Keeping the Brain in the Zone

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Neurotrauma

Keeping the Brain in the Zone Applying the Severe Head Injury GuideUnes to Practice Mary Kay Bader, MSN,

CCRN, CNRN, and Sylvain Palmer MD, FAGS

One of the greatest challenges for critical care nurses and the multidisciplinary team is caring for traumatic brain injury (TBI) patients with severe injuries. The care of these patients focuses on the need to assess patients in coma, to plan interventions to minimize increased intracranial pressure (ICP), to optimize cerebral perfusion pressure (CPP), and to measure patients' responses to interventions. The publication of the "Guidelines for the Management of Severe Head Injury" by the American Association of Neurological Surgeons (AANS) and the Brain Trauma Foundation in 1995 provided recommendations for practice based on a rigorous review of the medical scientific literature. 5 These guidelines focused on a patient population defined as severely brain-injured patients with Glasgow Coma Scale (GCS) scores between three and eight. Evidence produced from research studies reviewed by the AANS group questioned the validity of some of the traditional practices used for decades in managing increased ICP and led to the publication of guidelines summarizing the data. The recommendations represented a paradigm shift in the management

From the Division of Emergency and Critical Care Services (MKB), Mission Hospital Regional Medical Center (SP), Mission Viejo, California

of the TBI population. In addition to the medical research, three decades of nursing research related to the TBI population and ICP management has provided the team with results regarding ai1way, ventilato1y, positioning, and environmental stimulation management. The dissemination of these guidelines and the transition of evidence-based research into practice have challenged practitioners caring for the TBI population at the bedside. The multidisciplinary team must review the scientific literature, analyze current practice, construct new treatment plans, and implement these research-based interventions in clinical practice. The application of the published TBI guidelines and construction of standardized protocols has been analyzed by McKinley et al3 4 in a preliminary clinical trial involving 24 patients with severe head injury. The group found that ICP was more consistently managed and controlled in the group of patients with standardized, data-driven protocols using flow chart decision logic diagrams than the group of patients managed with preprinted and ad hoc physician orders. 34 The purpose of this article is to review the pathophysiology of brain injrny, summarize the severe head injury guidelines and research studies related to TBI, and translate this information into clinical practice. Clinical algorithms are presented to illustrate standardized

CRITICAL CARE NURSING CLINICS OF NORTH AMERICA I Volume 12 I Number 4 I December 2000

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care priorities for TBI patients with severe injuries during the resuscitation and intensive care phases of care.

The Pathophysiology of TBI Anatomy and ICP Head injury can produce a disruption in the balance inside the cranium. The three major components of the intracranial cavity are brain, blood, and cerebrospinal fluid. 21 Because the cranium is essentially a closed box, these three components are maintained in a constant balance. Any increase in one of the components results in decrease in one or both of the other two. The ability of the components to compensate and maintain a balance is limited when there is an expanding mass, such as cerebral edema or a hematoma. Once compensatory mechanisms are exhausted, increased ICP will result. 21 • 26 An ICP above 20 mm Hg is considered elevated in adults and requires aggressive intervention to minimize inju1y to the brain. 26 If untreated, increased ICP may produce ischemia or herniation of brain tissue, or both, with resulting injury to brain cells and to vital brain structures. 6

Primary and Secondary Head Injury A traumatic impact to the head resulting in biomechanical changes in the brain and cranium is called a primary head injury. 21 A primary injury causes focal or diffuse injuries such as fractures of the skull, tearing of blood vessels, and disruptions of brain tissue. 21 This kind of injury may lead to irreversible damage of brain cells. 22 Seconda1y head injuries are physiologic insults that occur after the primary injury and can contribute to further dysfunction and damage to the brain. 22 Examples of secondary injury include hypoxia, hypotension, hypocapnia, hypercapnia, hyperthermia, sustained increased ICP, systemic inflammatory response syndrome, anemia, electrolyte disturbances, vasospasm, hydrocephalus, seizures, and infections. 6• 21 The brain is especially sensitive to decreases in blood pressure and oxyof data from the Traumatic gen.7 Coma Data Bank (TCDB) found that those patients sustaining episodes of hypotension or hypoxia or both had worse outcomes than

those with no episodes. The data show hypotension had a more profound negative impact on survival and outcome in the TBI population than any other factor. 7 Dewitt et al1 2 suggest that the brain has an enhanced vulnerability to brain ischemia because of the brain's inability to increase cerebral blood flow when challenged with hypotension, hypoxemia, or anemia. These factors are within the team's control if recognized early and treated aggressively. The multidisciplinary team is key to recognizing and treating primary and secondary head injury. The maintenance of optimal cerebral hemodynamics and cerebral perfusion can prevent neurologic dysfunction and secondary neurologic injury.

Cerebrai Hemodynamics Cerebral lschemia and Cerebral Blood Flow

Cerebral ischemia is a state of inadequate blood flow to the brain, leading to inadequate oxygenation. This state can occur because of an increase in cerebral oxygen consumption or because of a decrease in blood flow and oxygen delivery to the brain. 16 Cerebral oxygen consumption is the amount of oxygen consumed by the brain. Fever, seizures, and trauma increase oxygen consumption, whereas hypothermia and medications such as barbiturates decrease oxygen consumption. 62 Oxygen delivered to the brain is the product of two factors: (1) arterial oxygen content, which is the product of arterial oxygen saturation and hemoglobin and (2) cerebral blood flow (CBF). 14 • 62 CBF is determined by taking the perfusion pressure gradient across the brain and dividing it by the vascular resistance, or in other words, the CPP divided by cerebral vascular resistance (CVR). 46 CVR cannot be measured directly, but technology is being developed to determine a reliable method. CVR is altered by the effects of oxygen, carbon dioxide, and CPP. A low Pao 2 and a high Paco 2 cause cerebral vasodilation, increasing CBF. A low Paco 2 causes cerebral vasoconstriction :rnd a decrease in CBF. CRF is normally maintained at a constant rate because of alterations in CVR controlled by autoregulation.

