manejo anestesico tce 2002

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Anesthetic management of traumatic

brain injury

Eric Bedell, MD*, Donald S. Prough, MDDepartment of Anesthesiology, University of Texas Medical Branch, 301 University Blvd.,

Galveston, TX 77555-0591, USA

Traumatic brain injury (TBI) represents a significant health issue in the United

States, with rates of 175300 per 100,000 per year and a death rate of 15 to 30

per 100,000, accounting for up to 56,000 deaths [1,2]. Although brain injury,

secondary to vehicular injury, was historically the most common form of TBI, in

the latter part of the twentieth century, gunshot wounds became the most common

form of fatal brain injury, surpassing motor vehicle accidents [3]. Between 1979

and 1992 in the United States, brain injury secondary to vehicular trauma

decreased from 11.4/100,000 to 6.6/100,000 persons (43%), while injury from

firearms increased from 7.7/100,000 to 8.5/100,000 (10%) [3]. Even with modern

diagnosis and treatment, the prognosis for the patient with TBI remains poor. In a

recent study of hypothermia as a treatment for acute brain injury, a mortality of

27% occurred in the control group [4]. Because of the prevalence of TBI, an

understanding of the management of this group of patients is vital to the modern-

day health care provider in general, and the clinical anesthesiologist specifically.

In head-injured patients, the concepts of primary and secondary brain injury must

be considered to correctly prioritize interventions. Primary brain injury, which is

the damage caused directly by the traumatic insult, can result from contusion of

the brain (either at the site of impact or distant from the impact site), shock wave

disruption, depressed bone fragments, vascular occlusion, expanding intracranial

masses (eg, epidural, subdural, or intraparenchymal hematomas) and other

mechanisms. This form of damage may require rapid induction of anesthesia to

facilitate surgical intervention. Secondary brain injury occurs after the primary

injury, often as a result of correctable or preventable causes such as hypotension,

hypoxemia, or intracranial hypertension, and may markedly influence outcome.

Care begins with a structured care team following an orderly treatment plan. A

neurosurgeon or trauma surgeon is usually the leader of the neurotrauma care

0889-8537/02/$ see front matterD 2002, Elsevier Science (USA). All rights reserved.

PII: S 0 8 8 9 - 8 5 3 7 ( 0 1 ) 0 0 0 1 0 - 4

* Corresponding author.

E-mail address:[email protected] (E. Bedell).

Anesthesiology Clin N Am

20 (2002) 417439


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team, which also may include anesthesiologists, intensivists, radiologists, radio-

logic technicians, laboratory personnel, general surgeons, and nursing personnel.

The actual care then provided depends upon the individual patients needs and theresources available.

This article reviews concepts of anesthetic management for the patient with

TBI. The recommended approaches to management are based upon physiologic

and pharmacologic data. Whenever possible, specific recommendations will

be made. At other times, conflicting information will be presented for readers

to consider.

Evaluation and stabilization

Upon initial presentation, a patient with TBI is usually considered to be at risk

for increased intracranial pressure (ICP), but this probability and its treatment

cannot become the only concern of the health care team. In any trauma patient,

priority must be first given to general evaluation and stabilization, with particu-

lar attention to the ABCs of airway, breathing, and circulation. Although

these activities will be discussed sequentially, they proceed concurrently in

most situations.

Initial evaluation includes a rapid review of all injuries and determination ofbaseline vital signs and level of consciousness. The head injury may not be the

only injury, and other injuries, such as chest or abdominal wounds, may be life-

threatening. A primary survey of the undressed patient, both front and back, with

a careful search for associated injuries should be performed. In moving the

patient, manual in-line axial stabilization of the cervical spine should be used

because of the risk that cervical spine injury could accompany head injury (see

below). A baseline level of consciousness should be ascertained. The Glasgow

Coma Scale (GCS) is a useful tool for such evaluation (Table 1). Studies

comparing the association between long-term outcome and GCS scores afterTBI have demonstrated that a lower initial GCS score is associated with higher

morbidity and mortality (Table 2). Changes from the initial GCS score are im-

portant in following clinical progress.

After rapid evaluation, the team directs attention to primary resuscitation,

particularly to the maintenance and protection of an adequate airway. In comatose

patients, an artificial airway usually must be established. The airway must be

reevaluated frequently, as a secure airway can rapidly be compromised. The

second priority is to provide adequate oxygenation and ventilation. The third

priority is to ensure the adequacy of circulation (including adequate peripheralvenous access and, if necessary, central venous or arterial access). Only after

addressing the ABCs should further care occur. The status of the ABCs must be

reviewed frequently to recognize and reverse deterioration.

When a trauma patient first presents for care, an individual (or group) should

be assigned to assess the airway. The decision to provide an artificial airway (ie,

intubate or perform a tracheostomy) can be difficult and can have long-term

E. Bedell, D.S. Prough / Anesthesiology Clin N Am 20 (2002) 417439418


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implications for management. It is important to appreciate the difference between

airway maintenance and airway protection. Airway maintenance means providingan unobstructed pathway for gas flow between the atmosphere and the terminal

alveoli. Airway protection means either the ability to recognize and overcome

compromise within the airway (eg, tongue, vomitus, or pharyngeal secretions) or

the presence of a patent mechanical airway.

