Critical Care Management of Traumatic Brain Injury

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CHAPTER 334 Critical Care Management of Traumatic Brain Injury

Claudia Robertson, Leonardo Rangel-Castilla

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Every year, about 1.5 million affected people die and several millions receive emergency treatment after TBI. Fatality and disability rates depend on the severity and mechanisms of the TBI, but unfavorable outcomes (death, vegetative state, and severe disability) can occur in more than 20% of affected patients after TBI.¹

The damage to the brain that occurs after traumatic injury is usually divided into two general types, primary and secondary (Fig. 334-1). The primary injury occurs before arrival at the hospital and, other than trauma preventive programs, cannot be modified by the physicians treating the individual patient. The severity of the primary injury, however, can be classified and quantified for prognostic purposes, and the primary injury often initiates a cascade of secondary injury processes that evolve over the first few postinjury days. Individual characteristics, including age, preinjury health, and certain genetic factors, can also alter the primary injury and subsequent response to the injury. For example, the ε4 allele of the apolipoprotein E gene is a genetic variant that has been associated with a worse outcome after TBI.² The injured brain is exquisitely sensitive to ischemia, and secondary ischemic insults can additionally damage the brain. Pharmacologic treatment of these secondary injury processes and modern emergency and critical care management to prevent secondary ischemic insults are the primary goals of the early treatment of TBI.

FIGURE 334-1 The outcome after traumatic brain injury is determined by a number of factors, including the severity and type of the primary injury, which initiates secondary injury processes and causes the injured brain to be more susceptible to secondary ischemic insults. BP, blood pressure; CaO₂, arterial concentration of oxygen; CBF, cerebral blood flow; ICP, intracranial pressure.

The science of pharmacologic treatment of the secondary injury processes involved in TBI is still in its infancy. Although a large number of injury mediators have been identified in experimental studies, treatment with agents that block these known injury mediators has not been demonstrated to improve neurological outcome in clinical studies. Corticosteroids, calcium channel blockers, free radical scavengers, N-methyl-D-aspartate (NMDA) receptor antagonists, hypothermia, and others have all been tested in large multicenter clinical trials, without significant improvement in outcome.

As a result, the outcome after severe head injury at the present time depends to a large extent on anticipation, recognition, and early treatment of secondary ischemic insults. Intensive care monitoring offers the opportunity to rapidly identify and therefore treat the secondary posttraumatic insults that may impair ultimate recovery. Modern intensive care management techniques attempt to provide the optimal environment for the injured brain to recover.

History of Head Trauma Management

Coma Data Banks

Systematic, multicenter efforts to study the management of TBI began in the 1970s. Initially, this work took the form of observational studies. Two large databases of prospectively collected clinical information resulted from this early interest and contributed scales for grading the neurological examination and computed tomography (CT) scan. Analyses of databases collected during large clinical trials in TBI patients have subsequently provided confirmation of most of the early findings, as well as updated prognostic scales.

The International Data Bank, which consisted of prospectively collected clinical information on 1000 comatose patients from three centers in Scotland, the Netherlands, and the United States, was reported in 1979.³ These investigators developed simple but practical scales for the assessment of coma (the Glasgow Coma Scale [GCS], Table 334-1) and for the assessment of neurological outcome (the Glasgow Outcome Scale [GOS], Table 334-2) and presented some of the early work on factors that determine outcome after neurological injury.^4,⁵ It was apparent from these studies that the outcome after severe head injury was dependent on the severity and type of the primary injury.

TABLE 334-1 Glasgow Coma Scale for Assessment of Coma and Impaired Consciousness

EYE OPENING	BEST MOTOR RESPONSE	BEST VERBAL RESPONSE
4 = Spontaneous	6 = Obeying	5 = Oriented
3 = To speech	5 = Localizing	4 = Confused
2 = To pain	4 = Withdrawing	3 = Inappropriate
1 = None	3 = Flexing	2 = Incomprehensible
	2 = Extending	1 = None
	1 = None

Data from Teasdale G, Jennett B. Assessment of coma and impaired consciousness. Lancet. 1974;2:81-84.

TABLE 334-2 Glasgow Outcome Scale (Original 5-Point Scale and Extended 8-Point Scale) for Assessment of Outcome

SUMMARY	GLASGOW OUTCOME SCALE	EXTENDED GLASGOW OUTCOME SCALE
	1 = Dead	1 = Dead
Sleep/awake, nonsentient	2 = Persistent vegetative state	2 = Persistent vegetative state
Conscious but dependent	3 = Severe disability	3 = Lower severe disability
		4 = Upper severe disability
Independent but disabled	4 = Moderate disability	5 = Lower moderate disability
		6 = Upper moderate disability
May have mild residual effects	5 = Good recovery	7 = Lower good recovery
		8 = Upper good recovery

Data from Jennett B, Bond MR. Assessment of outcome after severe brain damage. Lancet. 1975;1:480-484; and Wilson JT, Pettigrew LE, Teasdale GM. Structured interviews for the Glasgow Outcome Scale and the extended Glasgow Outcome Scale: Guidelines for their use. J Neurotrauma. 1998;15:573-585.

The Traumatic Coma Data Bank (TCDB) consists of prospectively collected clinical data on 1030 comatose patients from four centers in the United States.⁶ As part of this study, reported initially in 1991, and work from other individual head injury centers, the critical role of prehospital insults such as hypoxia and hypotension, the importance of prompt evacuation of intracranial mass lesions, and the importance of intracranial hypertension were more clearly identified.⁷^–⁹ In addition, a new classification of the primary injury based on CT scan findings (the Marshall CT classification) was developed from the TCDB data.¹⁰

The International Mission for Prognosis and Clinical Trial (IMPACT) database contains the data collected from most TBI clinical trials conducted over the past 20 years. The database contains information on 9205 patients with severe and moderate TBI from eight randomized placebo-controlled trials and three observational studies. The major emphasis during the first phase of the study was on information from the time of injury to the postresuscitation period and outcome at 6 months, thus providing a unique resource for prognostic analysis.¹¹ Using univariate and multivariate analysis, it was found that the most powerful independent prognostic variables were age, GCS motor score, pupil response, CT scan characteristics (including the Marshall CT classification) traumatic subarachnoid hemorrhage (SAH), and prothrombin time. Other important prognostic factors were hypotension, hypoxia, the eye and verbal components of the GCS, glucose, platelets, and hemoglobin. These results suggest the need for further research, including evaluation of the clinical impact of intervening aggressively to correct abnormalities in hemoglobin, glucose, and coagulation. The combination of prognostic factors also provides a solid foundation for estimation of the probability of each GOS category at 6 months for individual TBI patients.¹²

Traumatic Brian Injury Guidelines

In 2007, a joint undertaking of the Brain Trauma Foundation and the American Association of Neurological Surgeons (AANS), the Congress of Neurological Surgeons (CNS), and the AANS/CNS Joint Section on Neurotrauma and Critical Care updated evidence-based guidelines for the management of severe TBI.^13,¹⁴ In this third edition, six new topics were added and two were assigned to the prehospital guidelines. The levels of recommendation were changed from “standard, guideline, and option” to “level I, level II, and level III,” respectively. The purpose of the guidelines was to provide not only a road map for improving treatment but also a template for future research so that a sufficient body of class I and II studies for level I and II recommendations in the fourth edition could be generated. The main recommendations from the third edition of the “Guidelines for the Management of Traumatic Brain Injury” are summarized in Table 334-3.

TABLE 334-3 Summary of the Third Edition Guidelines for the Management of Severe Traumatic Brain Injury, 2007

See also Appendix 334-E1 online for a blank set of neurosurgical intensive care unit [ICU] admittance orders.

