Chapter 105 - Neurocritical Care - Anesthesiamiller8e:... · margin. 3. This is typically seen in severe lateral herniation (”midline shift”) when the anterior cerebral vasculature

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Neurocritical CareMICHAEL J. SOUTER • ARTHUR M. LAM

K e y P o i n t s

• Critical care of the nervous system is based on support of cerebral and spinal cord physiology and the prevention of secondary insults. This goal, in turn, depends on the comprehensive maintenance and adequacy of cardiopulmonary, gastrointestinal, renal, and endocrine function.

• Cerebral function is critically dependent on perfusion and oxygenation matching metabolism. Increased intracranial volume beyond the capacity of compensatory mechanism increases intracranial pressure (ICP) and may diminish perfusion adversely. The resulting cellular energy failure both initiates and propagates edema and inflammation.

• The resolution of cerebral edema depends on hydrostatic and osmolar forces applied to the blood-brain barrier. Excesses of perfusion pressure or intravascular hypotonicity worsen edema and must be avoided. Blood-brain barrier disruption varies over time and by pathologic process, and it affects the ability of hypertonic agents to exert an osmotic effect.

• Fever is frequently overlooked in the neurocritical care unit, but it significantly affects patient outcomes across a range of pathologic processes.

• Neurologic monitoring comprises placement of appropriate monitoring devices, as well as prompt response and institution of therapy to changes detected. The goal is to optimize the physiologic environment, despite the current lack of level 1 evidence to support the majority of monitors in common use. Clinical examination of neurologic function remains a crucial part of monitoring and care.

• The incidence of traumatic brain injury has declined, but this disorder remains a disease of the young, with enormous long-term socioeconomic impact. Prompt surgical appraisal is mandatory. Decompressive craniectomy after diffuse injury is not currently recommended. Hypothermia may still offer benefit in refractory intracranial hypertension. Corticosteroids are contraindicated.

• After the initial hemorrhage, mortality and morbidity from subarachnoid hemorrhage (SAH) arise from cerebral ischemia. Medical therapy for this complication involves augmentation of perfusion pressure, maintenance of blood volume, and optimization of oxygen delivery. Endovascular therapy with angioplasty with or without chemical vasodilation plays an important role in treating vasospasm. SAH may be accompanied by significant pulmonary, cardiovascular, or endocrine effects.

• Successful therapy for ischemic stroke is contingent on a time window of viability. Urgent appraisal and rapid treatment are crucial to a good outcome. Endovascular therapy and ultrasound are going to play an increasing role in conjunction with advances in magnetic resonance imaging.

• Injury to the spinal cord necessitates careful observation of respiratory adequacy because conditions may deteriorate before any observed improvement occurs. Fatigue is frequently a factor.

• Infectious disease of the central nervous system demands an aggressive approach to resuscitation, cerebrospinal fluid sampling, and early empiric antibiotic therapy, similar to that for sepsis.

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Critical care of the central nervous system (CNS) involves collaboration among several disciplines—neurosurgery, neuroanesthesia, neurology, neuroradiology, and electro-physiology. Each discipline offers unique contributions, which, in partnership, provide optimal care not only to the injured brain but also to the cardiopulmonary, endo-crine, gastrointestinal, and renal systems that support cerebral physiology. Integration of the complex goals of this care relies on the physician specializing in neurocriti-cal care, which increasingly is recognized as an important subspecialty.1

The use of a neurocritical care team, rather than sin-gle specialty care, has been associated with reduced in- hospital mortality and length of stay.2 Although the brain has a certain preeminence among the organs of the body, it relies on a stable platform of organ function else-where to enable homeostatic control and mechanisms of repair and recovery. Injury to the brain is associated with and precipitates a wide spectrum of dysfunction of other organ systems (Box 105-1). Although other specialists can train to be neurointensivists, anesthesiologists with

Global PyrexiaInflammatory activation

Cardiovascular Arrhythmia: bradycardia, tachycardia, atrial fibrillationHypertensionHypotensionLeft ventricular dysfunction

Respiratory ApneaPneumonia: aspiration, hypostatic, ventilator associatedPulmonary edemaARDS

Gastrointestinal Gastric erosionIleusConstipationPerforationMalabsorption

Renal DehydrationAcute renal failureUrinary tract infection

Hematologic AnemiaLeukocytosisCoagulopathy, disseminated intravascular coagulationDeep venous thrombosis, pulmonary embolism

Metabolic or endocrine Hyponatremia, hypernatremiaHyperglycemia, hypoglycemiaHypokalemia, hyperkalemiaHypomagnesemiaHypophosphatemiaCatabolic azotemiaRhabdomyolysis

BOX 105-1 Potential Systemic Complications Associated with Serious Brain Injury

ARDS, Acute respiratory distress syndrome.

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Chapter 105: Neurocritical Care 3099

training in neuroanesthesia and critical care are particu-larly well suited to demonstrate the combination of air-way and cardiovascular support skills that, together with an understanding of the physiology and pharmacology of the nervous system, may improve outcome.

INTRACRANIAL PHYSIOLOGY AND CEREBRAL AUTOREGULATION

The cerebrovascular circulation is constrained by a rigid perimeter of bone (see also Chapter 17). After exhaustion of limited compensatory mechanisms, the bony confines of the skull mandate increasing intracranial pressure (ICP) consequent to increasing intracranial volume. The change in ICP with change in intracranial volume is often referred to as the intracranial compliance curve, but it is more appropriately termed the intracranial elastance curve (Fig. 105-1).

Thus, an increase in elastance implies poor compli-ance, and a small change in volume can lead to an inordi-nate increase in pressure. These changes in volume arise from increments in intracranial tissue or fluid content (i.e., blood, interstitial fluid, or cerebrospinal fluid [CSF]). Tissue content is relevant insofar as mass lesions reduce intracerebral compliance and accentuate the effects of fluid changes.

Small increases in volume can be accommodated by an outflow of CSF from the cranial cavity into the spi-nal canal that produces the exponential pressure-volume relationship (see Fig. 105-1).