When evaluating the adequacy of the natural airway, quickly assess the level

of consciousness, examine the face and oropharynx for signs of injury or

obstruction, determine the presence or absence of bilateral breath sounds,

carefully examine for signs of airway obstruction (eg, stridor, retractions,

abdominal rocking), and establish the adequacy of arterial oxygenation usingpulse oximetry or arterial blood gas analysis. Also note vital signs (heart rate,

respiratory depth and frequency, blood pressure, temperature), review skin color,

and provide supplemental oxygen by means of a transparent, non-rebreathing

Table 2

Relationship of acute Glasgow Coma Scale (GCS) score to Glasgow Outcome Scale

Number (%) of cases

GCS score 3 4 GCS score 5 6 GCS score 7 9 Total cases

Dead/PVS 15 (78.9%) 19 (45.2%) 9 (25.7%) 43

SD/MD/GR 4 (21.2%) 23 (54.8%) 26 (74.3%) 53

Total cases 19 42 35 96

Abbreviations: The Glasgow Outcome Scale consists of five categories: death; PVS, persistent

vegetative state; SD, severe disability; MD, moderate disability; GR, good recovery.

FromJaggi JL, Obrist WD, Gennarelli TA, Langfitt TW. Relationship of early cerebral blood flow and

metabolism to outcome in acute head injury. J Neurosurg 1990;72:176182 [113]; with permission.

Table 1

Glasgow coma scale (GCS)

Component Response ScoreEye opening Spontaneously 4

To verbal command 3

To pain 2

None 1

Motor response (best limb) Obeys verbal command 6

Localizes pain 5

Flexion withdrawal 4

Flexion (decortication) 3

Extension (decerebration) 2

No response (flaccid) 1

Best verbal response Oriented and converses 5

Disoriented and converses 4

Inappropriate words 3

Incomprehensible sounds 2

No verbal response 1

Total score eye opening + motor response + verbal response 3B15

Reprinted fromTeasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical

scale. Lancet 1974;2:8184 [112]; with permission from Elsevier Science.

E. Bedell, D.S. Prough / Anesthesiology Clin N Am 20 (2002) 417439 419


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mask with high-flow 100% oxygen. The decision to provide an artificial airway

should be made by the team leader, and those managing the airway and should be

based upon specific indications. Table 3 lists some of the indications for trachealintubation. Individualization of care is important in managing the patient with

TBI, and as such, established protocols may require modification.

It is important to note that concern about increased ICP influences the

approach to the airway but does not contraindicate endotracheal intubation.

Endotracheal intubation in an unanesthetized patient will increase blood pressure,

heart rate, and ICP [5,6]. However, of greater clinical importance is the fact that

cerebral blood volume (CBV) is increased by hypoxia and hypercarbia [7], that

ICP is increased by untreated hypoxia [8], or hypercarbia [9], and that aspiration

of oral or gastric contents not only interferes with gas exchange but also increaseslong-term morbidity and mortality [10,11]. The increase in ICP with airway

manipulation can be reduced by appropriate use of medications [1214].

Having made the decision to provide an artificial airway, many techniques of

intubation and choices of drugs are possible. In general, the best technique is the

one with which the team members are most proficient. Head-trauma patients are

high-risk individuals in whom experimentation with new techniques or training

of inexperienced personnel may be imprudent. In general, there are two

approaches to the tracheal intubation of head-trauma patients: oral intubation

using direct laryngoscopy and nasal intubation (either blind or fiberopticallyguided). Each approach has advantages and disadvantages.

Associated cervical spine injury is present in approximately 2% [15] to 21%

[16] of trauma patients. Uncontrolled movement of the neck in patients with

cervical spine injury can precipitate neurologic injury, and is therefore to be

Table 3

Indications for endotracheal intubation

Absolute

Apnea, bradypnea (respiratory frequency < 6/min)

Hypoxia on 100% O2 (PaO2 < 70 mmHg, SpO2 < 90%)

Hypercarbia (PaCO2 > 65 mmHg)

Absence of airway protective reflexes (cough, gag, swallow)

Mechanical airway obstruction

Expanding oral or neck mass

Need for the administration of barbiturates, sedatives, or muscle relaxants

Hemodynamic instability/severe hypotension

Glasgow Coma Scale score < 8 (see Table 1)

Relative

Progressive tachypnea (respiratory frequency >35/min)

Flail chestPulmonary aspiration

Combative behavior

Hypothermia (core temperature < 34.5C)

Seizures

Increased intracranial pressure

Mild hypoxia or hypercarbia

Metabolic acidosis (pH < 7.25)



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avoided. Because of this possibility, the use of awake/sedated nasal intubation,

which does not require head movement, has been advocated [17]. Contra-

indications to awake nasal intubation include fractures of the skull base, LaForte fractures, bleeding diatheses, and midface disruption [18,19]. The technique

is much more difficult in patients with slow or absent respirations, and is

relatively contraindicated [20,21]. Fiberoptic visualization is often utilized but

has a number of limitations, including the requirement of a cooperative patient,

need for specialized equipment and training, and vastly increased difficulty when

the airway is contaminated with blood, vomitus, or excessive secretions [2022].

Direct laryngoscopy of patients with cervical injury can be used if accompanied

by manual in-line axial stabilization of the head and neck by an assistant [23]. In

the absence of in-line stabilization, neck movement, especially in the uppercervical spine, has been demonstrated in patients without neck injury [24].

Manual in-line stabilization (previously termed in-line axial traction) decreases

movement of the neck in cadaveric models of cervical spine injury [25], which

theoretically reduces the risk of aggravating cervical spine injury, but also

increases difficulty with visualization and tracheal intubation [26]. Regardless

of the intubation technique chosen, adequate planning and preparation should

precede intubation. The patient should be preoxygenated with 100% oxygen (O2)

by mask; intubating equipment and suction should be present and functioning; all

desired and emergency drugs should be present; and a means of establishing asurgical airway should be available if endotracheal intubation fails.