Multicenter Clinical Trials

Laboratory studies have provided a better understanding of the basic mechanisms of secondary injury to the brain after trauma. Anticholinergic agents, corticosteroids, calcium channel antagonists, free radical scavengers, NMDA receptor antagonists, bradykinin antagonists, and moderate hypothermia have all been studied in experimental head injury models and found to have beneficial effects. A number of potentially beneficial therapies derived from these laboratory studies have been tested in phase III clinical trials. As reviewed by Bullock and associates, a number of pitfalls can be encountered in taking a treatment from the laboratory to a successful clinical trial.¹⁵

The heterogeneity of TBI is considered one of the most significant barriers to translating effective therapeutic interventions from the laboratory to the clinical setting. The National Institute of Neurological Disorders and Stroke, in collaboration with other associations, including the Brain Injury Association of America, convened a workshop to outline a classification system for TBI. They proposed that a new multidimensional classification system be developed for TBI clinical trials and that preclinical models are vital in establishing the pathophysiologic mechanisms relevant to specific pathoanatomic types of TBI. Evaluation of targeted therapies for specific pathoanatomic lesions will probably require the inclusion of less severely injured patients with more homogeneous injuries.¹⁶

Pathophysiology of Traumatic Brain Injury

Primary Brain Injury

Two pathologic processes are uniquely characteristic of trauma: diffuse axonal injury (DAI) and contusion/hematoma formation. Diffuse injures are more common. In the TCDB series, 56% of patients with severe closed head injury had a diffuse injury and 42% had a focal mass lesion. However, the mortality rate is generally higher with a focal lesion, 39% versus 24% with a diffuse injury.⁶

Diffuse Axonal Injury

Histopathologic findings of DAI have been observed in 25% of patients who die of TBI.¹⁷ When more sensitive indicators of axonal injury are used, such as β-amyloid immunohistochemistry, as many as 90% of patients who die of TBI have DAI changes.¹⁸ Current thought about the development of DAI is that axotomy may not be complete immediately after the trauma. Secondary or delayed axotomy may predominate in many circumstances.

DAI is primarily a pathologic diagnosis, with microscopic damage scattered throughout the brain, but clinical correlations have been described. Traumatic loss of consciousness for less than 6 hours is considered a concussion and is usually associated with amnesia for the events related to the injury. Traumatic coma for longer than 6 hours is generally attributed to DAI. Three levels of DAI severity based on clinical criteria are recognized: (1) mild DAI—coma of 6 to 24 hours’ duration; (2) moderate DAI—coma lasting longer than 24 hours without decerebrate posturing; and (3) severe DAI—coma lasting longer than 24 hours with decerebrate posturing or flaccidity. Severe DAI has a 50% mortality.¹⁹

Hematomas/Contusions

Subdural hematoma is the most common focal intracranial lesion and occurred in 24% of patients in the TCDB with severe closed head injury.⁶ The hematoma is located between the dura and brain, usually results from a torn bridging vein between the cortex and draining sinuses, and is typically situated in the frontoparietal region. An acute subdural hematoma, identified within 72 hours after trauma, generally appears on CT as a high-density, homogeneous crescent-shaped mass paralleling the calvaria (Fig. 334-2). However, up to 10% of acute subdural hematomas may be isodense with brain because of the low hemoglobin content.²⁰

FIGURE 334-2 Categorization of primary brain injury (Traumatic Coma Data Bank categories). CT, computed tomography; GOS, Glasgow Outcome Scale; OR, odds ratio.

(From Marshall LF, Marshall SB, Klauber MR, et al. A new classification of head injury based on computerized tomography. J Neurosurg. 1991;75:S14-S20.)

The mortality rate in patients with subdural hematomas is high.²¹ The following CT scan findings are particularly predictive of outcome: hematoma thickness, midline shift, the presence of underlying brain swelling or contusions,^22,²³ obliteration of the basal cisterns, and the presence of traumatic SAH.²¹

Subdural hematomas cause brain damage by increasing intracranial pressure (ICP) and by shifting brain structures. Reductions in cerebral blood flow (CBF) below ischemic thresholds ²⁴ and marked reductions in cerebral oxygenation^25,²⁶ have been observed preoperatively and are rapidly reversed by surgical evacuation of the hematoma. The presence of blood in the subdural space may also have direct toxic effects, but experimental studies have not consistently demonstrated this mechanism.²⁷

The primary treatment of subdural hematoma is prompt surgical evacuation, and the longer the delay between injury and surgery, the more severe the ischemic damage that can occur. Surgical indications for acute subdural hematoma include (1) any subdural hematoma greater than 10 mm in thickness or with a midline shift of greater than 5 mm and (2) a subdural hematoma less than 10 mm in thickness and with a midline shift of less than 5 mm if the GCS score is less than 9 and decreases 2 or more points between the time of injury and hospital admission, asymmetric or fixed and dilated pupils, or ICP exceeding 20 mm Hg.²⁸ Mortality in patients arriving at the hospital in coma with subsequent surgical evacuation is between 57% and 68%.²⁸

Epidural hematomas, or collections of blood between the skull and the dura, are less common than subdural hematomas. Epidural hematomas occurred in 6% of patients with severe closed head injuries in the TCDB series.⁶ Although patients with subdural hematomas are generally comatose immediately, only a third of patients with epidural hematomas are unconscious from the time of injury, a third have a lucid interval, and a third are never unconscious.²⁹ An epidural hematoma is almost always associated with a skull fracture (91% in adults and 75% in children).³⁰ The blood comes from torn dural vessels, usually arterial, from the fractured skull bone or occasionally from torn venous sinuses. On CT (see Fig. 334-2), an epidural hematoma is characterized by a biconvex, uniformly hyperdense lesion. Associated brain lesions are less common than with subdural hematomas. Epidural hematomas may also develop in delayed fashion³¹ or on the contralateral side after evacuation of an initial epidural hematoma.³²

The outcome of patients with an epidural hematoma depends on their neurological status at the time of surgery. The mortality rate varies from 0% for patients who are not in coma, to 9% for obtunded patients, to 20% for patients in deep coma. The following parameters were found to be significantly related to outcome in patients with epidural hematoma: age, time from injury to treatment, immediate coma or lucid interval, presence of pupillary abnormalities, GCS motor score on admission, CT findings (hematoma volume, degree of midline shift, presence of signs of active hematoma bleeding, associated intradural lesion), and postoperative ICP.³³

The primary treatment of an epidural hematoma is prompt surgical evacuation. An acute epidural hematoma with a volume greater than 30 cm³ should be surgically evacuated regardless of the patient’s GCS score. An epidural hematoma less than 30 cm³ in volume, less than 15 mm in thickness, and with less than a 5-mm midline shift in a patient with a GCS score higher than 8 and no focal deficit may be managed nonoperatively with serial CT scanning and close neurological observation.³⁰ Mortality in patients undergoing surgery for evacuation of an epidural hematoma is approximately 10%.³⁰

Intracerebral blood can take the form of a hematoma or a contusion. Intracerebral hematomas are more common and occurred as the primary lesion in 10% of patients with severe closed head injuries in the TCDB series.⁶ Occasionally, it may be difficult to differentiate a traumatic intracerebral hematoma from spontaneous hemorrhage; however, the presence of associated contusion, fracture, or an air-fluid level in the sinus helps in identifying the hematoma as traumatic. A zone of surrounding hypodensity denotes contusion or edema.