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CPP is calculated by measuring the mean arterial pressure and subtracting mean ICP. Normal CPP in healthy adults is 50 to 150 mm Hg. 46 A CPP below 50 mm Hg causes a vasodilatory response in the arteries, leading to an increase in CBF. In the injured brain, Kelly has proposed that there is an alteration in the lower limit of autoregulation and that CPP levels of 60 to 70 mm Hg are needed to prevent the vasodilatory response and resulting increased ICP. 22 Kelly et al2 2 propose that CPP should be maintained at or above 70 mm Hg to reduce the risk of ischemia and control ICP. Rosner and Daughton have theorized that even in patients with intact autoregulation, CPP should be maintained above 70 mm Hg. In the event that CPP falls below 70 mm Hg, a vasodilatory response occurs, leading to increased CBF and ICP. Maintaining CPP above 70 mm Hg produces vasoconstriction and a reduction in ICP. 49 In summary, decreases in oxygen delivery can be caused by a variety of factors. CBF is reduced in the presence of a low CPP related to hypotension or intracranial hypertension as well as from a reduction in blood vessel diameter related to hypocapnia or vasospasm. Anemia, below a hemoglobin of 9 mg/dL, causes a reduction in oxygen-carrying capacity and delivery. 62 Hypoxia can also occur as a result of pulmonary complications such as pulmonary edema, atelectasis, and adult respiratory distress syndrome and results in a decrease in oxygen delivery.

Measuring Cerebral Oxygenation Measuring cerebral oxygenation is helpful in detecting episodes of cerebral hypoxia and ischemia. Cerebral oxygenation can be measured directly via implanted brain tissue oxygen sensors or indirectly via continuous measurement of jugular venous oxygen saturation. Monitoring techniques for direct measurement of brain tissue oxygenation are presently undergoing clinical trials. Investigators in Europe and in the United States are in the process of determining the best site for monitoring the oxygen, directly in the injured brain or at another location outside the injured area. The researchers are evaluating data to establish parameters indicative of tissue hypoxia

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and treatment strategies for abnormal values.19, 25, 35, 57, 59 The placement of a fiberoptic catheter into the internal jugular vein, which is positioned with the tip of the catheter near the jugular bulb, allows for measurement of global jugular venous oxygen saturation (Sjo2). Woodman and Robertson62 assert that Sjo2 measurement is a useful tool for detecting cerebral ischemia because it "reflects the balance between oxygen delivery to the brain and oxygen consumption by the brain." Situations that increase oxygen consumption or decrease oxygen delivery may be reflected in decreases in the Sjo2. Conversely, situations that decrease oxygen consumption or increase oxygen delivery may result in an increase in Sjo 2 . 62 The normal range for Sjo 2 is 55% to 71 %. 14· 53 An Sjo 2 less than 50%, a clinical situation known as cerebral oligemia or ischemia, is considered deleterious and has been associated with poor outcomes in studies. 18·48 In one study, the mortality in patients with jugular desaturations, defined as an Sjo2 less than 50% for a period lasting longer than 10 minutes, was compared with patients without desaturations. The group of patients without jugular desaturations had a mortality of 21%. Patients sustaining one episode of desaturation had a 37% mortality rate, whereas patients with multiple episodes of desaturation had a 69% mortality. 48 Common causes of cerebral oligemia include arterial hypoxia; anemia, which is defined as a hemoglobin less than 9 mg/ dL, hypocapnia, hypotension, intracranial hypertension, and cerebral vasospasm. 14· 62 The implications of poor outcome related to Sjo2 desaturations compel practitioners to monitor desaturations, diagnose their cause, and treat them aggressively. Proposed interventions related to increasing oxygen delivery include: (1) increased delivery of inspired oxygen; (2) increased carbon dioxide (Paco 2) levels; (3) transfusion of packed red blood cells; ( 4) enhancement of cerebral perfusion pressure and blood pressure with fluids and vasopressors; and (5) evaluation and treatment of cerebral vasospasm with transcranial dopplers, hypervolemic hypertensive hemodilutional therapy, and nimodipine. 51 · 62 Sjo 2 values greater than 75%, a clinical situation known as cerebral hyperemia, are indicative of an increase in cerebral blood flow relative to oxygen consumption. It may be

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indicative of a decrease or absence in oxygen extraction related to cerebral infarction. 53 An Sjo 2 greater than 75% may be associated with intracranial hypertension and increased cerebral edema. 53 The clinical implications of a high Sjo2 in the presence of increased ICP provides practitioners with possible interventions, such as hyperventilation, to reduce ICP. Lowering carbon dioxide below 35 mm Hg causes a decrease in blood delivery and a resulting drop in Sjo2 and ICP. Cruz has reported improved outcomes in patients managed with optimized hyperventilation and cerebral perfusion pressure (CPP) management when compared with a group treated with CPP therapy alone. 9 Understanding the concepts of brain injury and cerebral hemodynamics is essential to monitoring, intervening in, and evaluating care delivered to patients with severe TBI. Research related to medical and nursing interventions must be reviewed and applied to optimize patient outcomes.

lished articles related to severe head injury in adults with a GCS of 3 to 8. The members "used a meticulous process relying on scientific evidence rather than expert opinion." 5 Articles were reviewed and classified according to degrees of certainty and classification of evidence (Box 1). After classifying the articles, the information was collated into 14 topics (Box 2). The intent of the authors was to create guidelines emphasizing aspects of head injury management that would have the greatest impact on outcome. 5