Intravenous drugs can be used as adjuvants during intubation to create more

controlled and stable intubating conditions and to blunt the systemic effects of

intubation (increased blood pressure and ICP) [1214]. Drugs also can precip-

itate hypotension, result in total airway loss if intubation is unsuccessful, generate

life-threatening electrolyte imbalances (eg, hyperkalemia after succinylcholine in

chronically paraplegic or quadriplegic patients), trigger an anaphylactic or

anaphylactoid reaction, or interact in unexpected ways with the patients other

medications or other medical conditions. Only trained, experienced individualswho are prepared to recognize and manage drug-induced complications should

administer drugs.

Induction agents such as sodium thiopental, etomidate hydrochloride, and

propofol have been used to induce anesthesia before intubation. Each decreases

the systemic response to intubation, blunts ICP changes, and decreases the

cerebral metabolic rate for oxygen (CMRO2). Induction agents also cause apnea

and loss of protective airway reflexes; thus, an artificial airway must be secured,

and controlled ventilation must be initiated after their administration. Another

concern includes cardiovascular depression with propofol and thiopental, whichcan lead to hypotension, especially in the presence of uncorrected hypovolemia.

Hypotension is a primary risk factor for poor outcome after head trauma [2731].

Etomidate is unique in that induction doses usually cause little change in blood

pressure, although it reduces CMRO2 [32]. Etomidate administration, however,

can result in an exaggerated response to intubation, such as tachycardia, and has

been associated with myocardial ischemia in patients with high cardiac risk [33].



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Finally, ketamine, a dissociative anesthetic that preserves spontaneous ventilation

with limited cardiovascular compromise, would seem to be an appropriate agent

for use in establishing an airway in patients with TBI. This agent though, hasbeen associated with increased cerebral blood flow and increased ICP, and as

such, is relatively contraindicated as a single agent for patients with risk for or

preexisting increased ICP [34 36]. Whatever agent is chosen to blunt the

response to intubation, the individual providing the medication must be imme-

diately prepared to assume control of the airway, protect the patient from

pulmonary aspiration, assure adequate oxygenation and ventilation, and treat

systemic hemodynamic responses such as hypotension and tachycardia.

Muscle relaxants are often combined with induction drugs to secure the

airway. Succinylcholine hydrochloride, which is the only ultrashort-acting,depolarizing muscle relaxant presently approved by the Federal Drug Adminis-

tration, produces complete muscle relaxation within 60 to 120 seconds of

administration, with return of muscle strength in a matter of minutes. However,

it can lead to life-threatening hyperkalemia, trigger malignant hyperthermia, and

increase ICP [37,38]. The increase in ICP can be blunted by administration of an

adequate dose of an induction agent such as thiopental [39]. However, even

without treatment, the increase in ICP is transient and of questionable clinical

significance [39]. Increases in ICP secondary to hypoxia and hypercarbia are well

documented and much more likely to be clinically important.Nondepolarizing neuromuscular blocking agents, such as vecuronium bro-

mide, cis-atracurium bresylate, and rocuronium bromide, do not carry the risks of

hyperkalemia, malignant hyperthermia, and increased ICP. Given in large doses,

these drugs produce good-to-excellent intubating conditions within 120 to 180

seconds. However, profound relaxation will persist for 30 to 120 minutes,

mandating expeditious placement of an artificial airway.

All sedative/hypnotics and muscle relaxants used to facilitate endotracheal

intubation compromise protective airway reflexes. In trauma patients, it is

impossible to know when food was last ingested. There may be food, gastricsecretions, or blood within the stomach that may be aspirated into the lungs if

passive or active regurgitation occurs. Because of the risk of a full stomach, a

rapid sequence induction technique should be used when drugs are given that

remove protective reflexes. The rapid sequence induction consists of preoxygen-

ation and denitrogenation with 100% oxygen, application of cricoid pressure

[40], administration of induction agents and muscle relaxants, and immediate

direct laryngoscopy with intubation of the trachea. Positive-pressure ventilation is

avoided between the time of drug administration and intubation. Correctly

applied cricoid pressure is believed to decrease the risk of passive regurgitationand aspiration of gastric contents by mechanically occluding the esophagus at the

level of the cricoid ring. However, application of cricoid pressure in cadavers

caused cervical spine displacement in cases of ligamentous or bony disruption

[41], raising concerns about the safety of cricoid pressure in situations in which

cervical spine injury is present or likely. Even in healthy patients with no

identified risks for cervical spine instability, single-handed cricoid pressure



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(applied to only the anterior neck without posterior support) was associated with

a mean neck displacement of 4.6 mm (range of 08 mm) [42]. Therefore, the risk

of iatrogenic cervical cord injury in such patients must be weighed against therisk of gastric aspiration. Even with the risks of direct laryngoscopy, several

retrospective studies have suggested that direct laryngoscopy, even in the

presence of known cervical spine injuries, is as safe as alternate techniques

[43]. If endotracheal intubation is needed in a patient with known cervical spine

injury, other options such as blind nasal or fiberoptic intubation should be

considered if time and clinical circumstances permit. If direct laryngoscopy with

the application of cricoid pressure is to be used, the use of bi-manual cricoid

pressure (anterior compression of the cricoid cartilage with simultaneous support

of the posterior neck) has also been proposed [44]. Effective evaluation and acutestabilization of the head-trauma patient must precede all other interventions.