Most intracerebral hematomas are visualized as hyperdense mass lesions (see Fig. 334-2). They are generally located in the frontal and temporal lobes and can be detected on a CT scan immediately after the trauma. However, delayed intracerebral hematomas may also be manifested during the hospital course. A delayed hematoma is one that is seen on a repeated CT scan within 24 to 48 hours of the injury or operation but is not present on the initial CT scan. Commonly, a delayed hematoma is associated with clinical deterioration. Expansion of the intracerebral hemorrhage occurs in half the patients within the initial 24 hours, and larger hematomas exhibit the greatest expansion. Furthermore, the earlier the initial CT scan is obtained, the more likely it is that significant growth of the hematoma will be observed on subsequent scans.³⁴ Indications for surgery are (1) signs or neurological deterioration referable to the parenchymal lesion and medically refractory intracranial hypertension or signs of a mass effect on CT, (2) frontal or temporal contusions greater than 20 cm³ with a midline shift of 5 mm or cisternal compression in a patient with a GCS score of 6 to 8, and (3) any parenchymal lesion with volume greater than 50 cm³.³⁵ Factors that determine outcome in patients with intracerebral hematomas include GCS score, hematoma volume, and the occurrence of hypoxia.³⁶

Hemorrhagic contusions were present as the primary lesion in 3% of patients with severe closed head injuries in the TCDB series.⁶ Single contusions are located either below the region of the impact or opposite the region of impact. Contusions appear as heterogeneous areas of brain necrosis, hemorrhage, and infarction and represent mixed-density lesions on CT scan.³⁷ Multiple focal contusions have a “salt and pepper” appearance on CT. Ischemia may play a role in the pathogenesis of contusions, and regional CBF (rCBF) values averaging 17.5 ± 4.0 mL/100 g per minute have been measured in pericontusional tissue.³⁸

Classification of Primary Brain Injury

A number of injury severity schemes have been developed for predicting mortality after trauma and other critical illnesses. In general, these schemes have been developed in other patient populations and do not accurately predict outcome in neurologically injured patients. Rocca and colleagues studied 70 patients with TBI and found that the GCS was superior to the Acute Physiology Score (APS), the Simplified Acute Physiology Score (SAPS), and the Therapeutic Intervention Scoring System (TISS).³⁹ Alvarez and coworkers studied 401 patients with TBI and compared the predictive ability of the Acute Physiology and Chronic Health Evaluation (APACHE II), SAPS II, Mortality Probability Models (MPM II), and the GCS.⁴⁰ The MPM II system provided a good estimation of mortality. The SAPS II and APACHE II systems did not calibrate well, and the logistic regression model containing the GCS as an independent variable and developed in this group of patients was not as well calibrated as MPM II. Of all these systems, the GCS is the most commonly used neurological injury scale for adults because of its high interobserver reliability and generally good prognostic capabilities,⁴¹ but it is a poor discriminator for less severe TBI, which accounts for 80% to 90% of all cases.

Schemes that predict outcome well after TBI generally include age, severity of injury, and type of injury. For the severity-of-injury scale, the GCS, either the sum score or, for comatose patients, the motor score alone, is used. For the type of injury, a classification that separates focal and diffuse injuries is typically used. The CT classification of head injury based on information obtained from the initial CT scan was derived from the TCDB data.¹⁰ The scheme uses the status of the mesencephalic cisterns, the amount of midline shift, and the presence or absence of surgical masses. Diffuse injuries were defined in all patients with no mixed- or high-density lesions greater than 25 cm³. The category of diffuse injuries was divided into four subgroups: diffuse injury I included all head injuries with no visible pathology, diffuse injury II included all diffuse injuries with cisterns present and less than 5-mm shift, diffuse injury III included all diffuse injuries with compressed or absent cisterns but less than 5-mm shift, and diffuse injury IV included all diffuse injuries with more than 5-mm midline shift. Example of these diffuse injury categories are shown in Figure 334-2. The category of mass lesions, which included all patients with mixed- or high-density lesions greater than 25 cm³, was divided into those with the mass surgically evacuated (including operated subdural, epidural, and intracerebral hematomas) and those with nonevacuated mass lesions.

This CT classification scheme provided a better assessment of the risk for intracranial hypertension and a fatal outcome. Patients with diffuse injury I had the lowest mortality rate of 10%, whereas the diffuse injury II, III, and IV groups had mortality rates of 14%, 34%, and 56%, respectively. The mortality rate of patients with evacuated hematomas was 39%.

The IMPACT database studies have confirmed the usefulness of the TCDB classification but have also shown that individual CT characteristics such as traumatic SAH and the individual hematoma type (subdural versus epidural) have added prognostic value.²¹ Probably the most descriptive scheme at the present time is to use a combination of the TCDB classification plus these individual CT characteristics.

Secondary Brain Injury

Trauma initiates secondary injury processes in the brain that evolve during the early phase of hospitalization. Vascular changes are prominent and well described and can lead to additional injury to the brain if CBF is inadequate. Cellular processes are initiated that may lead to cell edema and cell death. Finally, inflammatory processes are initiated that can result in late vascular and cellular effects. These processes are manifested clinically by the development of intracranial hypertension and cerebral ischemia.

Traumatic Brain Swelling/Intracranial Hypertension

Brain edema and vascular engorgement have been used interchangeably to describe the brain swelling that accompanies severe TBI. Although the relative contribution of these two entities to the swelling process is controversial, there is increasing evidence that edema plays the predominant role. In experimental models of brain trauma, the water content of the brain is increased whereas cerebral blood volume is decreased, thus suggesting that edema is the major component of brain swelling after trauma.⁴² Clinical studies using magnetic resonance imaging (MRI) techniques to quantify water and blood content have confirmed these experimental findings in humans.⁴³

Brain edema can be vasogenic (secondary to opening the blood-brain barrier [BBB]) or cellular. Most experimental evidence, including recent data using diffusion-weighted imaging techniques to differentiate types of edema formation, suggest that the early, immediate increase in brain water after trauma is probably vasogenic whereas the gradual increase in brain water that occurs during the first few days after injury is cellular.^44,⁴⁵

The clinical manifestation of brain swelling is intracranial hypertension, which develops in 50% of patients in coma caused by severe head injury. It is a misconception that ICP will always be low after operative evacuation of a large intracranial hematoma. Intracranial hypertension occurs in 50% to 70% of patients after evacuation of an intracranial hematoma.^46,⁴⁷ This postoperative intracranial hypertension may be due to a postoperative hematoma, either at the site of the operation or at a new site, progressive swelling of a focal contusion, diffuse brain swelling, and other systemic complications. The incidence of intracranial hypertension is greater after evacuation of an intracerebral hematoma, 71%, than after evacuation of a subdural or epidural hematoma, 39%.⁴⁶ In patients with no mass lesions, elevated ICP has been observed to occur during the hospital course in 30%⁴⁶ to 80%⁴⁸ of patients.

The association between the severity of intracranial hypertension and poor outcome after severe head injury is well recognized. In one series, 77% of patients with ICP below 15 mm Hg had a favorable outcome as compared with just 43% of patients with ICP above 15 mm Hg.⁴⁹ Miller and coauthors reported that the mortality rate increased from 18% to 92% and the frequency of good outcomes decreased from 74% to 3% in patients with normal ICP versus patients who had intracranial hypertension that could not be reduced below 20 mm Hg.⁵⁰ Similarly, Saul and Ducker reported a 69% mortality rate in patients with ICP greater than 25 mm Hg as opposed to a mortality rate of 15% if ICP remained less than 25 mm Hg.⁵¹

The relationship between elevated ICP and a poor outcome is not simply a reflection of the severity of the initial neurological injury. Severe intracranial hypertension can result in secondary injury to the brain through ischemia produced by reduced cerebral perfusion pressure (CPP), and it can also distort and compress the brainstem. Although no randomized clinical trial has addressed this question, several clinical series have suggested that reduction of ICP to less than 20 mm Hg does reduce mortality after severe head injury.^46,⁵¹^–⁵³

Effects of Trauma on the Cerebral Vasculature

Many investigators have studied CBF after TBI and emphasized various patterns of CBF. A few studies have closely examined the evolution of TBI over time with serial measurements of CBF.^54,⁵⁵ These serial studies in particular have helped to develop the overall picture of the postinjury evolution of CBF.