Research Related to TBI and ICP In an effort to synthesize medical and nursing studies related to TBI and ICP, information

Box 1 CLASSIFICATION OF EVIDENCE AND DEGREES OF CERTAINTY USED BY AUTHORS OF TBI GUIDELINES Classification of Evidence

Evidence-Based Research AANS/Brain Trauma Foundation Guidelines The results of research conducted in head injury during the past 20 years have led to a better understanding of prima1y and secondary head injury. The studies related to secondary head injury raised an awareness in the neurosurgical community that the brain could suffer further damage after the initial event. 4· 5 The concept that the brain can be further damaged from delays in treatment; changes at the biochemical levels of the brain; and decreases in certain parameters, such as blood pressure, perfusion, oxygenation, carbon dioxide, and hemoglobin, increased practitioners' interest in examining current neurosurgical practices with respect to TBI. 5 On a national level, a study by Ghajar 17 demonstrated a variability in monitoring and treatment modalities among centers across the country. The results of this study and the failure in the past to develop guidelines that were purely objective in origin created a desire to establish research-based clinical guidelines. In a task force vras established of physicians with an academic expertise in head injury management. 5 The task force worked for 2 years reviewing pub-

Class I evidence: Class II evidence:

Class Ill evidence:

Prospective randomized controlled trials Prospectively collected data in clinical studies Retrospectively collected and analyzed data based on reliable data Types of studies: observational, cohort, prevalence, and case control Retrospective data collection Types of studies: clinical series, data bases, registries, case reviews, case reports, expert opinion

Degrees of Certainty Standards:

Guidelines:

Options:

"Represent accepted principles of patient management that reflects a high degree of clinical certainty" (pp 1-3) "Represent a particular strategy or range of management strategies that reflect a moderate amount of clinical certainty" (pp 1-3) "Are the remaining strategies for patient management for which there is unclear clinical certainty" (pp 1-3)

Data from Bullocl' R, Chestnut R, Clifton G, etal: Guide-

lines for the Management of Severe Head Injury. Brain Trauma Foundation/American Association of Neurological Surgeons, 1995.

KEEPll\JG THE BRA!l\J IN THE ZONE Box 2 SUMMARY: 14 TOPICS OF TBi GUIDELINES

X I. Trauma Systems and the Neurosurgeon Guideline: Organized trauma care systems should exist in all regions of the United States. Option: Neurosurgeons should be involved in planning, implementing, and evaluating care for patients with neurotrauma. II. Initial Resuscitation Option: Complete and rapid physiologic resuscitation should take place. Ill. Resuscitation of blood pressure and oxygenation Guideline: Hypotension and hypoxia must be avoided and treated. Option: Maintain mean arterial pressure> 90 mm Hg with a CPP > 70 mm Hg. IV. Indications for ICP Monitoring Guideline: ICP monitoring is indicated in TBI patients with an abnormal CT scan and GCS 3-8. ICP monitoring may be considered in patients with severe TBI if the patient's CT scan is normal and they have two of the following: age > 40 years, posturing, and hypotension (systolic BP < 90 mm Hg). V. ICP Treatment Threshold Guideline: Treatment of ICP should occur when ICP > 20-25 mm Hg. Option: Evaluating the patient's neurologic status and CPP data should coincide with treatment decisions of ICP. VI. ICP Monitoring Technology Recommendations: Ventricular catheters connected to an external transducer or with a fiberoptic transducer is the most reliable method of monitoring ICP. VII. Cerebral Perfusion Pressure (CPP) Option Maintain CPP > 70 mm Hg. VIII. The Use of Hyperventilation in the Acute Management of Severe TBI Standard: Chronic hyperventilation (Paco, 25 mm Hg or less) should be avoided after TBI if ICP is normal. Guideline: Prophylactic hyperventilation (Paco, < 35 mm Hg) in the first 24 hours should be avoided. Option: Hyperventilation may be used for short time periods in the event of worsening neurologic situations if all other methods to control ICP have been exhausted. Jugular venous oxygen saturation monitoring (Sjo 2 ) and cerebral blood flow monitoring may help to identify resulting cerebral ischemia from hyperventilation. IX. Use of Mannitol Guideline: Mannitol in doses of 0.25-1 g/kg is used for ICP control. Intermittent boluses may be more effective. Option: Mannitol can be used prior to ICP monitoring if the patient exhibits neurologic deterioration or transtentorial hernia-

XI.

XI I.

XIII.

XIV.

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lion; maintain se1·um osmolarity below 320 mOsm; maintain fluid replacement and euvolemia. Use of Barbiturates Guideline Patients with refractory intracranial hypertension in which all other medical and surgical therapies have failed to lower ICP may receive high-dose barbiturate therapy. Role of Glucocorticoids Standard: Glucocorticoids are not recommended for improving outcomes in severe head injury. Critical Pathway for the Treatment of Established lntracranial Hypertension A treatment algorithm which describes step-by-step interventions may assist the team in managing TBI patients. Nutritional Support of Brain-Injured Patients Guideline: Enteral or parenteral nutrition should be used to replace 140% of resting metabolism expenditure in nonparalyzed patients and 100% of resting metabolism expenditure in paralyzed patients. Option: Jejuna! feeding is preferred related to avoidance of gastric intolerance and ease of use. Antiseizure Prophylaxis Standard: Preventing late post-traumatic seizures using phenytoin, carbamazepine, or phenobarbitol is not recommended. Option: May consider use of anticonvulsant for patients at high risk for early posttraumatic seizures.