The cranial vault is compartmentalized by the falx cerebri and tentorium cerebelli, which creates the possi-bility of internal pressure gradients (Fig. 105-2). This may induce physical protrusion of brain tissue through the “apertures” of the compartments—herniation. Brain tis-sue may be injured directly but also indirectly by deform-ing and compressing vasculature adjacent to the dural margin.3 This is typically seen in severe lateral herniation (”midline shift”) when the anterior cerebral vasculature may be obstructed, thus producing frontal lobe infarction.

Pressure gradients are initially hydraulically equili-brated, with CSF moving between ventricular chambers and to the extracranial spinal space. The compensation achieved is limited by the CSF volume available to be displaced; ultimately, changes in volume will induce tis-sue displacement. This displacement may also contribute to impedance of CSF drainage either by occlusion of the foramina of Monro in the case of lateral herniation or by occlusion of the third ventricle and aqueduct by supraten-torial herniation through the tentorial gap. This situation typically gives rise to clinical features of midbrain struc-ture compression. Unilateral papillary dilation, ipsilateral or even contralateral paralysis (the Kernohan notch phe-nomenon), and abnormalities of respiration are apparent in the spontaneously breathing patient. If the herniation continues, it will result in cerebellar descent through the foramen magnum with consequent compression of the brainstem, thus producing bilateral papillary fixation, either tachycardia or bradycardia, and systemic hyper-tension.4 Changes in cerebral mass secondary to increase in venous blood volume also arise from obstruction to

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PART VIII: Critical Care Medicine3100

venous drainage by compression of the easily susceptible bridging veins draining from cortex to venous sinuses. Once an individual threshold of compliance is crossed, changes in volume exert a mass effect on the draining veins, which act as Starling resistors. This effect decreases drainage, which, in turn, amplifies and prolongs pressure

Intr

acra

nial

pre

ssur

e

Intracranial volume

Figure 105-1. Intracranial pressure-volume relationship.

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increases. Blood volume increases may be extravascular (i.e., hemorrhage) or intravascular (i.e., accumulation within a predominantly venous capacitance circulation). Venous circulation comprises approximately 75% of the cranial blood volume, whereas approximately 25% of ves-sels are arteries, arterioles, and capillaries.

The other main fluid mass effect is through edema, either cytotoxic or vasogenic.5,6 Cytotoxic edema results from hypoxia, with swelling of the intracellular compart-ment, whereas vasogenic edema in the interstitium usu-ally develops from a breach of the blood-brain barrier, often in response to high blood pressure.7

Thus, changes in the control of cerebral blood volume may have significant effects on ICP. The cerebral vascula-ture responds to changes in arterial pressure, arterial par-tial pressure of carbon dioxide (Paco2), or partial pressure of oxygen (PO2), by dynamically altering arteriolar caliber to maintain a constantly matched cerebral blood flow (CBF) sufficient to meet metabolic demands (Fig. 105-3). The pH, Paco2, potassium, and adenosine are among many purported metabolic mediators of flow.8

CBF control may be directly compromised by brain injury or by abnormalities of respiration and arterial blood pressure. In turn, this may increase venous vol-ume by allowing an excessive arterial inflow that venous

Tentoriumcerebelli

Oculomotornerve

Falx cerebri

Foramen of Monro

Fourth ventricle

• •

Figure 105-2. Schematic of intracranial compartments: coronal section.

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drainage cannot match, thereby increasing ICP. Conse-quently, untoward events, including hypotension, airway obstruction, fever, and seizures, produce what is termed a secondary physiologic insult. This has been demonstrated to induce further harm to the vulnerable brain and, in so doing, worsen outcome.6,9

A reduction in substrate delivery (i.e., oxygen and nutrients) to less than the threshold necessary to main-tain cellular viability produces cell injury with cytokine and chemokine release. This inflammatory amplification expands the injury,10 disrupts the blood-brain barrier function, and may directly lead to apoptosis. The disrup-tion of the blood-brain barrier creates vasogenic edema and allows serum proteins to cross into brain paren-chyma, with prolonged effects. This process is more evi-dent in the more metabolically active gray matter than in

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60

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00 50 100 150 200

CB

F m

L/10

0 g/

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Arterial

Venous

PO2 PCO2MAP

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Figure 105-3. The influence of changes in mean arterial pressure (MAP), arterial partial pressure of oxygen (PO2), and arterial partial pressure of carbon dioxide (Pco2) upon cerebral blood flow (CBF). Vascular diameter changes shown are in response to MAP.

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white matter.5 Most changes peak in the first 48 hours, but one study identified up to 25% of ICP peak increases occurring after day 5.11

GENERAL CARDIOPULMONARY CONSIDERATIONS

Any deterioration in ventilatory efficacy may adversely affect cerebral compliance (elastance) through carbon dioxide–induced vasodilation. Concerns have been expressed about the effect of positive end-expiratory pressure (PEEP) in this situation, but the decreased pul-monary compliance necessitating the PEEP also limits intrathoracic pressure transmission to the cerebral circu-lation.12 The net benefit of improved ventilatory efficacy from PEEP outweighs any mild disadvantages from its use. However, injudicious use of PEEP in circumstances of hypovolemia may reduce functional venous return and hence reduce cardiac output, with consequent effects on cerebral perfusion.12

Reductions in cardiac output and arterial blood pres-sure can initiate reflex cerebral vasodilation, which is the brain’s attempt to preserve CBF. Hypotension is a well-documented source of worsened morbidity,13,14 whether the decrease in blood pressure results from underresus-citation or iatrogenic mechanisms. This vasodilation increases venous blood volume and further diminishes cerebral perfusion pressure (CPP).15

Hypoxemia can cause direct as well as indirect injury to the brain. Hypoxemia less than 60 mm Hg is a significant contributor to secondary insult from vasodilatory ICP effects, in addition to the reduction in the oxygen gradi-ent to the cell. The resultant reduction in cerebral per-fusion, irrespective of primary cause, may cause further deterioration by depressing the level of consciousness, in turn leading to airway compromise, hypoventila-tion, and further decrease in oxygenation (Fig. 105-4). Consequently, pulmonary compromise is often seen in neurologic patients with altered mental status, as a result of impaired airway reflexes and repeated aspiration epi-sodes, culminating in a significant incidence of pneumo-nia, irrespective of the initiating pathologic process.16

Figure 105-4. A, Ventilatory-neu-rologic circle of dysfunction. Induced changes in partial pressure of carbon dioxide (Pco2) and partial pressure of oxygen (PO2) produce changes in cerebral blood volume (CBV), intra-cranial pressure (ICP), and cerebral perfusion pressure (CPP). This, in turn, impairs ventilatory control. B, Hemodynamic-neurologic circle of dysfunction. Similar to the diagram in A, systemic hypotension induces cerebral vasodilation, with increased CBV, increased ICP, and reduced CPP, which, in turn, increases vasodilation.