Martin and coworkers described a phasic pattern of cerebral hemodynamic changes in 125 severely head-injured patients with a GCS score lower than 8 who were studied prospectively with intravenous ¹³³Xe-CBF measurements, cerebral metabolic assessment, or transcranial Doppler (TCD) evaluations (or any combination of the three studies).⁵⁴ An early hypoperfusion phase occurred during the first 24 hours after injury and was characterized by low CBF and normal middle cerebral artery flow velocity (MCA-FV). This was followed by a hyperemic phase that occurred in about 40% of patients between postinjury days 1 and 3 when CBF was transiently increased with a rapidly rising MCA-FV but a normal hemispheric index. Later (postinjury days 4 to 15), a vasospasm phase occurred that was characterized by low-normal CBF values accompanied by high MCA-FV and an elevated hemispheric index. Hlatky and colleagues found a significant reduction in CBF during the first 12 hours after TBI; in patients with CBF lower than 18 mL/100 g per minute, intracranial hypertension played a major causative role in the reduction in CBF, and for levels of CBF between 10 and 40 mL/100 g per minute, the presence of regional hypoperfusion was a more important factor in reducing the average CBF.⁵⁶ These CBF patterns, which have been described primarily with global CBF measurements, can also occur regionally. Hypoperfusion, in particular, can occur in brain tissue surrounding a focal contusion or underlying a subdural hematoma. Schroder and associates observed rCBF values averaging 17.5 mL/100 g per minute in pericontusional brain.³⁸ McLaughin and Marion observed CBF values within contused brain and in pericontusional brain that were significantly lower than those in the rest of the brain.⁵⁷ Focal hyperemia has been observed in 38% of patients, particularly in tissue adjacent to intraparenchymal or extracerebral focal lesions.⁵⁸

Numerous studies have associated elevated CBF and outcome. In a study of 36 patients, the mortality rate was 67% in those with elevated CBF versus 9% in those with normal CBF and 27% in those with reduced CBF.⁶⁵ In contrast, other studies have found elevated CBF to be associated with a relatively good outcome.⁵⁵ Focal hyperemia has also been thought to be a finding associated with a favorable outcome.⁵⁸ Sometimes, hyperemia is defined by a low arteriovenous oxygen diffusion capacity (AVDO₂) or high SjvO₂ because this finding would suggest a CBF in excess of cerebral metabolic requirements. In terms of prognosis, however, the finding of an elevated SjvO₂ describes a wide spectrum of outcomes.⁶⁶ High SjvO₂ predicts a poor outcome if it is caused by a low cerebral metabolic rate of oxygen consumption (CMRO₂). In contrast, if high CBF is the cause of the elevated SjvO₂, it often predicts a favorable outcome.

Vasospasm and Head Injury Outcome

The TCDB study reported the occurrence of SAH in 39% of patients with severe head injury, although more recent studies have reported a higher frequency of traumatic SAH, probably because of the improved resolution of modern CT scanners.⁹

The incidence of ischemic injury secondary to vasospasm is more difficult to estimate because the neurological signs of ischemia are superimposed on the neurological deficits of the traumatic injury, but a few studies suggest that cerebral vasospasm may be an important cause of evolving injury in some patients. Chan and associates studied the relationship between increased FV and the development of cerebral infarction on CT in 121 patients.⁶⁷ They found that of 23 patients in whom a mean FV of greater than 100 cm/sec developed, an infarction in the territory of the involved cerebral vessel developed in 4.

Recently, Armonda and coauthors described a significant percentage of patients with severe TBI resulting from a blast or high-velocity gunshot wound to the head in whom cranial vascular injury developed.⁶⁸ Vasospasm was observed in up to 47% of these patients, the average duration of the spasm was 14 days with a range of up to 30 days, and vasospasm was associated with the presence of pseudoaneurysm, hemorrhage, the number of lobes injured, and mortality.

Secondary Ischemic Insults

Clinical studies have demonstrated an association between the occurrence of secondary insults and a poor neurological outcome. Jones and colleagues reported that secondary insults occurred in 91% of 124 patients studied with a computerized detection system.⁶⁹ The duration of hypotensive, febrile, and hypoxic insults was significantly associated with mortality. Gopinath and coworkers observed that the occurrence of secondary insults sufficiently severe that they resulted in desaturation of jugular venous blood was significantly related to a poor neurological outcome.⁶² Even when adjusted for other confounding factors, such as age, type of injury, and neurological status, the occurrence of just one episode of jugular desaturation was associated with a 2-fold increase in risk for a poor neurological outcome, and the occurrence of multiple episodes of jugular desaturation was associated with a 14-fold increase in risk for a poor neurological outcome.

It is likely that the major reason that a traumatized brain is so sensitive to secondary insults is that the regulatory processes that normally preserve CBF during reductions in blood pressure (BP), arterial PO₂, and hemoglobin concentration are dysfunctional after trauma. Therefore, goals for these physiologic parameters must be optimization of cerebral perfusion in the traumatized brain.

Causes of Secondary Ischemic Insults

Any pathophysiologic process that impairs cerebral energy metabolism can be a secondary ischemic insult after head injury. As shown in Figure 334-1, these processes can be divided into two general categories: (1) those that decrease the cerebral delivery of energy substrates and (2) those that increase cerebral energy consumption.

Cerebral oxygen delivery is the product of CBF and arterial oxygen concentration (CaO₂). CBF is normally closely regulated by the cerebral metabolic rate and will also be affected by CPP and arterial PCO₂. However, in disease states, CBF may be uncoupled from the metabolic rate and can be elevated or reduced from normal. CaO₂ is calculated from arterial oxygen saturation and the hemoglobin concentration and is normally around 20 mL/dL (9 µmol/mL). Both hypoxia and anemia can reduce CaO₂.

Cerebral oxygen consumption or CMRO₂ has a normal value of 3.4 mg/100 g per minute (1.5 µmol/g per minute). Numerous conditions are known to alter CMRO₂. Head injury, anesthesia, and hypothermia are known to decrease CMRO₂, whereas fever and seizures increase it.^63,⁷⁰^–⁷⁶ Recent studies using [¹⁸F]fluorodeoxyglucose-labeled positron emission tomography (FDG-PET) to study glucose metabolism after severe head injury have suggested that the cerebral metabolic rate of glucose (CMRGlc) may be elevated regionally and perhaps even globally at times when CMRO₂ is normal or reduced.⁷⁷ This “hyperglycolysis” may indicate mitochondrial damage and inability of the brain to metabolize oxygen normally. If energy metabolism is dependent on glucose metabolism, energy failure as a result of glucose depletion is another possible cause of secondary ischemic insults after severe head injury.

Neurological Intensive Care Monitoring

The two most important secondary injury processes that can be monitored, anticipated, and treated in the ICU are intracranial hypertension and cerebral ischemia. In addition, secondary ischemic insults can be anticipated and prevented or detected early and treated before sufficiently severe to injure the brain.

To accomplish these goals, severely head-injured patients should have their ICP monitored, preferably by ventriculostomy, and monitoring of cerebral perfusion with jugular bulb oximetry or brain tissue PO₂ (or both) and CPP monitoring may also be considered. In addition, head-injured patients should have close monitoring of systemic parameters, including the electrocardiogram, heart rate, BP, temperature (rectal), and fluid intake and output. An arterial catheter is usually indicated to continuously monitor BP and provide easy access for blood sampling and is required if pressor agents are needed to maintain adequate BP. Severely head-injured patients should be routinely monitored with pulse oximetry and capnography to avoid unrecognized hypoxemia or changes in ventilation. A central venous catheter and, in certain circumstances, a Swan-Ganz catheter may be useful to judge volume status. A Foley catheter is necessary for accurate measurement of urine output.

Monitoring Neurological Status

To assess the neurological status of the patient, evaluation of mental status and cranial nerve, pupillary, and motor functions should be included in the periodic neurological examination whenever possible. This will help in determining whether there is improvement, deterioration, or no change in the patient’s clinical condition. A 24-hour record of the patient should be available on one sheet, such as was described by Clifton and Grossman,⁷⁸ and should include information on vital signs and laboratory values. Computerized information systems are becoming more widespread in ICUs and can markedly reduce the burden of such record keeping.