BP = blood pressure: CPP = cerebral perfusion pressure: GCS = Glasgow Coma Scale: ICP = intracranial pressure; TBI = traumatic brain injury Data from Bullock R, Chestnut R, Clifton G, et al: Guidelines for the Management of Severe Head Injury. Brain Trauma Foundation/American Association of Neurological Surgeons, 1995.

will be formatted in phases of care and prioritized according to treatment strategies. The recommendations described in the Severe Head Injury Guidelines will be integrated into the appropriate sections.

Resuscitation: Prehospital, Emergency, and Operating Room The first section of the guidelines, Guideline I, presented data on patient outcomes related to trauma systems. The summarized data revealed that regions of the count1y with organized trauma systems have experienced a reduction in mortality in patients sustaining major trauma. 0 A recent study in Canada ex-

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plored the impact a dedicated clinical trauma service, revised standardized trauma protocols, and dedicated trauma nursing unit had on length of stay, costs, and mortality compared with the data collected from patients managed prior to the changes. Prior to 1996, the old style of managing the trauma patients used a compartmentalized care model with little coordination of care. The new changes produced a decrease in length of stay, decrease in costs, and an improved survival. ss To develop well planned trauma responses for head-injured patients, neurosurgeons should be a part of the team planning and integrating treatment interventions for the head trauma population. On arrival at the scene of the injury, the patient should be rapidly assessed for the ability to maintain a patent airway and for the presence of breathing. Securing an airway must occur simultaneously with stabilization of the spine. Once the airway is established or protected, breathing is supported using 100% oxygen. Hypoxia must be avoided because of its deleterious effects on outcome. Circulation is assessed by checking blood pressure, pulses, capillary refill, and skin signs and fluid resuscitation is initiated with intravenous access. Hypotension has been associated with increased morbidity and mortality in a munber of studies and must be rapidly identified and treated. 8· 13• is, 32 · 36- 37 Guideline III recommends aggressive management of hypoxia and hypotension (see Box 2). A brief neurologic assessment is included in the primary survey. Conducting the secondary survey provides for the comprehensive examination and includes identification of level of consciousness, neurologic signs of inju1y, and other multisystem injuries. Personnel at the scene should obtain information on mechanism of injury. Communication with a base station emergency department will facilitate the transmission of pertinent information to the receiving trauma center. On arrival at the receiving center, the headinjured patient is rapidly assessed by the trauma surgeon and interventions are implemented by the trauma team. Rapid physiologic resuscitation is recommended (Guideline II, see Box 2). Airway patency and adequate ventilations are assessed first. Headinjured patients with a GCS between 3 and 8 are candidates for endotracheal intubation.

Box 3 RAPID SEQUENCE INTUBATION PROTOCOL 1. Assist with ventilations using a 100% F10 2 by way of a non-rebreather mask if effective ventilatory effort is present or by bag-valvemask if ventilatory effort is ineffective or absent. 2 Apply cardiac monitor, pulse oximetry, and obtain blood pressure. Establish IV lines. 3. Set up suction and prepare intubation equipment. 4. Medication sequence and airway support: a. T - 5 minutes: Administer lidocaine 1.5 mg/ kg \VP (hold for seizures or complete heart block). b. T - 1 minute: 1) Administer etomidate 0.3 mg/kg \VP (induction agent lasts 8-15 minutes) 2) Apply cricoid pressure (unless contraindicated). Maintain assisted ventilations and cervical spine stabilization. 3) Consider atropine 0.02 mg/kg in pediatric patients < 8 years of age if bradycardic. c. T - 0: Administer choice of paralytic. d. T + 30 seconds: Check for jaw relaxation and intubate. e. Confirm tube placement with capnography, mist tube, and assess breath sounds. f. T + 5-8 minutes: Sedate as necessary with midazolam 0.1 mg/kg IV or lorazepam 0.01-0.05 mg/kg IV and consider analgesia with morphine sulfate 0.050.1 mg/kg IV. 5. Assess pulse oximetry and capnography. Monitor vital signs. 6. Document medications and patient tolerance in chart. IV = intravenous; IVP = intravenous push Courtesy of Mission Hospital Regional Medical Center, Mission Viejo, CA.

Specific criteria for intubation in the headinjured patient include the following: inability to maintain a patent airway, inability to maintain adequate ventilations, and inability to speak and follow commands. 22 Endotracheal intubation, or laryngoscopy and tracheal intubation, produces a noxious stimulation resulting in increased agitation, increased blood pressure, and increased ICP, which could further worsen a head-injured patient's status.10· 54 In addition, head-injured patients are at risk for aspiration if they have a full stomach. The risks associated with endotracheal intubation can be minimized by using a rapid

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sequence intubation protocol incorporating timed techniques and medications that help reduce the effects of the noxious stimulation. Rapid sequence intubation is a technique that uses rapid sedation and paralysis to facilitate intubation. A recent study found that 166 patients undergoing emergent endotracheal intubation with sedation and paralytics had no incidence of aspiration, airway trauma, or death. 28 The study compared the rapid sequence intubation group to 67 patients undergoing intubation without paralysis. The second group sustained the following complications: aspiration (15%), airway trauma (28%), and death (3%). 28 Supporting the airway with 100% oxygen delivered by bag-valve-mask ventilations is essential. Cricoid pressure is used during intubation to protect against regurgitation of gastric contents and to facilitate passage of the endotracheal tube into the tracheal opening. 11 Cervical spine stabilization must be maintained to reduce the risk of further injury in patients with cervical spine instability. Medications may be useful in blunting the effects of intubation. Lidocaine is used routinely as a pretreatment medication by a large number of centers as reported in a study by Silber. 51 Two theories related to lidocaine's actions on tracheal stimulation is its ability to block activation of local receptors in the airways and to inhibit centrally mediated responses that increase ICP in reaction to the noxious stimuli. 3 Sedative-hypnotic agents, such as thiopental and etomidate, are helpful to reduce or blunt the effects on ICP and reduce the cerebral metabolic usage of oxygen.<>. 22 Administration of these agents should take place 60 seconds prior to the administration of a neuromuscular blocker (NMI3). Both thiopental and etomidate are short acting, so supplemental sedation with midazolam within 10 to 15 minutes of administration can be helpful to maintain sedation. The choice of the NMB agent rests with the physician. The most frequently used NMBs are succinylcholine, vecuronium, atracurium, mivacurium, and rocuronium. 30· 54 All produce muscle relaxation and facilitate endotracheal intubation. Agents with the faster onset, for example, succinylcholine and rocuronium, are usually preferred. 30 54 The administration of analgesic agents, such as morphine sulfate or fentanyl, along with supplemental sedation