Necessary airway management should not be delayed or withheld because of fear

of increased ICP or the need for other diagnostic studies such as computed

tomographic (CT) scans, angiography, or cervical radiographs.

Having evaluated and dealt with airway, ventilation, and oxygenation issues,

the trauma team can proceed to hemodynamic evaluation. This evaluation

includes an estimation of intravascular volume, establishment of adequate

vascular access (peripheral venous, central venous, and arterial catheterization),

review of estimated blood loss, acquisition of baseline laboratory studies, andresuscitation. Because of the potential for unrecognized blood and fluid loss,

hypovolemia is always a possibility. Heart rate and blood pressure are insensitive

indicators of volume status. Young, previously healthy patients can lose nearly

30% of their blood volume yet not manifest overt hypotension in the supine

position. Reflex systemic hypertension is commonly observed with head trauma,

further confounding clinical assessment of intravascular volume.

The importance of avoiding hypotension cannot be overemphasized. Tables 4

and 5 illustrate the effects of hypotension on outcome after head injury. Fig. 1

graphically represents the influence of in-hospital hypotension on the long-term

Table 4

Outcome by secondary insult occurring from time of injury through resuscitation at Traumatic Coma

Data Bank Hospital Emergency Department for mutually exclusive insults

Number % of total Outcome (%)

Secondary insults of patients patients GR or MD SD or PVS Dead

Total cases 717 100 43.0 20.2 36.8

Neither 308 43.0 53.9 19.2 26.9

Hypoxia 161 22.4 50.3 21.7 28.0Hypotension 82 11.4 32.9 17.1 50.0

Both 166 23.2 20.5 22.3 57.2

Hypoxia, PaO2 < 60 mmHg; hypotension, systolic blood pressure < 90 mmHg.

Abbreviations: GR, good recovery; MD, moderate disability; SD, severe disability; PVS, persistent

vegetative state.

FromChesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining

outcome from severe head injury. J Trauma 1993;34:216222 [29]; with permission.



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outcomes of patients with head injury. Failure to recognize, intervene, and correct

hypotension, even at the earliest stages of management, is associated with poorer

outcome, and blood pressure should be the primary focus of initial evaluation and

resuscitation of the head-injured patient after airway management. Although

hypoxemia should be avoided, head injury appears to be much more adversely

influenced by hypotension.The choice of resuscitation fluid after head trauma is a matter of ongoing debate.

Relatively isotonic crystalloid solutions (lactated Ringers solution and 0.9%

saline) have been used extensively for years. It is important to remember that the

osmolarity of lactated Ringers solution is only 273 mOsm/L, while that of 0.9%

saline is 308 mOsm/L. Large volumes of lactated Ringers solution will decrease

serum osmolarity and thus increase total brain water [45,46]. Some institutions

limit the volume of lactated Ringers solution to 2000 mL, while others use 0.9%

saline as the crystalloid of choice. Because of crystalloid distribution throughout all

extracellular spaces, a ratio of 5:1 is required to replace blood loss (ratio ofinterstitial fluid volume to plasma volume). In major blood loss, this may represent

a considerable volume, especially because the ratio of crystalloid to blood loss

increases as protein dilution occurs [47]. Also, rapid infusion of unwarmed fluid

can lead to hypothermia. Despite years of treatment with fluid restriction of head-

injured patients, experimental and clinical data strongly suggest that there is little

correlation between total fluid administration and clinical outcome [48]; moreover,

if inadequate resuscitation results in hypotension, ICP may increase [49].

Hypertonic crystalloid solutions such as 3% and 7.5% saline have been used to

avoid the large volumes of isotonic crystalloids necessary for resuscitation.Hypertonic solutions increase intravascular volume by shifting water from the

intracellular to the extracellular space [50]. These agents increase intravascular

volume and improved hemodynamic stability in hypovolemic shock [51] and

reduce ICP but do not reliably restore cerebral oxygen delivery after experimental

head trauma [52]. The total volume of hypertonic saline should be limited to

minimize electrolyte imbalance and hyperosmolality.

Table 5

Outcome by secondary insult present at time of arrival at Traumatic Coma Data Bank Hospital

Emergency Department for mutually exclusive insults

Number % of total Outcome (%)

Secondary insults of patients patients GR or MD SD or PVS Dead

Total cases 699 100.0 42.9 20.5 36.6

Neither 456 65.2 51.1 21.9 27.0

Hypoxia 78 11.2 44.9 21.8 33.3

Hypotension 113 16.2 25.7 14.1 60.2

Both 52 7.4 5.8 19.2 75.0

Hypoxia, PaO2 < 60 mmHg; hypotension, systolic blood pressure < 90 mmHg.

Abbreviations: GR, good recovery; MD, moderate disability; SD, severe disability; PVS, persistent

vegetative state.FromChesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining

outcome from severe head injury. J Trauma 1993;34:216222 [29]; with permission.



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Fig. 1. Outcome (Glasgow Outcome Scale at 12 months after injury) as influenced by in-hospital hypotension (one or more ep

for 493 patients in the Traumatic Coma Data Bank (TCDB). Early hypotension is that present on arrival at the TCDB hospital

the patients stay in the intensive care unit beginning after the first shift. From Chesnut RM. Secondary brain insults after h

1995;3:366 375 [114]; with permission.