PCO2

PO2

Consciouslevel

Cerebralvasodilation

Systemichypotension

Airway controlcompromised

CPP

CPP

ICP

ICP

A B

CBVCBV

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Another potential mechanism is the release of cyto-kines from the brain in response to the inflammatory process triggered by an injury; this release may be suf-ficient to induce acute respiratory distress syndrome (ARDS) and systemic inflammatory response syndrome (SIRS).17,18 Moreover, the large tidal volume ventilation delivered during initial hyperventilation can enhance the development of ARDS19 (see also Chapters 101 to 103). This may create a therapeutic dilemma in the presence of cerebral pathophysiology. However, the “open lung” concept (i.e., small tidal volumes, high frequencies, and high PEEP) developed to minimize alveolar distention and reduce lung injury appears to be feasible in neuro-surgical patients despite theoretic concerns for adverse effects on ICP.20

The relationship between Paco2 and CBF can be exploited in examining the response of ventilated patients to tests of spontaneous breathing. Restoring Paco2 to normal may increase ICP, a finding indicating limited craniovascular compliance. Understanding this situation may guide subsequent therapy and ventilatory strategy, and ICP effects should be considered during any weaning process.

FLUIDS AND ELECTROLYTES

Normally, capillary fluid shift is a function of hydrostatic pressure pushing fluid out and the balance of osmotic forces retaining fluid within21:

Jv = Kf ([Pc − Pi) − σ [πc − πi])

where Jv is the net fluid movement between compart-ments, Pc is the capillary hydrostatic pressure, Pi is the interstitial hydrostatic pressure, πc is the capillary osmotic pressure, πi is the interstitial osmotic pressure, Kf is the filtration coefficient (this is a product of surface area and hydraulic conductivity), and σ is the reflection coefficient (the membrane impermeability toward osmotically active particles). In extracranial capillaries, these osmotic forces derive from oncotic pressure because smaller solutes can cross the capillary basement membrane following con-centration gradients and only large protein molecules remain to exert effect.

However, in the brain, because of the presence of tight junctions in the endothelium, this intact blood-brain barrier reflects smaller solutes (e.g., sodium and chloride ions), and this relative impermeability renders cerebral capillary fluid shift a function of hydrostatic and total osmolar forces, with the oncotic pressure playing a very small part and the fluid shift most dependent on the osmolar gradient. In the absence of externally adminis-tered osmotically active substances (e.g., mannitol), this gradient is largely determined by sodium concentration, as serum osmolality.

Serum osmolality = (serum Na) × 2 + glucose/18 + BUN/2.8

where Na is sodium and BUN is blood urea nitrogen.Thus, in general, hypotonic solutions should not be

used in the neurosurgical patient when edema is a signifi-cant consideration. The osmolalities of commonly used solutions are listed in Table 105-1.

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At the same time, the tighter endothelial connections and lipid bilayers also serve to reduce water permeability and hence the filtration coefficient. This physiologically limits the water shift across the vascular bed in response to changes in tonicity; otherwise, the brain volume would be significantly reduced by the large osmotic forces cre-ated by changes of only a few milliosmoles per kilogram. Net fluid shift across the blood-brain barrier therefore depends on water permeability, as defined by the filtra-tion coefficient, and solute permeability, as defined by the reflection coefficient. This process permits osmotic diuresis, in which substances reflected by the blood-brain barrier can exert a significant effect on brain water (e.g., mannitol and hypertonic saline).

Inadequate perfusion and supply of substrate, whether relative or absolute, induces energy failure. This pro-cess translates into real effects on the integrity and function of the blood-brain barrier, which is an energy-dependent physiologic construct, as opposed to a purely anatomic structure. Ischemia and rapid reperfusion are associated with the generation of matrix metalloprotein-ases that directly attack the proteins sealing the connec-tions between the endothelial processes that make up the blood-brain barrier.22 This condition creates a loss of integrity and increased porosity of the blood-brain barrier that pathologically affect the permeability and reflection coefficients. This acute blood-brain barrier disruption may allow solute shifts into the parenchyma and result in brain swelling, the extent of which depends on the “leakiness” of the blood-brain barrier, as well as the size and concen-tration of the osmotically active molecules on either side of the barrier.

Hence, intravascular fluid therapy must be carefully considered under circumstances of cerebral ischemia and inflammation. The brain exerts homeostatic control on metabolic and endocrine activity, and neurologic dysfunc-tion can manifest as untoward changes in fluid and elec-trolyte balance. Diabetes insipidus is a florid example of this, with polyuria, subsequent hypovolemia, and, if the disorder is left untreated, systemic hypotension. Iatro-genic causes may also include the use of osmotic diuret-ics, sedation, and analgesics. Sympathetic denervation as

TABLE 105-1 SODIUM CONTENT, OSMOLALITY, AND ONCOTIC PRESSURE OF COMMONLY USED INTRAVENOUS FLUIDS

FluidOsmolality (mOsm/kg)

Oncotic Pressure (mm Hg) Na+ (mEq/L)

Plasma 289 21 141Crystalloid0.9% NS 308 0 1540.45% NS 154 0 773% NS 1,030 0 515Lactated Ringer’s 273 0 130Plasma-Lyte 295 0 140Mannitol (20%) 1,098 0 0ColloidHetastarch (6%) 310 31 154Albumin (5%) 290 19

Na+, Sodium; NS, normal saline.