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is helpful to reduce further increases in ICP during the resuscitation. 22 An example of an RSI protocol used in one institution is illustrated (Box 3). Once the airway is secure, correct ventilatory management is key to decreasing ICP and maintaining cerebral blood flow. As stated earlier, a Paco 2 less than 35 mm Hg produces cerebral vasoconstriction and a resulting decrease in cerebral blood flow. 47 By decreasing the amount of blood flow to the head, the ICP will decrease. If ICP were the only variable affected by a low Paco 2, hyperventilation would prove beneficial. Studies examining cerebral blood flow after TBI have shown that CBF is at its lowest for the first 24 hours after brain injury. 2• 10 · 31 Hyperventilation in this situation could produce secondary injury related to low flow. Muizelaar ct al 41 studied the effects of hyperventilation in headinjured patients. The study found that those patients undergoing hyperventilation, defined as a Paco 2 25 ± 2 mm Hg for 5 days, had poorer outcomes at 3 and 6 months than the group with Paco 2s maintained at 35 ± 2 mm Hg. 41 Study results related to hyperventilation in TBI led to the recommendation, Guideline VIII, to use this modality only in certain clinical situations (see Box 2). Patients sustaining acute neurologic deterioration or increased ICP refractory to medical therapies may be candidates for hyperventilation for brief periods or longer. 5 Accompanying this statement was a recommendation to monitor Sjo 2, arterial-jugular venous oxygen content differences, or cerebral blood flow if hyperventilation must be used. By using these monitoring techniques, desaturations in cerebral oxygenation or abnormal cerebral blood flow could be detected and hyperventilation therapy could be adjusted to balance treatment of ICP and adequate cerebral oxygenation. In the prehospital scenario, hyperventilation in the presence of transtentorial herniation is acceptable for a brief period until definitive treatment is available and implemented. Maintaining an adequate cerebral perfusion is paramount in the resuscitative period to avoid hypotension. Guidelines III and VII support the concept of maintaining an adequate cerebral perfusion pressure of 70 mm Hg. Before the placement of an ICP monitor, the resuscitation team should establish a goal to maintain the mean arterial pressure (IVIAP)

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at greater than 90 mm Hg. Recommendations for fluid resuscitation include the administration of 0.9% normal saline, blood products, and colloid solutions. 9· 22 • 49 Normal saline is generally recognized as the fluid of choice, although some clinicians may prefer colloids such as albumin. 9· 22 ·49 In the event the patient is volume loaded, additional enhancement of blood pressure can be achieved with the use of vasopressors such as phenylephrine, dopamine, or norepinephrine. The ability to monitor adequate fluid resuscitation is enhanced with the placement of arterial and pulmonary artery catheters. Goals for adequate fluid volume resuscitation include a central venous pressure (CVP) between 5 and 10 mm Hg or pulmonary capillary wedge pressure (PCWP) of 10 to 15 mm Hg. 22 The use of analgesics, NMB, and sedative agents is useful in managing increases in ICP during intubation and is helpful when trying to limit ICP increases during the resuscitation. Mannitol is another medication used to reduce ICP (see Guideline IX in Box 2). Mannitol acts to increase preload and perfusion pressure, decrease hematocrit and blood viscosity, and increase cerebral oxygen delivery.42 Because of its diuretic effect, concurrent assessment of fluid volume is important. Fluids are replaced as needed to maintain euvolemia. While rapid interventions to stabilize airway, breathing, circulation, and ICP are implemented, a secondary survey is completed to determine the presence of other injuries. Interventions such as placement of an indwelling Foley catheter and nasogastric tube are completed. Cervical spine and chest radiographs are generally completed in the emergency department. A CT scan of the brain follows. If an abnormality is seen on the CT scan requiring surgery or there is a need to monitor ICP, the patient is transported to the operating room for surgical intervention. Placement of an ICP monitor is indicated in patients sustaining severe TEL Bader et al 1 proposed that ICP monitors should be placed in the operating room to limit the risk of infection. The indications for monitoring and the most accurate type of ICP catheters are described in Guidelines IV and VI (see Box 2). the r::comOnce the r11onitor is in mended threshold for ICP treatment is 20 mm Hg, although a range of 20 to 25 mm Hg is cited in Guideline V (see Box 2). 5· 6

Priorities in the operating room focus on maintaining adequate oxygenation, ventilation, and perfusion and reducing ICP. Immediate airway and hemodynamic goals include 0 2 saturation greater than 94%, Paco 2 30 to 35 mm Hg, and MAP greater than 90 mm Hg. Placement of an Sjo 2 catheter and monitor is helpful to monitor the effects of therapy in the operating room. Anesthetic agents that reduce the cerebral metabolic usage of oxygen (CMR0 2) and ICP are used to assist with control of ICP. Thiopental, etomidate, and propofol are common agents used for induction of anesthesia. 33 Adjunctive medications such as inhalation agents, narcotics, barbiturates, propofol, and NMB are used to maintain anesthesia and airway control.33 Establishing an organized approach to managing patients with TEI enhances the resuscitative efforts by the team (Box 4). Setting physiologic goals helps to coordinate multidisciplinary interventions. Ensuring the rapid movement of the patient through the system is paramount. Once operative interventions are completed, the patient is transferred to the intensive care unit for definitive care. Repeat CT scanning is often performed during transfer, assessing the results of surgery and possible progression of pathology. Scanning at this time often avoids the need to mobilize critically ill patients from the ICU after they have been stabilized.