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Isotonic colloidal solutions (hetastarch, pentastarch, albumin, and blood) are

useful for acute volume expansion, and are given in a ratio of 1:1 to replace blood

loss. Because of concerns about compatibility, infection, and availability, the useof blood products for initial resuscitation should be restricted to severe ongoing

hemorrhage, severely compromised oxygen delivery, and bleeding diatheses

[53,54]. Six percent hetastarch and 5% albumin are frequently given instead of

packed red cells or crystalloid. Hetastarch, in volumes greater than 20 mL/kg, has

been associated with abnormal clotting profiles and a risk of increased bleeding

[55,56], while 5% albumin, as a human product, is expensive, limited in

availability, and has been associated in rare instances with anaphylactic reactions.

Meta-analyses suggest that overall survival is not increased by the use of albumin

or colloid [57] and perhaps is even worsened [58]. In the future, synthetic bloodproducts, such as recombinant hemoglobin, may become available for use in

resuscitation. These agents would allow rapid volume expansion without the risks

of incompatibility, infection, or scarcity while improving oxygen delivery [59].

To date though, these agents have not been efficacious, and the only agent studied

in a clinical setting was withdrawn because of increased patient mortality [60].

Hypotonic solutions and glucose-containing solutions deserve special men-

tion. Because of redistribution of hypotonic solutions throughout total body

water, 5% dextrose in water (D5W) is ineffective as a resuscitation fluid. Only

7% of intravenously administered D5W remains intravascularly after equili-bration; therefore, the volumes required to resuscitate even limited blood loss

may cause severe hyponatremia and may aggravate cerebral edema. Hyper-

glycemia in conjunction with TBI has been associated with worsened outcome

both in animal and human studies [61 63]. Consequently, glucose-containing

solutions, unless required to correct hypoglycemia, should be avoided in head

trauma. Because hypovolemia, hypotension, and shock are so important, and

because it is not clear which fluid is best (given the above caveats), the choice of

resuscitation fluid is more a matter of personal preference than a choice based

upon clear scientific outcome studies.With the ABCs addressed, attention can shift to the management of specific

injuries. For the purposes of this article, we will assume an isolated TBI. (In

clinical practice, other injuries could be of higher priority and require more

prompt attention. The early goals of management are to diagnose the extent of all

injuries, to resuscitate and stabilize the head-injured patient, and to expedite

needed surgical intervention.)

Management

After the initial evaluation and resuscitation are completed, the management of

blood pressure and ICP becomes paramount and is based on the interrelationships

between brain trauma, intracranial pressure, and hemodynamic manipulations.

Conventionally, invasive ICP monitoring is used if GCS is 8. This is usually

deferred for patients scheduled for immediate craniotomy. In those patients



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scheduled for non-neurosurgical procedures under general anesthesia (eg, extrem-

ity surgery), one should consider placement of ICP monitoring devices for those

with GCS 12 as they are at risk for intraoperative deterioration, and stronglyconsider placement for those with an initial GCS 8.

Irreversible ischemic cell damage occurs rapidly when there is inadequate

cerebral blood flow (CBF) that contributes to brain injury [27] on a global,

regional, or focal level. The actual determinants of CBF are complex, and

there are no tests or studies to monitor CBF real-time in an emergency setting.

The supervisory physician must thus make empirical management decisions

about the adequacy of CBF, based on the clinical situation and on an estimation

of cerebral perfusion pressure (CPP), which is defined as mean arterial blood

pressure (MAP) minus ICP or central venous pressure (CVP), whichever ishigher. In clinical practice, a CPP of 60 80 mmHg generally is considered

adequate [64].

CPP represents the blood pressure gradient across the brains vascular bed, and

thus determines blood flow through the brain. This relationship can be modeled

through a modification of Ohms Law, which states that the pressure gradient

(arterial pressure minus venous pressure) equals the flow times the resistance:

Pressure Flow Resistance

This model must be used with care. It would be easy to mistakenly assume thatthe resistive element in the equation is fixed. In reality, there is great variability in

cerebral vascular resistance due to local and systemic factors. Both experimental

and clinical brain trauma are associated with acutely increased cerebrovascu-

lar resistance.

In healthy, nontraumatized patients, cerebral vascular resistance is regulated

predominantly at the precapillary arterioles to maintain a constant blood flow

adequate to supply the needs of the brain tissue. Classic examples of these

changes are listed in Table 6. These changes in resistance are the foundation for

the concept of cerebral autoregulation, which holds that CBF is regulated throughalterations in arteriolar muscular tone under a wide variety of situations to

maintain a balance between CBF and CMRO2. Normal autoregulatory profiles

for humans are well described, and are shown in Fig. 2, although these responses

are altered in disease states and after TBI. In normal individuals, there is a direct

relationship between blood pressure and cerebral vascular resistance, allowing for

a constant blood flow over a wide range of MAPs.

Table 6

Effect of systemic and local factors on cerebrovascular resistance

Causes of cerebral vasoconstriction Causes of cerebral vasodilation

Increased blood pressure Decreased blood pressure

Decreased PaCO2 Increased PaCO2Decreased blood viscosity Increased blood viscosity

Barbiturates Hypoxia (SaO2 < 60 mmHg)

Decreased cerebral metabolic demands Increased cerebral metabolic demands



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After TBI, vascular reactivity is acutely altered [65]. Pressure autoregulation

is lost at lower levels of CPP [66]. In experimental animals, loss of autoregu-

lation has led to increased neurologic injury with even mild hemorrhagic hypo-

tension [67]. Moreover, in the acute interval after both experimental [67]

and clinical [27] traumatic brain injury, CBF is substantially reduced; one thirdof patients have decreased regional or global CBF to a level that can cause

cerebral ischemia within 8 hours of injury [68]. Posttraumatic impairment of

pressure autoregulation may further reduce CBF at blood pressures that might

otherwise be considered safe, which may explain the worsened outcome

associated with hypotension.