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a consequence of brainstem or spinal cord injury may also contribute to reductions in venous return as a result of increased vasodilatation and peripheral venous pooling.23

The increased sympathetic discharge commonly accompanying cerebral insults can also manifest as extra-cerebral stress on the entire body with increased incidence of gastric stress erosion, hypercatabolism, hyperglycemia, and impaired glucose tolerance.24

Nutrition requirements are often increased after brain injury, and evidence suggests improved outcome with the early use of enteral nutrition (see Chapter 106).25

Hyperglycemia is a potent aggravator of cerebral insult.26 However, tight glycemic control with aggressive insulin therapy worsens the outcome of critical care patients in general and may worsen cerebral metabolic stress (see also Chapter 39).27,28 Moderate glycemic control is advocated.

FEVER AND INFECTION

More than 50% of patients in neurologic intensive care units (ICUs) develop fever.29 This condition is an often overlooked insult to the compromised brain, thus increas-ing oxygen utilization and metabolic stress.29 Patients within the ICU have multiple risk factors for infection and sepsis, including the presence of a variety of indwell-ing catheters (e.g., arterial, venous, CSF). Other poten-tial causes of fever include intracranial hemorrhage and

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idiosyncratic drug effects (e.g., the anticonvulsant phe-nytoin).29,30 Fever is associated with a worsened outcome after neurologic injury, including intracranial hemor-rhage, subarachnoid hemorrhage (SAH), and stroke. A meta-analysis of available studies demonstrated an increase in neurologic morbidity and mortality associated with fever.31

Although hypothermia has not proven to be a success-ful intervention for patients with traumatic brain injury (TBI)32 or SAH,33 this finding does not equate to a lack of beneficial effect of normothermia compared with hyper-thermia, and many clinicians are increasingly aggressive in preventing and treating fever.34

To provide appropriate treatment for fever, it is neces-sary to perform daily reappraisal to delineate the source of fever, given the large number of potential causes. However, in many cases a cause cannot be determined, and empiric treatment including scheduled administration of acet-aminophen, application of cooling blankets, and, increas-ingly, more invasive methods of cooling are required.

MONITORING

The avoidance or correction of secondary physiologic insults necessitates the aggressive use of physiologic mon-itors (see Chapter 49 and Fig. 105-5). This monitoring does not obviate the need for regular clinical examination

Figure 105-5. Schematic of avail-able intracranial monitoring, with near-infrared oximetry (NIRS), intracranial pressure (ICP, either by ventriculostomy or parenchy-mal probe), brain tissue oximetry (Pbo2), microdialysis, and jugular venous oximetry (Sjo2).

MicrodialysisICP/PbO2

Ventriculostomy

SjO2

NIRS

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of the CNS, with observation of the response to stimuli. Monitors (e.g., processed electrical activity, cerebral oxy-genation, and ICP) are merely surrogates of actual cere-bral function. Similarly, attention should be paid to the basics of fluid volume status, respiratory rate, cardiovas-cular stability, and metabolic consumption.

INTRACRANIAL PRESSURE

ICP monitoring quickly became a standard of care after its introduction to clinical use in the 1970s, thereby mak-ing subsequent determinations of utility and effective-ness difficult. Nevertheless, a NIH sponsored randomized controlled trial has been performed in Latin America, demonstrating no overt benefit of ICP monitoring.36 Noninvasive monitors have not established sufficient reli-ability and remain the subject of research. While recent data suggests that ICP monitoring has minimal effect on outcome,35 monitoring must guide therapy to be effective and ICP data should remain as one of the components influencing but not replacing clinical appraisal. Most neurosurgical centers still insert such devices routinely in the management of patients with TBI and SAH, by using defined thresholds (e.g., ICP > 25 mm Hg) to trigger treat-ment interventions, including osmotic agents (e.g., man-nitol or hypertonic saline) or operative treatments (e.g., decompressive craniotomy or CSF drainage).

ICP sensors may represent only the compartment pres-sure where they were placed (see Fig. 105-2), and they may not be sensitive to acute transients in pressure on the other side of the falx or tentorium.37 Intraparen-chymal fiberoptic devices are less invasive and easier to place, but they may be calibrated only ex vivo and can-not drain CSF. Thus, provided the ventricles are acces-sible, ventricular catheters remain the “gold standard” of measurement, albeit at the expense of an increased risk of infection of approximately 6%.38

When the ventricles are small, this monitoring becomes technically difficult, and the risks of hemor-rhage and contusion are increased.

ICP devices can be quickly placed with a minimum of morbidity in experienced hands and, provided suit-able attention is paid to the issue of potential drift from calibration,39 generally offer useful insights to guide therapeutic interventions. However, placement of these devices is contraindicated in the presence of coagulopa-thy or platelet dysfunction.

Observation of ICP monitoring trends reveals charac-teristic patterns that may have prognostic implications (e.g., the Lundberg “A” or “plateau” ICP wave indicating critical cerebral compliance40 and impending herniation).

CEREBRAL BLOOD FLOW

Important threshold values for function were identified by Symon and others (Table 105-2).41 The initial meth-ods of quantitative CBF measurements were laborious and time consuming and did not offer accurate regional estimates.42 These methods were replaced by the use of isotopic tracers that allow basic regional flow measure-ment (e.g., inhaled or intravascular xenon-133) or a combination of imaging and qualitative assessment

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(i.e., single photon emission computed tomography [SPECT]). Calibrated imaging techniques such as positron emission tomography (PET) and stable xenon or contrast computed tomography (CT) perfusion42 have become standard in many centers. Magnetic resonance imaging (MRI) of perfusion is rapidly evolving and may provide quantitative flow measurement in the near future.

Although providing potentially useful information on regional perfusion, these methods often involve trans-porting the patient outside the ICU, a maneuver that may be clinically inappropriate in unstable circumstances.