Monitoring for Secondary Injury Processes: Intracranial Hypertension

ICP cannot be reliably estimated from any clinical feature after severe head injury. Clinical symptoms of raised ICP, such as headache, nausea, and vomiting, are impossible to elicit in comatose patients. Papilledema is uncommon after head injury, even in patients with intracranial hypertension.⁷⁹ In one study, although 54% of patients had increased ICP, only 3.5% had papilledema on funduscopic examination. Other neurological signs, including pupillary dilation and decerebrate posturing, can occur in the absence of intracranial hypertension. CT signs of brain swelling, such as a midline shift and compressed basal cisterns, are predictive of raised ICP, but intracranial hypertension can occur without these findings.

Techniques for Monitoring Intracranial Pressure

Historical Aspects

Recording of cerebrospinal fluid (CSF) pressure was initially performed through lumbar puncture in the late 1800s. Continuous pressure recordings of ICP were first reported in 1951 by Guillaume and Janny.⁸⁰ In 1960, Lundberg reported the results of ventricular catheter pressure recordings in 143 patients with various neurosurgical diagnoses.⁸¹ This was a landmark work that emphasized both the safety and importance of monitoring ICP.

Currently Available Techniques

Although several new types of monitors have recently been marketed, the ventriculostomy catheter remains the preferred device for monitoring ICP and the standard against which all the newer monitors are compared. The ventriculostomy catheter is positioned with its tip in the frontal horn of the lateral ventricle and is coupled by fluid-filled tubing to an external pressure transducer that can be reset to zero and recalibrated against an external standard. The ventriculostomy catheter provides the most reliable measurement of ICP throughout the normal and pathologic ranges.⁸² In addition, the ventriculostomy ICP monitor allows treatment of elevated ICP by intermittent drainage of CSF. However, the risk for ventriculitis and intracranial hemorrhage is highest with ventriculostomy,⁸³ and proper placement of the catheter tip in the lateral ventricle can be difficult in patients with small, compressed ventricles.

When the ventricle cannot be cannulated, alternative devices can be used. A number of non–fluid-coupled devices have become available for ICP monitoring and have replaced the subarachnoid bolt as an alternative to ventriculostomy in most institutions. The microsensor transducer ⁸⁴ and the fiberoptic transducer⁸⁵ are the most widely available. These miniature pressure transducer–tipped catheters can be inserted in the subdural space or directly into brain tissue. The main advantage of these monitors is their ease of insertion, especially in patients with compressed ventricles. They provide more reliable measurements of ICP than do subarachnoid bolts and fluid-coupled catheters in the subdural space because they have no lumen to become obstructed. The transducers, however, cannot be reset to zero after they are inserted into the skull, and they exhibit drift over time.⁸⁶

For surgical patients, the ICP monitor may be inserted at the end of the surgical procedure. Those who do not require surgery are immediately transferred to the ICU after the initial CT scan, and an ICP monitor is then inserted. A pressure tracing should display the pulsatile nature of the ICP. A dampened tracing may not be a reliable measure of ICP.

ICP monitoring is continued for as long as treatment of intracranial hypertension is required, typically 3 to 5 days. A secondary rise in ICP has been observed 3 to 10 days after injury in 30% of patients with intracranial hypertension ⁸⁷ as a result of the delayed development of intracerebral hematoma or cerebral vasospasm or because of systemic factors such as hypoxia or hypotension. Souter and colleagues associated an increase in the blood leukocyte count with late intracranial hypertension.⁸⁸

Complications

The two major complications of ICP monitoring are ventriculitis and hemorrhage. Infection may be confined to the skin wound, but ventriculitis occurs in 1% to 10% of patients. Factors that predispose to ventriculitis are intraventricular hemorrhage, SAH, cranial fracture with leakage of CSF, craniotomy, systemic infections, catheter manipulation, leaks, and irrigation. The duration of catheterization has been correlated with an increasing risk for CSF infections during the first 10 days of use. Although prophylactic catheter exchange remains a practice option, the available data suggest that this procedure does not reduce the risk for infection.⁸⁹ Systemic prophylactic antibiotics are ineffective in reducing the incidence of infections, but antibiotic-impregnated ventriculostomy catheters reduce the risk for CSF infection from 9.4% to 1.3%.⁹⁰ Systemic prophylactic antibiotics and routine catheter exchange are not recommended in the current TBI guidelines (see Table 334-3—level III recommendation). The best strategies for reducing the risk for ventriculitis associated with ICP monitoring are meticulous aseptic technique during catheter insertion, the use of antibiotic-impregnated catheters, and minimization of the duration of monitoring.

The second major complication of ICP monitoring is intracerebral hemorrhage. Although the risk for hemorrhage has been shown to be consistently low (1% to 2%), it is an important complication to recognize and treat.⁸³ Patients with coagulopathies are at greater risk for the development of this complication. Some evidence suggests that patients with an international normalized ratio of 1.6 or less have a very low risk for hemorrhage if a parenchymal catheter is placed.⁹¹

Normal Intracranial Pressure Values

Normally, resting ICP is less than 10 mm Hg. Sustained ICP of greater than 20 mm Hg is clearly abnormal. ICP between 20 and 40 mm Hg is considered moderate intracranial hypertension. ICP greater than 40 mm Hg represents severe, usually life-threatening intracranial hypertension. These thresholds for the severity of intracranial hypertension assume normal BP. When a temporal mass lesion is present, however, herniation can occur at ICP values of less than 20 mm Hg.⁹²

Different authors have recommended treatment of ICP when greater than 15, 20, or 25 mm Hg. No studies have clearly established one of these values as the most appropriate threshold for treatment. Marmarou and coworkers observed an increasingly worse outcome with greater durations of time that ICP was higher than 20 mm Hg.⁹³ Contant and associates observed a worse outcome with greater durations of time that ICP was higher than 25 mm Hg.⁹⁴ The current TBI guidelines (see Table 334-3) recommend treating ICP above 20 mm Hg (level II recommendation) or using clinical and CT characteristics in addition to the ICP value to determine the need for treatment (level III recommendation).¹³

Indications for Intracranial Pressure Monitoring

Monitoring of ICP can result in serious complications and is therefore indicated only in patients at significant risk for the development of intracranial hypertension. Indications from the current TBI guidelines are listed in Table 334-3.^13,⁹⁵ ICP should be monitored in all salvageable patients with severe TBI, defined as a GCS score of 3 to 8 after resuscitation and abnormal findings on CT (level II recommendation). ICP monitoring is indicated in patients with severe TBI and normal CT findings if two or more of the following features are present at admission: age older than 40 years, unilateral or bilateral motor posturing, or systolic BP lower than 90 mm Hg (level III recommendation). Patients with a GCS score higher than 8 might be considered for ICP monitoring if they require treatment that would not allow serial neurological examinations, such as prolonged anesthesia for surgery to treat multiple injuries or prolonged pharmacologic paralysis for ventilatory management, or if they require a treatment that might raise ICP, such as positive end-expiratory pressure (PEEP). A severe coagulopathy is the only major contraindication to ICP monitoring.

Monitoring for Secondary Injury Processes: Cerebral Ischemia

As with intracranial hypertension, there are no reliable clinical findings for cerebral ischemia. The neurological signs caused by brain injury usually obscure any focal findings that might be caused by secondary ischemia. Therefore, cerebral perfusion must be monitored to detect secondary cerebral ischemia after TBI.

The ideal monitor for cerebral ischemia after TBI does not yet exist. This ideal monitor would give regional information about CBF because there can be marked regional differences in CBF after trauma. This ideal monitor would also give continuous information because CBF evolves over time after injury. Techniques that are available fall under two general categories, those that monitor cerebral perfusion or blood flow and those that monitor CBF indirectly through cerebral oxygenation.