In contrast, hypertension after TBI could increase intracranial hemorrhage or

disrupt the upper limits of pressure autoregulation leading to excessive CBV

[69,70]. Initially, a patient with TBI may manifest systemic hypertension. In

some patients, an increase in MAP may be necessary to overcome increased ICP(and thus maintain CPP). Treating systemic hypertension before ruling out

increased ICP may lead to inadequate CPP [71], while failure to treat systemic

hypertension in the presence of an intracranial bleed may lead to hematoma

expansion and higher ICP. Evidence of increased ICP and the presence of

systemic hypertension should be an indication for early diagnostic procedures.

A judgment should be made about the presence of increased ICP or about

Fig. 2. The relationship of cerebral blood flow (CBF) to cerebral perfusion pressure (CPP), PaCO2,and PaO2. Units on the abscissa are in mmHg. From Michenfelder JD. The awake brain. In:

Michenfelder, JD, editor. Anthesthesia and the brain: clinical, functional, metabolic, and vascular

correlates. New York: Churchill Livingstone; 1998. p. 321 [115]; with permission.



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whether the hypertension is leading to further patient compromise before treating

systemic hypertension aggressively. With the availability of CT scanners in most

medical centers, the rapid diagnosis of intracranial mass lesions should bepossible without significant delay. In summary, it is prudent to keep in mind

the possible alterations in cerebral vascular reactivity and avoid even mild

hypotension, while at the same time guarding against uncontrolled or sustained

hypertension. A reasonable guideline for blood pressure management is a CPP of

60 to 100 mmHg.

Changes in arterial carbon dioxide tension (PaCO2) also influence CBF.

Cerebral vascular reactivity to PaCO2was noted in the early 1950s in association

with high-altitude military aircraft [72]. It was hypothesized that severe hypo-

capnia had deleterious effects [73], reflecting the basic question, Can hypocarbiaproduce cerebral vasoconstriction sufficient to precipitate cerebral ischemia?

Animal studies and clinical electrophysiologic data have not supported the concept

that hypocarbia induces cerebral ischemia in normal brain [74,75]. The study of the

effects of hypocarbia on abnormal brains (eg, TBI) has yielded different results.

Animal studies have demonstrated that hypocarbia, in association with anemia,

hypotension, or brain retraction, can lead to ischemia injury, and there is growing

evidence that hypocarbia may be associated with worsened long-term outcome in

head-trauma patients [7678]. The routine use of hyperventilation in head-trauma

patients is, therefore, no longer recommended. Two relative indications for the useof hyperventilation include acute increases in ICP and the need to improve surgical

exposure. Use of prolonged hyperventilation may require the insertion of a

regional or focal measure of the adequacy of cerebral oxygenation, such as jugular

venous oximetry or brain tissue oxygen sensors (see below).

Management of ICP also contributes to maintaining an adequate CPP.

Intracranial pressure is the relationship between the volume of the skull and its

contents. This relationship is described by the elastance curve, which relates ICP

and intracranial volume (Fig. 3). As the volume of the intracranial contents ap-

proaches the available space (the knee of the curve), the pressure increasesrapidly. Beyond this point, even small additional volume increases can dramat-

ically increase ICP.

The intracranial contents can be arbitrarily divided into four groups: solid

mass, water, cerebrospinal fluid (CSF), and intravascular blood. Management

techniques can be aimed at all four areas with varying degrees of success. Solid

intracranial contents include nonwater brain parenchyma plus missile compo-

nents, bone fragments, and hematomas. These elements cannot be pharmacolog-

ically or physiologically manipulated. Surgical decompression or decreasing the

relative volume of the other intracranial contents remain the only practicaloptions. Therefore, it is vital to understand the techniques, risks, and potential

benefits of altering the volume of the other intracranial components in the

management of ICP.

CSF drainage can be used to decrease ICP as well as to control hydrocephalus

and improve surgical exposure. Pharmacologic manipulation of CSF production

and elimination using acetazolamide is slow in onset and difficult to titrate. The



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intraoperative adjustment of CSF volume is not a primary technique for the

management of ICP during anesthesia unless a ventriculostomy is in place.

However, graded CSF drainage is used to control ICP in some centers.

Reducing intracranial water content is important in the management of

intracranial hypertension associated with TBI. Brain water content depends upon

the cellular integrity and function of the bloodbrain barrier, the osmolality of

blood, and the osmolality of the fluid administered. Brain water is minimally

influenced by changes in colloid osmotic pressure, but is highly influenced byacute changes in osmolality [79]. Hypotonic fluids increased brain water [46],

and hypertonic fluids decreased brain water in animals [50]. Overall brain water

can also be reduced through administration of osmotic agents such as mannitol

(in doses of 0.51 g/kg). Although countless clinicians have observed decreased

ICP after administration of these agents, the precise mechanism of action of

mannitol has been questioned [80]. In contrast, glucocorticoids do not decrease

traumatic brain edema [81], despite their established efficacy in reducing vaso-

genic edema associated with brain tumors. Glucocorticoids are indicated for the

acute treatment of spinal cord injury, and should be initiated as soon asreasonable following injury [82].

Adjustment of intracranial blood volume remains the mainstay of acute ICP

management. CBV is approximately 3.5 mL/100 g brain tissue in healthy

individuals [83], or about 50 mL, approximately one-fourth of which is arterial

and three-fourths venous. It is important to appreciate the difference between CBV

and CBF, and the difference between arterial and venous blood volume. CBF is the

Fig. 3. Elastance curve for the cranial vault. Additional volume is well tolerated if reserves are good;

however, as intracranial volume increases to a critical point, intracranial pressure (ICP) increases

rapidly with further small increments in intracranial volume.