Thermodilution is a focal technique in which small thermocouples are placed cortically. Blood flow is related to temperature diffusion at the probe.43 An alternative approach has been to use jugular venous temperature dif-fusion to assess flow. Whether this measure reflects CBF reproducibly may depend on the ratio of jugular venous drainage to overall cerebral venous flow.44 It remains to be seen whether these devices can be developed into reli-able and consistent monitoring tools.

TRANSCRANIAL DOPPLER MONITORING

Transcranial Doppler monitoring uses the Doppler shift effect to assess flow velocity in insonated arteries (see also Chapter 49).45 This method is often used as a surrogate of flow for examining accessible vessels and, in skilled hands, offers considerable insights into dynamic flow. This tech-nique has the advantage of being a bedside, relatively speedy, and noninvasive monitor of flow within the main components of the circle of Willis through the ophthal-mic, temporal, and foramen magnum acoustic windows. It has excellent temporal resolution and, being noninvasive, allows repetitive measurements with little or no risk. In a small proportion of patients, predominantly older women and black patients, temporal bone thickness may prevent monitoring.46 Extrapolation of velocity to flow relies on an assumption of relatively constant diameter of the large con-ductance vessels. Under different circumstances, changes in velocity can be used to assess alterations of vascular caliber (e.g., arterial vasospasm after SAH)47 or intracranial steno-sis (Fig. 105-6). For the middle cerebral artery, vasospasm can be distinguished from hyperemia by examining the ratio between the intracranial flow velocity and the extra-cranial carotid artery flow velocity (the Lindegaard index). A ratio greater than 3 is generally indicative of vasospasm, whereas a ratio less than 3 is consistent with hyperemia.48 A similar ratio has been developed for the posterior circu-lation by comparing the flow velocity in the basilar artery with that of the extracranial vertebral artery. A value greater

TABLE 105-2 FUNCTIONAL THRESHOLDS OF CEREBRAL BLOOD FLOW

CBF (mL/100 g/min) Result

50 Normal20 EEG slowing15 Isoelectric EEG6-15 Ischemic penumbra<6 Neuronal death

CBF, Cerebral blood flow; EEG, electroencephalogram.

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Figure 105-6. Transcranial Doppler images of elevated cerebral blood flow velocities in the middle cerebral and vertebrobasilar vessels.

than 2 with an elevated flow velocity in the basilar artery is reportedly consistent with vasospasm,49 although this finding has been questioned by concurrent angiographic comparisons.50

AUTOREGULATION AND VASOMOTOR REACTIVITY

Monitors of CBF can assess the response of the cerebral vasculature to changing circumstances of metabolism and blood pressure (i.e., autoregulation).51,52 Static cere-bral autoregulation can be determined with sustained manipulation of blood pressure by using either a tilt test or a direct vasopressor as clinically appropriate, whereas

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dynamic autoregulation can be assessed using rapid deflation of previously inflated thigh cuffs above sys-tolic blood pressure. Alternatively, autoregulation can be assessed by monitoring CBF velocity through tran-scranial Doppler in response to spontaneous fluctuation of blood pressure by using transfer function analysis, although these techniques are likely to be less reliable than the stimulus-response paradigm.53 The presence or lack of autoregulation may guide subsequent treat-ment and prognosis because frequently the loss of autoregulation is associated with a poor outcome.54,55 Cerebrovascular reserve or vasomotor reactivity, as determined by CBF response to changes in Paco2, can be assessed either with rebreathing or addition of carbon

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dioxide to the breathing circuit or with administration of acetazolamide.53

JUGULAR BULB OXIMETRY

The Fick principle may be reversed to examine the venous oxygen saturation which, assuming a constant hemato-crit and metabolism, can offer an assessment of the ade-quacy of CBF and associated oxygen delivery relative to cerebral oxygen consumption:

If AVDO2 = (CMRO2/CBF), then CaO2 − CjvO2 = (CMRO2/CBF)

Ignoring the contribution of dissolved oxygen, then:

(SaO2 − SjvO2) × Hgb × 1.34 = (CMRO2/CBF)

where AVDo2 is the arteriovenous oxygen content differ-ence; CMRo2 is the cerebral oxygen metabolic rate; Cao2, Cjvo2, Sao2, and Sjvo2 are the arterial oxygen and jugu-lar venous oxygen contents and saturations, respectively; Hgb is the hemoglobin concentration; and 1.34 is the oxygen affinity constant.

In vivo, catheters are placed in retrograde fashion through the internal jugular vein to its jugular bulb at the foramen or even beyond, to the large sinuses (Fig. 105-7).56,57

These catheters provide information related to both perfusion and oxygen consumption, in a manner anal-ogous to the use of mixed venous oximetry for shock management. Both desaturation (<50%, suggesting inadequate delivery or excess consumption) and abnor-mally high saturation (>75%, suggesting hyperemia or stroke) have been associated with poor outcome.58,59 The derivable arteriovenous oxygen content difference is possibly a more accurate assessment of the adequacy of flow and is related to outcome.60 Jugular venous oximetry has been criticized as being insensitive to focal changes because it reflects the averaged global cerebral venous oxygen saturation from the confluence of hemispheric venous drainage. Consequently, some authors have suggested using oxygen consumption in combination with the cerebral arteriovenous gradient of lactate to make stoichiometric assessments of aerobic versus anaerobic metabolism.61 These authors use meta-bolically directed management strategies, as opposed to management of cerebral hemodynamics,62 that is, goal-directed therapy based on metabolic indices (jugu-lar venous oxygen saturation), rather than on hemody-namic indices (ICP and CPP).