Monitors of Cerebral Perfusion

Cerebral Perfusion Pressure

The simplest measure of cerebral perfusion is CPP, which is calculated by subtracting ICP from mean arterial blood pressure (MAP). The normal lower limit of autoregulation for CPP is 50 mm Hg. In severely head-injured patients, the ability to autoregulate may be impaired, and CBF may be inadequate even with CPP values greater than 50 mm Hg. CPP can be reduced through either decreases in BP or increases in ICP. As a monitor for cerebral perfusion, CPP is widely available and convenient but limited in that only ischemia caused by increased ICP or by decreased BP is assessed.

Transcranial Doppler Flow Velocity

TCD ultrasonography uses a pulsed ultrasonic signal in the 2-MHz range that is transmitted through thin areas of the skull. Blood flow volume and FV are not synonymous. However, flow volume is directly proportional to FV and may be obtained by multiplying the velocity by the cross-sectional area of the vessel insonated. Because TCD measures FV in the arteries at the circle of Willis, the radius of the vessel is not generally known, and collateral blood flow is variable, TCD ultrasonography cannot provide quantitative data on regional tissue perfusion.

Several studies assessing the relationship between peak FV and changes in CBF have suggested that changes in MCA-FV may be used as an indicator of relative changes in blood flow. Kofke and colleagues, investigating the relationship between MCA-FV and CBF assessed by stable xenon–CT during balloon test occlusion of the carotid artery in 31 patients, found a significant correlation in the alteration of flow detected by the two methods.⁹⁶ More recently, changes in MCA-FV and changes in CBF evaluated by stable xenon–CT in patients with various intracranial pathologies, including 8 with closed head injury, have shown close correlation.⁹⁷

During arterial spasm, FV increases through the narrowed segment proportional to the reduction in the vessel’s diameter. Severe vasospasm, with a larger than 50% reduction in vessel diameter, is associated with an FV of greater than 200 cm/sec.⁹⁸ However, an increase in FV may also reflect hyperemia, which is often seen as a posttraumatic event. To differentiate between these two hemodynamic phenomena in the absence of direct CBF measurements, the MCA-to–extracranial internal carotid artery FV ratio, also known as the Lindegaard or hemispheric index, has been measured. In the presence of hyperemia, raised FV in both the extracranial and intracranial vessels does not alter the ratio; however, with vasospasm, FV is high only in the intracranial vessels, which results in a high hemispheric index. The mean hemispheric index in normal individuals is 1.76 ± 0.1, and pathologic values suggestive of vasospasm are generally higher than 3.⁹⁹

Cerebral Blood Flow

Techniques for Monitoring Cerebral Blood Flow

Recently, newer technologies have made measurement of CBF more feasible in critically ill patients. Measurement of global CBF by the classic Kety-Schmidt technique in which nitrous oxide is used as the diffusible indicator can be performed at the bedside with a minimum of expense and equipment. Measurement of rCBF by stable xenon–CT or perfusion CT is possible and can even be performed in the ICU with a portable CT scanner (examples are shown in Fig. 334-3). However, these measurements of CBF are intermittent and require the patient to be hemodynamically stable during the time required for the measurements. Therefore, transient reductions in CBF or reductions in CBF in an acutely unstable patient are difficult to document with these technologies.

FIGURE 334-3 Examples of cerebral blood flow imaging with stable xenon–enhanced computed tomography (CT) (left) and CT perfusion (right). The top image is from a patient with a temporal contusion. The bottom image is from a patient with a hemispheric infarction after evacuation of an acute subdural hematoma.

The stable xenon–CT method relies on the radiodensity of xenon and its inertness and rapid diffusion into tissues. An initial non–contrast-enhanced scan helps in choosing the levels for CBF measurement. Baseline scans, usually at four levels, are followed by multiple scans at each of the four levels at 1-minute intervals during the inhalation of 28% to 33% xenon. The baseline pre-xenon scans are subtracted from the subsequent xenon scans to provide quantitative enhancement values in Hounsfield units. Clearance curves proportional to brain and arterial xenon concentrations from an end-tidal analyzer are converted into CT enhancement units. Blood flow is then calculated from the Kety-Schmidt equation for each CT voxel. Studies in normal volunteers have indicated that xenon at a concentration of 30% has an effect on cerebral hemodynamics and causes arterial vasodilation and enhancement of CBF.^100,¹⁰¹ This probably occurs as a result of an increase in metabolism and a vasodilatory effect of xenon. Some studies have observed a small increase in ICP averaging 6.9 ± 7.7 mm Hg during CBF measurements with xenon-CT,¹⁰² whereas others have not.¹⁰³

Perfusion CT imaging uses a nondiffusible indicator technique to calculate blood flow. The imaging study is performed by collecting a continuous (kinematic) sequence of scans after an intravenous bolus of an iodine contrast agent. Each image is subtracted from a baseline image to develop a time enhancement curve. Perfusion is then calculated by the slope method.

Local Cerebral Blood Flow Sensors for Brain Implantation

Two methods for continuously measuring local CBF are now commercially available, the thermal diffusion method and the laser Doppler method. Both methods are invasive and require the probe to be placed on the surface of the brain at surgery or into the brain through a bur hole. In addition, both methods measure CBF in only a small volume of brain, which may or may not be representative of the whole brain. However, the continuous nature of the measurements gives a dynamic picture of brain perfusion. Although there is extensive documentation of the reliability of these methodologies in the laboratory, experience in the ICU is currently limited.¹⁰⁴^–¹⁰⁷ Nonetheless, especially for patients undergoing a craniotomy, these methods may become practical for monitoring CBF postoperatively.

Thermal diffusion flowmetry (TD-CBF) uses heat transfer as a tracer for the measurement of blood flow. The sensor consists of two gold disks embedded in a 3-mm Silastic leaf or two bands on an intraparenchymal catheter. One disk is heated slightly above brain temperature (to a maximum of 44°C), whereas the other is neutral. The leaf probe is laid on the surface of the brain, and the catheter version can be implanted into the brain parenchyma. The difference in temperature between the two disks is monitored and converted to blood flow in mL/100 g per minute by the monitor and displayed digitally. Carter and Atkinson ¹⁰⁸ modified a thermal sensor described by Brawley¹⁰⁹ and were able to quantitate the flow measured by the thermal sensor. They derived a mathematical formula by comparing TD-CBF with ¹³³Xe-CBF¹¹⁰ and further confirmed its reliability through comparison with hydrogen clearance.¹¹¹ In TBI patients, the CBF values obtained with the catheter probe have good correlation with those obtained with stable xenon–CT.¹¹²

Laser Doppler flowmetry (LDF) is a technique in which CBF is measured indirectly from the magnitude of the frequency shift of monochromatic light by a moving column of blood. The most accurate recordings are obtained when the probe is in direct contact with the region of interest but away from obviously visible vessels, which will bias the capillary flow. The most useful application of LDF is for continuous monitoring of CBF in the ICU. Its high temporal resolution allows the detection of transient hemodynamic events, although the information involves relative changes in local CBF.

Cerebral Blood Flow Adequacy

Measures of cerebral oxygenation, such as SjvO₂ and brain tissue PO₂ (PbtO₂), have been used in place of quantitative CBF measurements because they give an indicator of the adequacy of CBF relative to cerebral metabolic requirements. Because cerebral metabolic requirements may be reduced after TBI, normal CBF values may not apply. When CBF is low (25 to 30 mL/100 g per minute), it can be difficult to decide whether it is an appropriate response to lower cerebral metabolic requirements or whether the brain is hypoperfused. A measure of cerebral oxygenation can be helpful in making this distinction. If the brain is hypoperfused, oxygen extraction will be increased and SjvO₂ will be reduced. If CBF is appropriate for the brain’s metabolic requirement, SjvO₂ will be normal. Frequently, this information is more clinically useful than the absolute CBF values.