Intensive Care Unit Management Transition of the patient from the resuscitation phase to the ICU phase can be challenging. Reassessment of oxygenation and ventilation must take place. Oxygenation and ventilation are maintained via mechanical ventilation. The Fro 2 delivered is based on Pao 2 and arterial oxygen saturation. Titration of the Paco 2 levels is dependent on many factors. When ICP is less than 20 mm Hg, Paco 2 levels are maintained at or above 35 mm Hg. In the event ICP is elevated, Sjo2 must be assessed to determine if lowering Paco 2 is possible. If the Sjo 2 is more than 55%, hyperventilation can be used to lower ICP. If the Sjo 2 levels is less than 55%, hyperventilation should not be used because it will result in further decreases in cerebral blood flow. Maintaining airway clearance requires suctioning when secretions interfere with oxy-

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Box 4 MANAGING PATIENTS WITH TBI RESUSCITATION PHASE ALGORITHM ED Priorities Intubate/oxygenate/ventilate Use RSI protocol: Lidocaine, etomidate, neuromuscular blocker, morphine sulfate, and midazolam Maintain Sao 2 > 94%/Pao2 > 60 mm Hg and Paco 2 35 mm Hg Ensure spine stabilization/maintain neck in neutral position IV access/fluid resuscitation Maintain MAP > 90 mm Hg Use 0.9% NS or 5% albumin for euvolemia Use dopamine/phenylphrine for BP support Place arterial line access Obtain C-spine/chest radiographs Rapid CT scan of brain Administer mannitol 0.25-1.0 g/kg IV for signs of increased ICP OR Priorities Maintain Sao2 > 94%/Pao 2 > 60 mm Hg and Paco 2 30-35 mm Hg Maintain MAP > 90 mm Hg with fluids, blood products, and vasopressors Place central access and consider PA catheter Place Sjo 2 catheter Sedation/analgesia to reduce ICP/CMR02 Use propofol for ICP control if patient normotensive Place ventriculostomy/ICP monitor CMR02 = cerebral metabolic usage of oxygen; MAP = mean arterial pressure; Sao2 = arterial oxygen saturation; Sjo, = global jugular venous oxygen saturation Courtesy of Mission Hospital Regional Medical Center, Mission Viejo, CA.

genation and ventilation. Nursing research studies have demonstrated that ICP increases with endotracheal suctioning. 23 • 43 • 52· 56 Strategies to blunt the untoward effects of suctioning on ICP include (1) administering medications before the procedure (i.e., lidocaine, opiates, and NMB); (2) using hyperoxygenation with 100% oxygen before suctioning; and (3) limiting the suctioning attempts to twice. The use of aggressive hyperventilation for short periods during the suctioning procedure has been examined by Kerr et al and found to limit increases in ICP. 24 Before the routine acceptance of this practice, the effects of hyperventilation on blood flow must be examined further to ensure there are no episodes of cerebral desaturations or ischemia.

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Assessment of cerebral perfusion and intracranial hemodynamics is accomplished by using invasive hemodynamic monitoring tools, that is, arterial, pulmonary artery, and Sjo2 catheters. CPP requires monitoring MAP and ICP. A minimum CPP of 70 mm Hg is desirable in patients with intact autoregulation. When interventions are needed to raise CPP, the CVP, PCWP, systemic vascular resistance (SVR), stroke volume, and cardiac index must be assessed. Preload is increased through the administration of fluids to a PCWP of 10 to 15 mm Hg. Afterload is assessed by way of SVR and is manipulated with vasopressors if it is low and vasodilators if it is high. Contractility is reflected in stroke volume, and enhancement is accomplished with agents such as dobutamine. Optimizing CPP is imperative for maintaining cerebral blood flow. Assessment of Sjo2 reflects oxygen delivery and consumption. Sjo 2 assessment must coincide with assessment of ICP and other factors. Strategies to raise a Sjo2 that is less than 55% include increasing Fro 2; raising Paco 2 levels; increasing blood pressure via fluids or vasopressors; administering medications to decrease CMR0 2 , such as lorazepam, morphine sulfate, NMB, propofol, and barbiturates; administering mannitol to increase perfusion pressure and oxygen delivery; and reducing factors related to increased CMR0 2 such as fever and fighting the ventilator. A strategy to lower a Sjo2 greater than 75% is hyperventilation resulting in lower Paco 2 levels. Selecting the correct interventions requires careful consideration of multiple parameters. Maintenance of an ICP less than 20 mm Hg is desirable (see Guideline V in Box 2). Assessment of the ICP waveform provides insight into the compliance of the brain. The pulse waveform produced by an ICP has a Pl, P2, and P3 wave. A brain is said to be compliant if the PlP2P3 waveform looks like a descending staircase. If P2 increases and is higher than the first Pl wave, the brain is said to have a loss of compliance. 16 In patients with an intraventricular ICP catheter, drainage of CSP can lower ICP. Hyperventilation, used in conjunction with Sjo 2 assessment, and enhancement of MAP to increase CPP greater than 70 mm Hg, reduces ICP as discussed previously. Maintenance of neutral neck and body position, the administration of certain