BRAIN TISSUE OXYGEN TENSION

In conceptually similar assessments of in vivo oxygen-ation, miniaturized Clark electrodes have been developed and combined with ICP catheters to provide simultane-ous estimations of tissue oxygen tension and ICP. Patho-logic levels are thought to be lower than 15 mm Hg with normal values in the 20- to 45-mm Hg range.63 These brain tissue O2 tension (Pbo2) devices have been used in a variety of pathologic conditions, thus guiding ther-apy and providing insight into the adequacy of cerebral perfusion,63 although Pbo2 may alert to poor outcomes independent of CPP.64 However, many concerns remain regarding measurement errors, calibration drifts, and

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uncertainty of the generalizability of the local measure-ment.65 Nevertheless, in patients without focal lesions, important physiologic feedback is provided in response to therapeutic manipulations of arterial blood pressure and oxygenation.66 The hope is that these questions will be addressed by ongoing clinical trials of Pbo2-guided treatment protocols.67

CEREBRAL MICRODIALYSIS

Interest in the use of cerebral microdialysis probes to assess the biochemical milieu of the brain is significant. These probes are placed through a burr hole and cycle small volumes of dialysate through the catheter to an extracranial collection system. Consequently, various substances can diffuse across the semipermeable mem-brane (e.g., lactate. pyruvate, glucose, glycerol, gluta-mate),68 for collection and subsequent analysis using a bedside high-pressure liquid chromatography device. This device gives graphic and numeric displays of trended concentrations for the preceding collection interval (usu-ally 1 hour). This information then relates to the in vivo biochemistry of the brain. Although this technique is intuitively attractive, unresolved questions have ham-pered its wider implementation, not the least of which is the question of the optimal site of placement, in relation both to disease and to anatomic region of gray matter versus white matter.68

These issues were addressed by a consensus state-ment on placement of microdialysis catheters, with the aims of improving accuracy in the comparison of results and allowing generalization from accumulated experience.69 Improvements in membrane technology now permit larger molecules to cross into dialysate, thus creating the possibility of research into microvascular peptidomics.68

Figure 105-7. Lateral cervical spine radiograph showing appropriate positioning of the jugular venous oximetry (Sjo2) catheter above the lower border of the C1 vertebra (the arrow tip is actually within the jugular foramen).

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ELECTROENCEPHALOGRAPHY

The electroencephalogram (EEG) records electrical activ-ity generated and detected by appropriately placed elec-trodes in a radial and axial array, as defined by the 10/20 system, an internationally standardized system of record-ing (see also Chapter 49). The consequent waveforms are displayed and recorded. The spectrum of component frequencies, together with amplitude and power, can be quantified and analyzed in a variety of fashions by what are termed processed EEG monitors. These devices can pro-vide important diagnostic information in patients in the neurocritical care unit who cannot be otherwise assessed. The EEG tends to be used in a diagnostic snapshot mode for isolated assessments, and it is underused as a continu-ous monitor within the ICU. This underuse is a function of the difficulty involved in its application and interpreta-tion, which necessitate dedicated equipment and person-nel. A 24-hour continuous recording of EEG is, in general, more fruitful than a snapshot recording.

Moreover, both in TBI and in SAH, significant numbers of patients develop nonconvulsive status epilepticus,70,71 a condition that constitutes a regularly overlooked but significant source of morbidity and stress on the brain. Whereas the EEG is a difficult monitor to use, definite indications exist for its deployment, and the neurocriti-cal care physician should be familiar with the basic prin-ciples of its function and use.

Some related devices have also been developed from processed EEG to monitor the depth of anesthesia. Although these devices have been used to monitor the level of sedation in critically ill patients, they are not designed for—and should not be used to—monitor neu-rologic integrity or seizure activity.

NEAR-INFRARED SPECTROSCOPY

The idea of pulse oximetry for the brain, as conceptual-ized in the early 1990s, is attractive. It relies on the prin-ciple of reflectance spectroscopy, in which near-infrared light traverses bone transparently, to be scattered and reflected to a degree inversely proportional to the con-centration of light-absorbing materials in tissue (e.g., hemoglobin and other tissue chromophores). The sur-face detector is constructed and calibrated to detect light that has ostensibly traversed down to cerebral cortex and back. An adjacent detector is positioned to detect a signal from superficial tissues, and both signals are then used in an algorithm to derive an estimated tissue saturation. However, the devices employed have been troubled by issues of reliability, specificity, and cross contamination from other cytochrome-containing tissues.72,73 Slightly more enthusiasm exists for their role as trend monitors of flow, especially in children and patients with extracranial carotid artery disease.74,75

RADIOLOGIC IMAGING

Imaging can be employed as a monitoring technique, albeit on a protracted time scale.76 The two major modali-ties are CT and MRI. CT is by far the most useful and commonly used technique because it is the most efficient



method. MRI, although more time consuming, is more sensitive for brainstem lesions, as well as for axonal inju-ries. Both CT and MRI can provide information on the vascular tree, but conventional contrast angiography remains the gold standard. Assessment of intracranial masses, diffuse injury, or hemorrhage can be subse-quently used to guide therapy, triage, and prognosis.77

To provide meaningful comparison of therapeutic modalities in clinical trials, it is important to standardize and categorize CT images. The Marshall scale has been used in TBI to stratify degrees of hemorrhage and con-tusion within the cranial vault, and it correlates with outcome (Table 105-3).78,79 The Fisher scale assesses the volume of subarachnoid blood after a diagnosis of SAH.80 There again, it has strong relationship with outcome regarding the development of vasospasm (Box 105-2A),81 the correlation of which was further improved by the modified Fisher scale (Box 105-2B). 82 These scales rely on experienced interpretation for accuracy. Inconsis-tent application of the Marshall scale has been reported, a finding suggesting an urgent continued need for standardization.83

A more recent and exciting development in CT scan-ning is the capacity to estimate specific gravity of tissue (eSG), thus delivering insight into cerebral edema and tis-sue swelling. Such measurements taken from the first CT scan (average 4 hours from injury) have performed well as predictors of outcome at 6 months, and they also cor-relate with ICU length of stay and time spent ventilated.