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rate at which blood traverses the cerebral vascular bed (generally 55 mL/min-

100 g), while CBV is the actual volume of blood contained within the vascular bed.

CBF and CBV are not directly coupled; an increase in CBF does not necessarilylead to an increase in CBV. An acute increase in CBF may lead to reflex arteriolar

vasoconstriction and an overall decrease in CBV (and thus a decrease in ICP)

[64,84]. Similarly, the management of arterial and venous blood volumes must be

considered separately. The arterial vascular system will autoregulate based upon

local and systemic factors, while the volume in the venous circuit usually responds

passively to external factors such as venous distending pressure.

Alteration of arterial CBV remains a principal tool in management of ICP after

head trauma. By manipulating the reactive arterial vascular system, it is possible

to induce arterial vasoconstriction and to decrease arterial CBV. Table 6 listssome of the arterial responses to various local and systemic challenges. Peri-

arteriolar hydrogen ion concentration ([H+]) powerfully influences cerebral

arteriolar tone. Clinical management usually emphasizes PaCO2. As the PaCO2increases, [H+] increases. Arteriolar diameter increases, leading to a concomitant

decrease in cerebral vascular resistance, an increase in CBF, and an increase in

CBV. The opposite occurs with decreased [H+] (decreased PaCO2). The effects of

lowering PaCO2 are rapid in onset (23 minutes) and remain for a number of

hours. This acute effect is lost, however, as buffering of periarteriolar [H+]

diminishes the effect of hyperventilation on arteriolar vascular tone. By 24 hours,the initial vasoconstriction is gone, and an abrupt return to normal PaCO2 may

lead to cerebral vasodilation and increased ICP [85]. In normal brain, increases in

CO2 to greater than 80 mmHg do not lead to greater cerebral vasodilation, as

relaxation is maximal. Similarly, in normal brain, hyperventilation to PaCO2below 20 mmHg does not lead to further vasoconstriction, as either local factors

or mechanical factors inhibit further vasoconstriction.

After cerebral ischemia or TBI, the role of PaCO2 is less clear. Excessively

low PaCO2 may contribute to or cause ischemia [78] and worsen long-term

cellular survival. The measurement of cerebral oxygenation using cerebralvenous oxygen saturation has shown that hyperventilation can lead to significant

decreases in saturation [86]. Although low PaCO2 may constrict normal arterio-

les, thereby shunting blood to ischemic areas [87], this Robin Hood process of

stealing blood from rich tissue beds to give to poor regions has been

difficult to prove. Redistribution of blood flow from normal areas to ischemic

areas has been unpredictable [88] and ideally requires continuous real-time

monitoring for proof of efficacy. Hyperventilation should thus be restricted to

short intervals with specific goals such as acutely decreasing ICP or improving

surgical exposure, and consideration for the use of jugular venous saturationmonitoring should be made [89]. PaCO2 should be allowed to return toward

normal as soon as the acute indications pass. It is intriguing to note that the

effects of hyperventilation can be modified in patients with TBI. Use of

supplemental inspired oxygen to develop hyperoxia (arterial oxygen tension

[PaO2] > 200 mmHg) has been shown to ameliorate the effects of hyperventila-

tion and improve jugular saturation in patients with TBI [90,91]. The utility of



16/23

hyperoxia as a clinical tool is as yet unproven, but represents an ongoing area of

provocative research.

Hypoxia remains one of the most potent arteriolar cerebrovascular dilators.Hypoxia or ischemia leads to marked vasodilation, increased arterial vascular

volume, and increased ICP. Normal systemic oxygenation does not necessarily

imply adequate cerebral oxygenation; CBF and oxygen-carrying capacity must

also be adequate. Techniques for monitoring transcranial cerebral oxygen

saturation [92,93], jugular venous oxygen saturation [94], and brain tissue partial

pressure of oxygen (PO2) are being developed or are available to provide real-

time information about the adequacy of cerebral oxygenation. In the future, these

techniques may become available for routine evaluation of head-injured patients.

At present, maintenance of adequate CPP and oxygen-carrying capacity remainthe primary tools for preserving cerebral oxygenation.

The phenomenon of pressure autoregulation is also critical in regulating CBV.

Cerebral arteriolar smooth muscle responds to increased intravascular pressure

with increased vascular tone within the range of pressure autoregulation. As

blood pressure increases, arteriolar vasoconstriction maintains constant flow and

decreases arterial blood volume. By the same mechanism, decreased blood

pressure (or hypotension) produces arteriolar dilation and increases arterial blood

volume. Because hypotension-induced reflex vasodilation may increase CBV and

ICP in head-injured patients [49], protection against hypotension remains a keycomponent in the management of arterial blood volume and ICP.

Red cell rheology and blood viscosity play a role in arterial vasoconstriction.

Decreasing hematocrit decreases blood viscosity, which leads to vasoconstriction

of normal brain arterioles [95]. Thus, hemodilution increases CBF and results in

reflex vasoconstriction, which has been termed blood viscosity autoregulation

[96]. The clinical importance of this phenomenon is controversial [97]. Admin-

istration of mannitol alters red cell deformability and decreases viscosity

unrelated to changes in hematocrit [98]. This observation may explain mannitol-

induced decreases in ICP that are not related to total brain water or hemodilu-tion [99101].