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medications, control of stimulation and care activities, and thermoregulation are additional interventions used to control ICP. Neck and body position has been studied by a number of researchers to determine the effects of turning the head and body and elevating the head on ICP. Venous blood flow from the brain to the heart is affected by turning the neck 45° to 90°. The neck turning causes ICP to increase because of compression of the internal jugular vein. 29 · 52 • 60 • 61 ICP may increase with turning or flexing the body. 27 • 3s, 39 • 61 Positioning the head of bed up to 30° decreases ICP. Fluid volume status must be considered, and patients should be euvolemic when elevation takes place. In patients with hypovolemia, the head of bed should remain flat because of untoward effects of hypotension when the bed is elevated. 6 A variety of medications is helpful in reducing or controlling ICP. Morphine sulfate, as continuous intravenous (IV) infusions between 5 and 10 mg/h, assists with analgesia and depresses airway reflexes stimulated during suctioning. 6• 22 Continuous IV infusions of sedative agents, lorazepam, or midazolam, reduce agitation and help control ICP. NMB agents provide chemical paralysis and mitigate increases in ICP caused by suctioning, increased motor tone, shivering, or fighting the ventilator. 6• 22 • 23 Propofol and barbiturates act to decrease CMR0 2 and ICP, although in high doses they can lower MAP. 6 The advantage of propofol is that the drug has a shorter half-life than barbiturates and can be titrated off rapidly. 44 Barbiturates are considered useful in situations when all medical and surgical therapies have failed to control ICP (see Guideline X in Box 2). The choice of medications depends on the specific indication or need. Some agents will eliminate the neurologic examination. Most often, the patient with TEI receives a combination of medications to control ICP. One medication no longer recommended in the treatment of the TBI population is glucocorticoids (see Guideline XI in Box 2). This standard statement is based on the lack of evidence that glucocorticoids improve outcome in head injury. Control of the patient's environment includes reducing external stimulation, spacing nursing activities, and controlling the effects of noxious stimuli produced from suctioning

and care activities. Controlling external stimulation such as lights and noise may reduce ICP. In some studies, environmental noise and conversation increased ICP. 39• 56 Other studies exploring family presence, auditory stimuli, or conversation found that they did not affect ICP. 20 · 45 • so, 58 The spacing of nursing activities provides the patient time to recover from any adverse events or stimulation. Monitoring patient's responses to stimulation allows the practitioner to evaluate individualized reactions. Adjustments in the environment may help control ICP elevations. Hyperthermia increases CMR0 2 and adversely affects outcome. 22 Maintaining normothermia, maximum of 37.5°C, is paramount. The use of acetaminophen, cooling blankets, and fans helps to offset any increases in temperature. Mild hypothermia may be desirable in TBI, but research is still underway to determine the efficacy of hypothermia. Ensuring support of body systems is important for reducing morbidity associated with brain injury. Aggressive pulmonary hygiene with suctioning, vibration, and repositioning (including special beds) and the use of inline treatments with bronchodilators help to prevent pulmonary complications. Supporting nutritional needs in the TEI population is beneficial (see Guideline XIII in Box 2). The use of enteral nutrition or parenteral nutrition contributes to wound healing, improved weaning from mechanical ventilation, maintenance of gut function, and reducing infection. 22 The use of support stockings and pneumatic compression boots may reduce the risk of deep vein thrombosis. 22 Maintenance of skin integrity and muscle tone and position helps reduce the complications of immobility. Prevention of early seizures with anticonvulsants is indicated, but the continued use of anticonvulsant therapy for the prevention of late seizures is not recommended (see Guideline XIV in Box 2). The integration of the care priorities and recommendations into a clinical pathway, protocol, or guideline ensures a standardized approach to patients with TEI (see Guideline XII in Box 2). An algorithm representing the management priorities during the ICU phase, which incorporates considerations of ICP and Sjo 2, is described (Fig. 1). Psychologic support of the patient, family, and significant others is imperative during all

KEEPING THE BRAIN IN THE ZOf\IE

I

423

1. Position Head of Bed 30° if euvolemic 2. Reduce environmental stimulation 3. Drain CSF for ICP >20 mm Hg

4. Monitor Sjo2 5. Maintain Paco 2 35 mm Hg 6. Target CPP Therapy >70 mm Hg 7. If MAP/CVP/PCWP is low with CPP <70 a. 5% albumin/NS 500 mL until CVP 5-10 mm Hg/PCWP 10-15 mm Hg b. Use phenylphrine/dopamine to increase CPP >70 mm Hg once volume loaded 8. Continuous Ativan 0.01-0.05 mg/kg N for sedation 9. Continuous MS 3-8 mg/h for analgesia l 0. Use NMB for paralysis as indicated 11. Maintain Temperature 36-37°C. Treat fever aggressively

12. If ICP continues >20 mm Hg and/or Sjo2 <55%, see below

I ICP >20 & Sjo 2 >55%

ICP >20 & Sjo 2 <55%

*Decrease Paco 2 to keep Sjo 2 >55

1' Increase

* Mannitol 0.25-1.0 g/kg IV;

* Optimize Hgb >9

keep serum osmo <320; give fluids *Titrate propofol 10-100 µ,g/kg/min

Paco 2 to keep Sjo 2 >55%

*Allow Paco 2 to rise till Sjo 2 >55% or ICP >20

* Increase F102 as needed

* Optimize Hgb >9

., Mannitol 0.25-1.0 g/kg IV

* Mannitol 0.25-l.O

*Add barbituates at 50 mg/h

keep serum osmo <320; give fluids

* Wean propofol and increase

·'Titrate propofol 10-100 µ,g/kg/min

barbiturates to l-3 mg/kg/h

ICP >20 & Sjo2 <55%

g/kg IV; keep serum osmo <320; give fluids

* Add barbiturates at 50 mg/h

* Titrate propofol

* Wean propofol and increase

* Add barbiturates

barbiturates to l-3 mg/kg/h Figure 1 Management of traumatic brain-injured patients: ICU phase algorithm. NS = normal saline; MS = morphine sulfate. (Courtesy of Mission Hospital Regional Medical Center, Mission Viejo, CA)