TABLE 105-3 MARSHALL SCALE: COMPUTED TOMOGRAPHY CATEGORIES FOR HEAD INJURY

Category Definition

Diffuse injury I No visible intracranial pathologic processDiffuse injury II Cisterns are present with midline shift of

0-5 mm and/or lesion densities present; no high- or mixed-density lesions at >25 mL

Diffuse injury III Cisterns compressed or absent, with midline shift of 0-5 mm; no high- or mixed-density lesions of >25 mL

Diffuse injury IV Midline shift of >5 mm; no high- or mixed-density lesion of >25 mL

Evacuated mass lesion (V)

Any lesion surgically evacuated

Nonevacuated mass lesion (VI)

High- or mixed-density lesion of >25 mL; not surgically evacuated

Grade 1 No blood detectedGrade 2 Diffuse deposition of subarachnoid blood, no

clots, and no layers of blood >1 mmGrade 3 Localized clots and/or vertical layers of blood

≥1 mm in thicknessGrade 4 Diffuse or no subarachnoid blood, but intrac-

erebral or intraventricular clots present

BOX 105-2A Fisher Scale (Computed Tomography Scan Appearance)



The relative objectivity and quantitative nature of this method may offer advantages over other scoring systems.84

CLINICAL EXAMINATION

Comprehensive neurocritical care encompasses the ability to perform a competent neurologic examination. Repro-ducible and objective assessment of neurologic function is as important a monitor as some of the sophisticated technology mentioned earlier, with the advantage that it offers better insight into global function of the nervous system and allows integration of information in an inher-ently complex dynamic system. One of the most basic yet important examinations is the pupillary light reflex, the unilateral absence of which may indicate midbrain compression from uncal herniation and neurologic emer-gency. Bilaterally absent papillary reflexes signify immi-nent or established cerebellar herniation, but this may be reversible with rapid efficacious treatment.

Clinical scales have been devised for common neuro-logic settings. The Glasgow Coma Scale (GCS) is a well-known, universally if inconstantly applied scale (Table 105-4). It relies on independent assessment of eye open-ing, speech, and best motor movement in response to pro-gressive trials of command, voice, and noxious stimuli.85 The Hunt and Hess scale (Table 105-5), when applied to patients with SAH, offers classification and prognostica-tion of mortality.86 The World Federation of Neurologic Surgeons (WFNS) scale is the preferable rating because it

Grade 0 No blood detectedGrade 1 Thin* subarachnoid blood, no intraventricular

hemorrhageGrade 2 Thin subarachnoid blood, with intraventricular

hemorrhageGrade 3 Thick subarachnoid blood, no intraventricular

hemorrhageGrade 4 Thick subarachnoid blood, with intraventricular

hemorrhage

BOX 105-2B Modified Fisher Scale (Computed Tomography Scan Appearance)

*Vertical thickness of 1 mm separates thin from thick subarachnoid hemorrhage.

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uses the more prevalent GCS but with a modifying com-ponent of focal deficit (Box 105-3).87 Knowing and using these scales are crucial to understanding the terminology and practice of neurocritical care.

MULTIMODALITY MONITORING

No single monitor credibly and reliably offers insight into the functioning physiology of the brain. Instead, various surrogates of function are offered. Many criticisms can be directed at each individually, but an interesting concept is that of multimodality monitoring, which uses a combi-nation of parameters to improve on accuracy of diagnosis and guidance to management.88 Although it is an attrac-tive concept, the precise implementation of this idea is still in its early days, with little methodologic standard-ization; this standardization may be facilitated by rapidly approaching commercial development.

COMMON DISEASES IN THE NEUROCRITICAL CARE UNIT

HEAD INJURY

The treatment of TBI was one of the initial emphases of neurocritical care (see also Chapter 81). Changes in road traffic legislation and enhancements in passenger protec-tion have led to a decline in the incidence of TBI in the United States, to the degree that motor vehicle accidents have been replaced by falls as the chief cause of injury.89 These causes, together with assaults and off-road and sporting injuries, still contribute to what is referred to as a silent epidemic,89 accentuated by ongoing military con-flicts and their hallmark blast injuries,90 as well as a preva-lence consequent on concentration in a predominantly youthful population. Outside of wartime, these causes usually share a common factor in the contribution from alcohol consumption.91,92

In all circumstances, brain structure is deformed by the transmission of kinetic energy. The distribution of this damage covers a wide spectrum from localized con-tusion to diffusely scattered foci, varying with the cir-cumstances of the incident and the architecture of the victim’s brain. Typically, cerebral contusions are located at the bony prominences of the skull, at the sphenoid wing and petrous ridge.93 This variability in inflicted

TABLE 105-4 GLASGOW COMA SCALE

6 5 4 3 2 1

Eyes N/A N/A Opens eyes spontaneously

Opens eyes in response to voice

Opens eyes in response to noxious stimuli

Does not open eyes

Verbal N/A Is oriented, converses normally

Is confused, disoriented

Utters inappropriate words

Makes incomprehensible sounds

Makes no sounds

Motor Obeys commands Localizes to noxious stimuli

Has flexion to noxious stimuli

Has abnormal flexion to noxious stimuli

Extends to noxious stimuli

Makes no movements

N/A, Not applicable.

t Tzu Chi General Hospital JC September 20, 2016.sion. Copyright ©2016. Elsevier Inc. All rights reserved.

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pathologic features introduces significant heterogeneity in presentation and behavior, and it confounds some broader assumptions on time course and care. A patient with a temporal lobe injury may behave very differently from a patient with a posterior fossa lesion.

TBI may also be classified according to whether it is blunt or penetrating. Penetrating injury may again have widely varying consequences depending on site, depth, and energy, but is generally fatal if it bilaterally traverses the midbrain.94 Although initial mortality from penetrat-ing injury is higher, outcome in survivors is similar to that for nonpenetrating injury.95

Vascular injury may affect more superficial arterial blood vessels, as seen in the middle meningeal artery injury typical of pterional fracture. This injury com-monly results in an extradural hematoma.96 These rap-idly expanding collections can result in swift neurologic deterioration and devastating results, if not treated quickly. The mortality is between 15% and 20%.97 Alternatively, cortical bridging veins between cortex and the dural venous sinuses are often torn by rota-tional or acceleration-deceleration forces to produce an accumulating subdural hematoma. This may mani-fest slowly and may even be unaccompanied by signs of external trauma. In the time taken for the venous hematoma to develop, symptoms may be subtle and, unfortunately, may be disregarded. The slow expansion exerts a cumulatively damaging effect, which by the time severe signs eventually manifest may be just as or even more destructive than a rapidly expansile lesion.98 This injury is prevalent in older patients, in whom the process of senile cerebral atrophy results in greater tension on the bridging veins crossing an increasing

