transport her immediately to the operating room.

View larger version (76K): [in this window] [in a new window]   Figure 2 Unenhanced CT scans of A.P.’s brain and face show injuries.

The neurosurgical operative team assisted the neurosurgeon with placement of an ICP catheter and a LICOX brain tissue oxygen catheter. The initial ICP was 35 mm Hg, a considerable elevation from the normal value of less than 20 mm Hg. The PbtO₂ was 3 mm Hg, a critical level (normal PbtO₂ is 20 to 35 mm Hg). During the next 30 minutes, the ICP increased to 50 mm Hg and the PbtO₂ stayed at 3 mm Hg. The team was using multiple interventions during this period in an effort to reduce ICP and improve PbtO₂. Team members administered an FIO₂ of 100%, maintained the PetCO₂ at 35 mm Hg, administered analgesic agents and mannitol, and attempted to increase the mean arterial pressure to greater than 80 mm Hg but were successful only for a short period.

The neurosurgeon elected to perform a craniectomy when the team was unable to control the ICP. By the time the bone was removed, the ICP had reached 60 mm Hg. As the bone was removed and the sub-dural hematoma evacuated, the ICP decreased to 8 or 10 mm Hg and the PbtO₂ increased dramatically to 20 to 45 mm Hg. Because of the unstable pelvic fracture and A.P.’s critical condition, hoping to stabilize the fractures, the orthopedic surgeon placed a C-ring on the pelvis. Pins were placed in the leg fractures for traction to be applied once the patient reached the ICU. A.P. had a large 7-cm laceration across her forehead, so the plastic surgeon quickly repaired it. The physician team elected not to repair the facial fractures because of A.P.’s critical condition. By the time the operative procedures were completed, the ICP had once again increased to more than 40 mm Hg, and the PbtO₂ had decreased to 2 mm Hg (Figure 3). Despite multiple interventions, the team could not increase the PbtO₂ to more than 2 mm Hg or decrease the ICP to less than 40 mm Hg. A.P.’s condition was highly unstable and grave.

View larger version (28K): [in this window] [in a new window]   Figure 3 Course of events during the operating room phase for A.P. Fluids administered during this phase included 9 units of fresh-frozen plasma, 21 units of red blood cells, 10 units of cryoprecipitate, 10 units of platelets, and 4 L of isotonic sodium chloride solution. Medications administered included 200 µg/min phenylephrine and 150 µg/kg per minute propofol.

ICU Phase
Initial 24 Hours
A.P.’s neurological condition was grave. Her GCS score was 1 (eye opening), 1 (motor response), and 1 (verbal response), and both pupils were 6 mm in diameter and nonreactive. Her ICP was greater than 40 mm Hg, and her PbtO₂ was between 2.5 and 3.5 mm Hg. The ventilator was set to maintain an FIO₂ of 40% and a pressure setting and rate to maintain the PetCO₂ at 35 mm Hg. Intravenous administration of fluids and vasopressors was continued. In addition to phenylephrine, dopamine was added and titrated in an effort to increase the CPP to 70 mm Hg. Because the ICP values were between 40 and 50 mm Hg, the maximum CPP achieved was 40 to 59 mm Hg. The team was unable to bring A.P. into the zone of control or meet the goals that had been established for this phase, which were maintaining an ICP less than 20 mm Hg and a PbtO₂ greater than 20 mm Hg.

Within hours of A.P.’s admission to the ICU, the team continued to struggle. The ICU nurse and respiratory care practitioner decided to increase the FIO₂ to 70%, a change that resulted in an increase of the PbtO₂ to 6.2 mm Hg within 30 minutes. The FIO₂ was increased to 100%, and the PbtO₂ increased to 23 mm Hg within 25 minutes of that change. Once the target PbtO₂ was reached, the team focused on decreasing the ICP (Figure 4). Despite aggressive fluid and vasopressor therapy, the CPP remained in the range of 40 to 50 mm Hg, lower than the goal of 70 mm Hg. Epinephrine was added to the phenylephrine and dopamine in an attempt to increase CPP.

View larger version (31K): [in this window] [in a new window]   Figure 4 Course of events from 12 PM to 7 PM during the first 24 hours of team management for A.P. in the intensive care unit.

Because the PbtO₂ was greater than 20 mm Hg, the team sought to decrease the FIO₂ from 100%. Each time the FIO₂ was decreased, the PbtO₂ decreased precipitously to less than 5 mm Hg. Use of 100% FIO₂ was resumed immediately to keep the PbtO₂ greater than 20 mm Hg. Full systemic support was instituted.

The interventions in the first 24 hours were focused on optimizing oxygen levels and lowering ICP. Although the PbtO₂ goal was achieved, the ICP was dangerously elevated to 40 to 60 mm Hg. The team was encouraged by the ability to maintain PbtO₂ but frustrated with the ICP. A.P. was in for a rough hospital course.

Days 2 to 26
The team continued to focus their interventions on decreasing the ICP to less than 20 mm Hg and maintaining the PbtO₂ at greater than 20 mm Hg. During day 2, the ICP remained between 40 and 50 mm Hg despite drainage of cerebrospinal fluid, maintenance of PetCO₂ at 28 to 30 mm Hg, aggressive CPP therapy, repeated administration of mannitol boluses, and use of high doses of propofol intravenously. The CPP was maintained between 50 and 60 mm Hg with fluid therapy and maximum dosages of dopamine, phenylephrine, and epinephrine as intravenous infusions. At one point, the PbtO₂ decreased to 12.4 mm Hg despite the FIO₂ remaining at 100%. A.P.’s hematocrit was 0.24, so the surgeons ordered 2 units of packed red blood cells. The CPP increased by only 5 mm Hg, but the PbtO₂ increased from 12.4 to 22 mm Hg. After the red cells were transfused, PbtO₂ fluctuated when the FIO₂ was decreased to less than 100%. Despite several attempts to decrease the FIO₂ on day 2, it appeared that high-flow FIO₂ was the only intervention that would keep the PbtO₂ greater than 20 mm Hg. No change in A.P.’s neurological status occurred: both pupils remained 7 mm in diameter and fixed. No motor movement or doll’s eyes, blink, or gag reflex was detected.