Vascular autoregulation is determined by many factors, including viscosity and

CBF. In addition, if oxygen-carrying capacity is decreased below the metabolic

requirements of the brain, cerebral vasodilation will occur. The difference of the

impact of hemodilution-induced vasoconstriction and vasodilation secondary to

inadequate oxygen delivery is difficult to determine clinically. In practice, the

optimal hematocrit for head-injured patients remains undefined.

Pharmacologic interventions are another important means of altering arteriolar

resistance and arterial blood volume. Table 7 lists some commonly administereddrugs and their effects on cerebral arterial tone. Volatile inhalational agents and

nitrous oxide cause arterial vasodilation; although hyperventilation modifies

drug-induced cerebral vasodilation, it does not reliably prevent increases in

ICP. Therefore, intravenous agents such as narcotics, benzodiazepines, and short-

acting hypnotics have been used for anesthesia in cases of head trauma. With

either inhalational or intravenous techniques, hypotension must be avoided. Some



17/23

intravenous agents, including propofol and thiopental [102], cause systemic

vasodilation or myocardial depression, which may lead to hypotension, especially

in conjunction with uncorrected hypovolemia. Therefore, blood pressure must be

monitored and hypotension treated promptly and aggressively. Because of the

risks and benefits of different anesthetic approaches, the clinician should becareful about the choice of drugs for individual patients.

Cerebral venous blood volume depends upon CBF, gravity, and restriction to

outflow. Increased blood viscosity decreases flow (by increasing resistance),

leading to increased blood volume. Decreasing the venous pressure differential

(by increasing CVP [103], lowering the head [104], or inducing cerebral

venodilation) will increase venous CBV. Increasing the resistance to venous

outflow by bandaging the neck or extreme lateral rotation of the head can

increase venous CBV [83,105]. Maneuvers that facilitate cerebral venous

drainage and therefore potentially decrease venous CBV, are listed in Table 8.However, if such maneuvers decrease CPP (eg, head elevation leading to

hypotension), the benefits of improved venous return may be negated [106].

Attempts to limit secondary brain injury should ideally include the initiation of

protective measures that would improve the outcome of damaged cells and protect

normal tissue from harm. The concept of brain protection is used extensively in

Table 7

Effects of selected drugs on cerebral vascular resistance, systemic vascular resistance, and myocar-

dial contractility

Drug CVR SVR Myocardial

Ketamine Decreased Increased Increased

Halothane Decreased Unchanged Decreased

Isoflurane Decreased Decreased Unchangeda

Sevoflurane Decreased Decreased Unchangeda

Nitrous oxide Decreased Unchanged Decreased

Barbiturates Increased Decreased Decreased

Benzodiazepines Increased Decreased Unchanged

Narcotics Variable Decreased Unchanged

Etomidate Increased Unchanged Unchanged

Propofol Increased Decreased Decreased

Abbreviations:CVR, cerebral vascular resistance; SVR, systemic vascular resistance.a Note that systemic arterial dilation may preserve cardiac output, thus masking myocar-

dial depression.

Table 8

Techniques to decrease cerebral venous blood volume

Avoid extremes of neck rotation

Avoid direct jugular compression

Elevate head (caution: hypotension negates effect on CPP)

Decrease blood viscosity (mannitol)

Avoid sustained increases in intrathoracic pressure

Avoid cerebral venodilators (e.g., nitroglycerine, etc.)

Abbreviations:CPP, cerebral perfusion pressure; ICP, intracranial pressure.



18/23

cardiac surgery and neurosurgery. Techniques to decrease the likelihood of

permanent ischemic injury to brain, such as active hypothermia preceding

complete circulatory arrest, are now accepted practices [107]. The efficacy ofthese techniques after ischemic or traumatic insults is less established. Preliminary,

single-institution studies evaluating hypothermia and long-term outcome after

head trauma suggested that decreasing the temperature of the brain shortly after

injury improved morbidity and mortality [108 110]; however, a recent multicenter

trial did not reproduce these earlier findings [4]. An interesting finding in that trial

was the fact that the worst outcome occurred in patients who arrived at the hospital

and were rapidly rewarmed. A variety of drugs that influenced outcome after

ischemic and traumatic brain injury in experimental animals have also been studied

in clinical trials but to date have not been shown to improve outcome. At present,the most important goal is the reestablishment of adequate brain tissue oxygenation

to limit further cellular compromise. Based upon the clinical presentation, a

specific care plan should encompass patient needs, and allow for rapid evaluation

and treatment and flexibility based upon new research.

Summary

The management of TBI remains an important and frustrating component of thepractice of anesthesiology and critical care medicine. The difficulties in manage-

ment of TBI as well as the poor response rates to medical therapy after TBI are not

new. The following passage appeared in the introductory chapter of a text on TBI

from 1897: The manner of treatment is of importance in only a minority of cases,

since many subjects of intracranial injury are fated to die whatever measures may

be adopted for their relief, and a still greater number are destined to recover though

left entirely to the resources of nature. It is probable that in by far the larger

proportion of cases in which the issue is determined by treatment it is met in the

initial stage, and by insuring restoration from primary shock [111].Although secondary insults from factors such as hypotension, hypoxemia, and

hyperventilation increase morbidity and mortality, data are not yet available to

indicate whether scrupulous prevention and prompt treatment of secondary

injuries will reduce morbidity and mortality. In addition, no specific intervention

to date has improved overall long-term outcome. With ongoing research, perhaps

active interventions will become available. Until that time, thoughtful and care-

ful attention to physiologic management provides the greatest opportunity for a

good outcome.

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