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BADER and PALMER

phases of care. Preparation of the family and significant others for the patient's emergence from come and potential temporary or permanent disabilities is essential. The patient's transition from coma to arousal and awareness is monitored closely by the team. Ongoing interventions to support body systems are completed. Following the critical phase of care, the patient is assessed for neurologic deficits and systemic effects of the injury by the multidisciplinary rehabilitation team. Placement of the patient in acute rehabilitation or a skilled nursing care facility will be based on this assessment and tolerance to therapy.

Results of Application of Algorithms to Practice At a trauma center in the west, the transition of the severe head injury guidelines to clinical practice was accomplished following multidisciplinary meetings held to review current practices and discuss the recommendations made in the document. A review of the literature enhanced the team's knowledge of current studies related to head injury. The team sought out information on the technology of Sjo 2 monitoring and brought the catheters into the hospital for use with head-injured patients with severe injuries. Construction of a clinical guideline document and associated algorithms was based on the information presented. Education of all disciplines by the neuroscience clinical nurse specialist and neurosurgeons assisted in the dissemination of the new guidelines. Twenty-four-hour

support for the trauma team was provided by the neuroscience clinical nurse specialist. Treatment decisions were discussed by all disciplines, and a multidisciplinary integrated approach was implemented. Each phase of the trauma patient's care was carefully monitored and reviewed. A small group of ICU nurses and the neuroscience clinical nurse specialist developed critical thinking algorithms to assist the bedside nurse with decision making because multiple parameters had to be considered prior to an intervention. A retrospective and prospective review of 3479 trauma records was undertaken to compare data on patients with severe TBI admitted to the trauma center prior to and following the implementation of the clinical guidelines. Inclusion criteria for patient selection required admission GCS 3 to 8 or deterioration from a higher GCS within 48 hours of admission and CT scan changes indicative of brain injury; presence of ICP monitoring; age greater than or equal to 8 years; and closed head injury. Exclusion criteria for the study included patients less than 8 years of age; penetrating head injury; patients pronounced brain dead or those who died within 24 hours of admission; and patients with GCS 3 to 8 and absence of CT or clinical examination evidence of injury, positive ETOH and absence of injury, or post-ictal period on admission with absence of injury. Trauma records of 1937 patients fromJanuary 1, 1994 to June 1997, the pre-TBI guidelines group, were reviewed, which resulted in a sample of 37 patients meeting inclusion criteria. Trauma records of 1542 patients from June 1997

Pre-TBI Guidelines

Post-TBI Guidelines

Indicator

1/94-6/97

6/97-12/99

Number of Patients Average Age Sex: Male/Female Mean Admit GCS Mean ISS Scores Mean ICP Days Mean Ventilator Days Mean ICU Length of Stay Mean Hospital Length of Stay Mean Charges

37 41.35 y 33/4 6.4 32.82 9.97 17.46 21 03 24.35 $196,128.00

54 38 y 43/11 6.7 28.27 11.1 18.8 21.6 25.2 $285,927.00

GCS = Glasgow Coma Scale; ICP = intracranial pressure; TBI = traumatic brain injury; ISS = Injury Severity Score

KEEPING THE BRAIN IN THE ZONE

to December 1999, the post-TBI guideline group, were reviewed and resulted in 54 patients meeting criteria. The two groups' mean GCS, age, mean ICP days, mean ventilator days, and mean ICU and hospital length of stay were similar (Table 1). Outcomes at 6 months were classified according to the Glasgow Outcome Scale (GOS). The scale rates outcome as follows: GOS 5 = good outcome; GOS 4 = moderate disability; GOS 3 = severe

OUTCOME PRE-TBI GROUP (n = 37) 1994 (n = 10) 1995 (n = 9) 1996 (n = 14) 1997 (partial) (n = 4) Percentage Totals POST-TB! GROUP (n

GOS

=

Glasgow Outcome Scale; TBI

=

disability; GOS 2 = persistent state; and GOS 1 = death. The group managed with the new guidelines, post-TBI guidelines group, had improved outcomes compared to the prc-TBI guidelines group (Table 2). Data are being collected and analyzed on an ongoing basis. Changes in practice will be recommended and implemented by the TBI multidisciplina1y team based on the data results and new scientific literature.

GOS 4-5

GOS 2-3

GOS 1

2

3 5

4 2 4

1

4 4 5 3

27.03%

29.73%

43.24%

5

3 5 1

= 54)

1997 (partial) (n = 9) 1998 (n = 22) 1999 (n = 23) Percentage Totals

425

6 12 20 70%

2 13%

17%

traumatic brain injury

Providing care to the TBI patient population with severe injuries requires an integrated multidisciplinary approach. The team in clinical practice must be willing to examine its own practice, seek out the latest information on TBI, and critically analyze the information. Members must be open to changing their own practice when the data presented support change. Interventions based on scientific evidence provide a strong foundation for delivering care. The standardization of these interventions into protocols facilitates team communication and coordination. Measuring outcomes is imperative for evaluating the effectiveness of current treatment algorithms. Changes in treatment practice should be based on the measured outcomes and advances in the scientific literature.

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Address reprint requests to Mary Kay Bader, MSN, RN, CCRN, CNRN 15 Las Alforjas Rancho Santa Margarita, CA 92688 e-mail: [email protected]