Jugular Venous Oxygen Saturation

Initial experiences with fiberoptic oxygen saturation catheters placed in the jugular bulb were unsatisfactory. However, more recently available catheters have been found to have much improved performance.¹¹³^–¹¹⁵ A number of studies have assessed the role of monitoring jugular venous saturation in patients with severe TBI. In 1995, Robertson and coauthors published the findings from a series of 177 patients with severe TBI and demonstrated that 39% of the patients had at least one episode of desaturation and that good recovery or moderate disability occurred in 44% of the patients with no episodes of desaturation, in 30% of the patients with one episode, and in 15% of the patients with multiple episodes of desaturation.¹¹⁶ Mortality was higher in patients with one episode or multiple episodes of desaturation (37% and 69%) than in those with no episodes (21%).

High SjvO₂ values have also been associated with a poor outcome. In 1999, in a series of 450 patients who underwent jugular venous saturation monitoring, Cormio and colleagues reported that high SjvO₂ (>75%) occurs with hyperemia or after infarction because nonviable tissue does not extract oxygen.⁶⁶ In addition, these patients were found to have a worse outcome at 6 months after injury than those with a mean SjvO₂ of 56% to 74%.

Side of Catheterization

Early studies suggested that either jugular bulb would provide similar SjvO₂ information in most healthy people. However, as early as 1945 it was observed that in patients who have focal lesions, there may be a significant difference in the oxygen saturation values obtained in the right and left jugular bulbs.¹¹⁷ This variability occurs because of the often incomplete mixing of cerebral venous blood before the sagittal sinus divides into the right and left transverse sinuses.

Stocchetti and coworkers compared simultaneous measurements of SjvO₂ in the right and left jugular bulbs of 32 patients with severe head injury.¹¹⁸ The average difference in SjvO₂ between the right and left jugular bulbs was 5%. Fifteen patients had a maximal right to left difference in SjvO₂ of greater than 15%. Three additional patients had differences greater than 10%. Metz and colleagues compared bilateral SjvO₂ measurements in 22 patients with severe head injury.¹¹⁹ They found that the greatest success in identifying transient ischemic episodes was achieved if the following strategy was used. When the injury is diffuse, the catheter should be placed on the side of dominant flow. When the injury is focal, the catheter should be placed on the side of the lesion.

These studies are clear that when focal lesions are present, there may be significant differences in the oxygen saturation measured in the left and right jugular bulbs. If the monitoring strategy is to use SjvO₂ as a monitor of global oxygenation, cannulating the dominant jugular vein is the most logical because it will be the most representative of the whole brain. However, if the strategy is to identify the most abnormal oxygen saturation, the recommendations of Metz and colleagues should be followed.¹¹⁹

Normal Jugular Venous Oxygen Saturation

Gibbs and coworkers studied 50 healthy young males and observed that their SjvO₂ ranged from 55% to 71% (mean of 61.8%).¹²⁰ More recently, Chieregato and associates measured SjvO₂ in 12 subjects undergoing selective bilateral catheterization of the inferior petrosal sinus for the diagnosis of Cushing’s disease and found that even lower values could exist in normal awake subjects.¹²¹ That these values for SjvO₂ are lower than normal mixed venous oxygen saturation indicates that the brain normally extracts oxygen more completely from arterial blood than do many other organs.

In head-injured patients, the average SjvO₂ is higher than normal and the range for SjvO₂ is considerably wider than it is in normal subjects. In a series of 116 patients who underwent continuous measurement of SjvO₂ for the first 5 to 10 days after a severe head injury, SjvO₂ averaged 68.1% ± 9.7% (range, 32% to 96%) in 1329 measurements.⁶² PjvO₂ averaged 37 ± 7 mm Hg (range, 22 to 85 mm Hg).

From studies examining ischemic thresholds, it appears that normal brain metabolism can be altered at SjvO₂ values of less than 40% to 50% but that values of less than 20% would be required for irreversible ischemic injury.¹²²^–¹²⁷ The current TBI guidelines (see Table 334-3) recommend treating patients with an SjvO₂ of less than 50% (level III recommendation).

Complications

Potential complications can be divided into those associated with insertion of the catheter, including carotid artery puncture, injury to nerves in the neck, and pneumothorax, and those associated with the catheter remaining in the jugular vein, including infection, an increase in ICP, and venous thrombosis.

Carotid puncture is the most common complication associated with internal jugular vein catheterization. However, it rarely has serious consequences, and the risk can be minimized by making certain that the puncture is lateral to the carotid pulsation. The vast majority of arterial punctures can be managed conservatively by applying local pressure for 10 minutes.

Line sepsis is a complication that is commonly associated with all types of indwelling catheters. Most studies have reported an overall rate of zero to five episodes of infection per 100 catheters.¹²⁸ Proper sterile technique in placement and maintenance of the jugular bulb catheter should minimize this risk.

ICP can be increased by maneuvers that obstruct venous return from the brain, and it is reasonable to be concerned that a catheter in the jugular vein might raise ICP. However, the 4 or 5 French catheter used for SjvO₂ monitoring is quite small relative to the lumen of the internal jugular vein. Stocchetti and coauthors reported that there was a slight increase in ICP “of no clinical significance” during catheter insertion.¹²⁹

Coplin and colleagues reported that 8 of 20 patients investigated with ultrasonography after jugular bulb catheterization had nonobstructive, subclinical thrombi.¹³⁰ Symptomatic thrombosis of the internal jugular vein is very uncommon with jugular bulb catheters but could have serious consequences. Depending on normal flow to the thrombosed internal jugular vein, the obstruction could impair venous return from the head and elevate ICP.

Brain Tissue PO₂

The major limitation of SjvO₂ as a monitor of CBF adequacy is that regional ischemia will not be identified. In circumstances such as brain trauma, where regional differences in CBF may occur, PbtO₂ as a monitor of cerebral oxygenation may have an important advantage. Normal values for PbtO₂ are 20 to 40 mm Hg, and critical reductions in PbtO₂ are 8 to 10 mm Hg. The current TBI guidelines (see Table 334-3) recommend treatment if PbtO₂ is lower than 15 mm Hg (level III recommendation). Hoffman and associates found that PbtO₂ in patients with ischemia detected by single-photon emission computed tomography averaged 10 ± 5 mm Hg versus 37 ± 12 mm Hg in normal brain.¹³¹ Valadka and coworkers found that the likelihood of death after a severe head injury increased with increasing duration of time with a PbtO₂ value lower than 15 mm Hg and with any occurrence of a PbtO₂ value lower than 6 mm Hg.¹³² van den Brink and coauthors reported a prospective study of 101 patients and found that PbtO₂ values of less than 10 mm Hg that lasted longer than 30 minutes were associated with increased mortality and a worse outcome.¹³³ In 2005, Stiefel and colleagues reported a series of 53 patients with severe TBI treated with ICP and CPP treatments goals and the addition of an oxygen-directed therapy protocol aimed at maintaining PbtO₂ greater than 25 mm Hg; they found a significant decrease in mortality (44% to 35%) in those treated with an oxygen-directed therapy.¹³⁴ In 2008 in a prospective study of 26 children with severe TBI who were managed with continuos PbtO₂ monitoring, Figaji and coauthors found a significant association between poor outcome and reduced PbtO₂.¹³⁵

Summary of Monitoring Options for Secondary Cerebral Ischemia

It is clear from the description of the available devices that none are ideal in the head injury setting. No single monitor gives continuous high-resolution rCBF information. At the present time, a reasonable strategy is to use intermittent measurements of rCBF, preferably by the stable xenon–CT or perfusion CT method, to obtain information about whether regional abnormalities in flow exist. If there are no hypoperfused regions, a global monitor such as SjvO₂ should suffice. If there are significant regional abnormalities in flow, it may be better to use PbtO₂ or one of the local CBF probes as a local monitor of the hypoperfused area in addition to a global monitor such as SjvO₂.