On day 3, a CT scan of the brain revealed an epidural collection of blood underneath the scalp on the side where the craniectomy had been done. Despite A.P.’s critical state and poor prognosis, the team pressed on with care. The neurosurgeon took A.P. back to the operating room and evacuated the hematoma. The ICP decreased from values between 40 and 50 mm Hg to values between 20 and 30 mm Hg (Figure 5). CPP improved and was maintained at greater than 70 mm Hg. During day 3, the PbtO₂ decreased, with lower levels of PaCO₂ and FIO₂ as well as decreases in CPP (Figure 5). Adjustment of FIO₂ occurred, with fluctuations between 50% and 80% FIO₂. PaCO₂ changes from 32 to 27 mm Hg resulted in a decrease of 8 mm Hg in PbtO₂. Full vasopressor support was maintained. No change in the neurological findings occurred during this time.

View larger version (39K): [in this window] [in a new window]   Figure 5 Course of events from 24 hours to 72 hours of the team management for A.P. in the intensive care unit.

By day 7, A.P.’s pulmonary status had improved. The inverse inspiratory/expiratory ratio therapy was stopped, and the FIO₂ was at 50%. Her ICP was controllable and was maintained at less than 20 mm Hg with drainage of cerebrospinal fluid. She required less vasopressor support and had been weaned from the intravenous infusions of metaraminol, norepinephrine, and epinephrine. The most interesting phenomenon was related to the PaCO₂ levels needed to maintain PbtO₂ greater than 20 mm Hg. Because A.P.’s ICP was low, the team allowed the PaCO₂ to increase until the PbtO₂ was maintained consistently at greater than 20 mm Hg. The PaCO₂ ranged from 45 to 50 mm Hg during this time. Her neurological status continued to improve; both pupils reacted to light and were equal in diameter at 4 mm.

A.P.’s status continued to improve, and the neurosurgeon began weaning her off therapies. Weaning was done in an orderly fashion to minimize relapses or elevations in ICP (Figure 1). During the course of several days, A.P. was weaned off all vasopressors. She went to the operating room on day 11 for repair of the pelvic and leg fractures. On day 12, the LICOX catheter was removed. A.P.’s GCS score was 4 (eye opening), 5 (motor response), and 1 (verbal response). She was moving both upper extremities spontaneously, with 4/5 motor strength on the right side and 2/5 motor strength on the left side. On day 14, A.P. went back to the operating room for a tracheostomy, placement of gastric and jejunostomy tubes, and repair of the facial fractures. Physical, occupational, and speech therapies were started. By day 22, A.P. was weaned from the ventilator, and she was transferred to the surgical unit by day 26.

A.P. continued to improve. She began turning her head and tracking nurses and her family as they moved around the bed. A.P. started to follow commands. She was up in a bedside chair at least 3 times a day. Any time she was out of bed, she used a helmet to protect her head where the bone had been removed. As A.P. continued to improve, she was evaluated for acute rehabilitation. A.P. was transferred to acute rehabilitation on day 50 and was discharged home on day 78.

At 3 months, A.P. underwent a cranioplasty and the bone was replaced. She returned home able to walk, talk, dress, eat, and participate in life’s activities. It has been 18 months since A.P.’s accident, and she is independent in her activities of daily living.

	Outcomes Associated With Integrated Care: Oxygen Monitoring/Traumatic Brain Injury Guidelines

Top Putting It All Together Applying Brain Oxygen... Outcomes Associated With... Conclusion References

 
The outcomes of patients with severe traumatic brain injury have been greatly improved through the use of ICP/brain oxygen monitoring and the application of the Brain Trauma Foundation/American Association of Neurologic Surgeons’ Guidelines for the Management of Severe Head Injury.^2,20 At Mission Hospital, Mission Viejo, Calif, all outcomes for patients with severe traumatic brain injury are tracked for at least 6 months after the patients are discharged from the hospital. In order to maintain consistency, inclusion and exclusion criteria were established. The inclusion criteria included the following: GCS scores of 3 to 8, blunt mechanism of injury, abnormal findings on CT scan and/or clinical examination, and age 8 years or greater. Exclusion criteria were penetrating trauma, pronounced brain dead within 24 hours of ICU admission, age less than 8 years, and normal findings on CT scan and presence of alcohol/drug intoxication, seizure, or a non–central nervous system injury leading to depressed level of consciousness. Since we instituted the guidelines for traumatic brain injury and brain oxygen monitoring in the forms of catheters in the jugular bulb and the brain, the outcomes have improved dramatically (Table 6).

	Conclusion

Top Putting It All Together Applying Brain Oxygen... Outcomes Associated With... Conclusion References

	References

Top Putting It All Together Applying Brain Oxygen... Outcomes Associated With... Conclusion References

 

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This Article Full Text (PDF) Respond to This Article Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Bader, M. K. Articles by March, K. Search for Related Content PubMed PubMed Citation Articles by Bader, M. K. Articles by March, K.