Figure 334-4 illustrates how this strategy might be used to identify and guide the treatment of focal ischemia after a head injury. This patient was initially admitted with a subdural hematoma (Fig. 334-4, left CT scan), which was evacuated promptly on arrival at the hospital. At surgery, a PbtO₂ catheter was placed near contused brain underlying the evacuated hematoma. Initially, PbtO₂ was normal, but over postinjury hours 36 to 46, PbtO₂ gradually decreased to 5 mm Hg with no changes in any other physiologic parameters. Note that SjvO₂, which is a measure of global oxygenation, remains low-normal (≈55%) despite the very low PbtO₂ and that CPP was 65 to 70 mm Hg. Administering 100% oxygen raised PbtO₂ to 15 mm Hg (Fig. 334-4, top graph). A CT scan (Fig. 334-4, middle scan) showed increased swelling around the contusion, and stable xenon–CT showed a large area with rCBF values of less than 10 mL/100 g per minute at the contusion site. Dopamine was started and phenylephrine added later to increase blood pressure. As CPP increased with this treatment, PbtO₂ returned to normal (Fig. 334-4, bottom graph), and a repeated stable xenon–CT scan (Fig. 334-4, right scan) showed significant improvement in CBF.

FIGURE 334-4 Example of identification of focal ischemia and treatment guided by brain tissue PO₂ (PbtO₂). This patient was admitted with a subdural hematoma (left computed tomography [CT] scan), which was evacuated promptly on arrival at the hospital. A PbtO₂ catheter was placed near contused brain underlying the evacuated hematoma. Initially, PbtO₂ was normal, but over postinjury hours 36 to 46, PbtO₂ gradually decreased to 5 mm Hg. Note that jugular venous oxygen saturation (SjvO₂), which is a measure of global oxygenation, remains low-normal despite the very low PbtO₂ and that cerebral perfusion pressure (CPP) was 65 to 70 mm Hg. Administration of 100% oxygen raised PbtO₂ to 15 mm Hg (top graph). A CT scan (middle scan) showed increased swelling around the contusion, and xenon-CT showed a large area with regional cerebral blood flow (CBF) values greater than 10 mL/100 g per minute at the contusion site. Dopamine was started and phenylephrine was added later to increase blood pressure. As CPP increased with this treatment, PbtO₂ increased (bottom graph), and repeated xenon-CT (right scan) showed significant improvement in CBF.

In this case, the progressive focal ischemia in the area of the contusion could possibly have been suspected from the changing appearance of the CT scan; however, stable xenon–CT and PbtO₂ provided a convenient way to grasp the severity and extent of the ischemia, and PbtO₂ also provided a good method for monitoring the effectiveness of the treatments applied in the ICU. The challenge with this strategy for monitoring is placing the local monitor in an area of the brain that is vulnerable to the development of ischemia.

Monitoring for Secondary Ischemic Insults

Secondary ischemic insults are global and usually transient. Therefore, a global, but continuous measure of CBF adequacy, such as SjvO₂, would be useful for monitoring for secondary insults. In addition, physiologic variables that are a common cause of secondary ischemic insults should be monitored.

Monitoring for Cerebral Causes of Secondary Ischemic Insults

Intracranial Hypertension

Intracranial hypertension was the most common cause of jugular venous desaturation in a prospective study of 116 patients with severe head injury; it accounted for 44% of the total number of episodes.⁶² As discussed earlier, ICP should be monitored, preferably by ventriculostomy.

Seizures

Seizures can dramatically increase CMRO₂ and CMRGlc. In rats in which seizures were induced by bicuculline, CMRO₂ was increased by 150% to 250%.⁷⁴ If CBF is marginal or uncoupled from the cerebral metabolic rate, ischemia can occur during the seizure.

The overall risk for seizures after TBI ranges from 2.5% to 5% with all types of injury, but it is 7% to 39% with cortical injury and neurological sequelae.¹³⁶ Because patients are often sedated and pharmacologically paralyzed for treatment of intracranial hypertension, seizure activity may be subclinical. For this reason, continuous monitoring with electroencephalography (EEG) is useful for this high-risk group of patients.¹³⁷

Seizures are not a common cause of jugular venous desaturation and can significantly reduce SjvO₂ if CBF is unable to meet the increased cerebral metabolic requirements. Increases in extracellular glutamate have also been reported during posttraumatic seizures.¹³⁸

Monitoring for Systemic Causes of Secondary Insults

Hypotension

Autoregulation is the ability of the brain to maintain normal CBF over a wide range of BP values, normally from a mean BP of 50 to 150 mm Hg. After TBI, the cerebral vasculature can lose the ability to autoregulate completely and CBF rises and falls with BP, or the lower limit of autoregulation, which is normally 50 mm Hg, can be shifted to a higher pressure. The consequence is that low BP values that are normally tolerated without sequelae can result in cerebral ischemia after TBI. Lewelt and colleagues showed in a fluid percussion injury model that autoregulation was severely impaired after both low-level and high-level injuries.¹³⁹ Normally in the cat, CBF is constant until CPP falls below 60 mm Hg. After a fluid percussion injury, CBF decreased proportionally to a CPP below 80 mm Hg. Chan and coauthors described similar findings in patients with head injury, with MCA-FV measured by TCD and SjvO₂ decreasing as CPP was reduced below approximately 70 mm Hg.¹⁴⁰

Hypotension is common in head-injured patients on admission to the hospital. The TCDB study of 717 patients reported that 35% had a systolic BP lower than 90 mm Hg on arrival in the emergency department.⁸ Hypotension on admission increased the mortality rate by 150%. Miller and Becker found in a group of 225 patients that the presence of a systolic BP lower than 95 on arrival in the emergency department was associated with a twofold increase in mortality rate.¹⁴¹

Hypotension is also common during hospitalization and is associated with a worse outcome. In another TCDB study, 29% had a systolic BP lower than 90 mm Hg during their ICU stay.¹⁴² Hypotension during the hospitalization was associated with a significantly worse outcome. In a prospective study in which SjvO₂ was monitored in 116 patients, hypotension was the third most common cause of jugular venous desaturation and accounted for 10% of the episodes.¹⁴² Marmarou and associates analyzed 428 patients who had hourly recordings of ICP, MAP, and CPP and reported that the proportion of time that MAP was lower than 80 mm Hg was significantly related to a poor neurological outcome.⁹³ Pietropaoli and colleagues observed in a study of 53 patients who underwent early surgery for traumatic intracranial hematomas that intraoperative hypotension (systolic BP <90 mm Hg) was associated with a mortality rate of 82% as opposed to 25% in patients without hypotension.¹⁴³

For these reasons, BP is a particularly important physiologic parameter to monitor after severe head injury. Usually, placement of an arterial catheter is indicated so that BP can be monitored continuously, and the goal should be a MAP greater than 80 to 90 mm Hg so that CPP remains at a value of at least 60 mm Hg.

Hypocapnia

Induced hyperventilation constricts cerebral blood vessels and thereby reduces global CBF and cerebral blood volume. The effect of changes in PaCO₂ on cerebral vessels is mediated by the change in pH induced in extracellular fluid.¹⁴⁴ CO₂ reactivity is preserved in most patients with severe head injury,¹⁴⁵ and therefore hyperventilation can rapidly lower ICP through the reduction in cerebral blood volume. The effects of hyperventilation on ICP are immediate, but the duration of the effect is brief because the pH of the brain, at least in normal individuals, soon equilibrates to the lower PaCO₂ level. Hyperventilation will clearly reduce ICP, but this potentially beneficial effect is attained at the expense of cerebral perfusion. Whether hyperventilation can actually result in cerebral ischemia in head-injured patients is controversial. However, several studies suggest that excessive hyperventilation after severe head injury can be a secondary ischemic insult. In a prospective study in which SjvO₂ was monitored in 116 patients with severe head injury, hypocapnia was the second most common cause of jugular venous desaturation and accounted for 36% of the episodes.⁶²

If areas of the brain that are marginally perfused have impaired CO₂

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