TABLE 105-5 HUNT AND HESS GRADING SYSTEM

Grade Clinical PresentationSurvival (%) (approximate)

Grade 1 Asymptomatic or mild headache 70Grade 2 Moderate to severe headache,

nuchal rigidity, and no neurologic deficit other than possible cranial nerve palsy

60

Grade 3 Mild alteration in mental status (confusion, lethargy), mild focal neurologic deficit

50

Grade 4 Stupor and/or hemiparesis 20Grade 5 Comatose and/or decerebrate

rigidity10

Grade 1 GCS score of 15, motor deficit absentGrade 2 GCS score of 13-14, motor deficit absentGrade 3 GCS score of 13-14, motor deficit presentGrade 4 GCS score of 7-12, motor deficit absent or presentGrade 5 GCS score of 3-6, motor deficit absent or present

BOX 105-3 World Federation of Neurologic Surgeons Scale

GCS, Glasgow Coma Scale.

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istance, thus rendering these vessels all the more sus-eptible to rupture.

In all these scenarios, the primary pathologic process is ccentuated by secondary features of elevated ICP, dimi-ution of arterial inflow, and consequent reduction in PP, with resulting tissue hypoxia and cell death, as pre-iously described in discussion of the intracranial pres-ure-volume relationship (see Fig. 105-1).

This process can also be modified adversely by oss of autoregulation, which may result in further ncreases in ICP. This condition is often seen in dif-use injury, in which although individual foci may be mall, they additively combine to produce a total bur-en of inflammatory change sufficient to overwhelm utoregulation.99

Traumatic SAH (tSAH) is seen in up to 60% of admis-ions for TBI.100 Some variability of detection and report-ng exists, but despite this, tSAH has a substantial effect n outcome.101 Prolongation of the QTc interval is seen n 67% of patients with tSAH, and QTc prolongation is eemingly proportional to severity.102 Approximately 0% of patients with tSAH may also develop vasospasm, hich can lead to secondary ischemic insult. The diagno-

is and management of the vasospasm are facilitated by he use of transcranial Doppler monitoring. Vasospasm is lso being recognized as a feature in the pathologic pro-ess of blast injury.90

Management of TBI in the ICU should include com-rehensive examination and assessment using such prin-iples as outlined in Advanced Trauma and Life Support ATLS) because occult injuries can escape initial screening et subsequently exert a delayed physiologic compromise n the arrival of the patient in the ICU, or worse, in the T scanner. These injuries may accentuate the primary rain injury by contributing to secondary physiologic nsult.14

Overall, the common goal of treatment of TBI is o maintain cerebral perfusion. In patients with mass esions resulting in anatomic distortion with mass ffect, surgical removal of lesions is indicated. Early ecompressive craniectomy for patients with diffuse

njury has not proven useful and may have worsened utcome,103 although results of a larger trial are awaited. edical management may be required both before and

fter surgical intervention or as an alternative in cir-umstances of diffuse injury. Such treatment strategies ithin the ICU revolve around the reduction of ICP nd the maintenance of cerebral perfusion, which may ot be compatible goals. Although therapeutic resolu-

ion of ICP with osmotic diuresis is a logical approach, t may have unintended consequences on central vas-ular volume and myocardial function.104 After an ini-ially beneficial effect in reducing intracerebral volume,

annitol then leaves the vasculature through the kid-ey. This process also reduces cardiovascular volume,

hus diminishing cardiac output and arterial blood ressure and possibly replacing one physiologic insult or another.

Mannitol has diminished in popularity, to be sup-lanted by hypertonic saline.105 This solution demon-trates a good resuscitation profile, with none of the elayed hypotension observed with mannitol.106 Some of

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he same concerns with the use of mannitol also apply o the use of hypertonic saline (i.e., diffusion of osmoti-ally active particles into the brain interstitium in cir-umstances of injury or compromise of the blood-brain arrier).107 This approach may create rebound effects n reduction of plasma osmolarity as hypertonic saline dministration is reduced, with an increase in brain water. his finding has been observed with differential effects in ontused versus noncontused brain.108 Although bolus sage of hypertonic saline has been shown to be useful,

t remains to be seen whether sustained infusions or the ractice of persistent-induced hypernatremia offer any

mprovement in outcome.Although the choice of resuscitation fluid does not

ave any effect in a large study of trauma victims,109 a post oc analysis of subgroup data demonstrated increased ortality associated with the use of albumin in TBI.110

his finding is somewhat at odds with the demonstration f potential benefit in stroke,111 and a prospective trial is eeded.

Control of the vascular blood volume may also be reg-lated by manipulation of the partial pressure of carbon ioxide (Pco2), which most frequently requires intubation f the trachea and mechanical ventilation.

Controlled hyperventilation is frequently practiced o reduce blood volume and hence ICP.112 Studies have emonstrated adverse consequences of aggressive hyper-entilation, and most authorities agree on limiting the eduction in Pco2 to avoid ischemia.113

The Brain Trauma Foundation publishes guidelines n the management of brain trauma, which are regularly pdated. These guidelines concentrate on the principles utlined previously, namely, reduction of ICP while pre-erving perfusion pressure.114 They also provide state-ents of consensus on the merits of these strategies.

hey recommend a target Pco2 of between 30 and 35 mm g,108 with a CPP of 60 to 70 mm Hg. Higher CPP values ave no benefit and may worsen outcome.115,116

Hypertension in excess of autoregulatory control can nduce both excess blood volume and the formation of asogenic edema across a compromised blood-brain bar-ier.7 This concept underpins the Lund group protocol, hich gives priority to limiting the Starling forces across

he capillary bed to avoid the formation of edema.117 hese investigators recommend a CPP of 50 mm Hg sing β-blockers as required, the reduction of metabolic emand with barbiturates, and intravenous colloid dministration.118

Any evidence of comparative effectiveness was estricted to case series, offering outcomes similar to hose with CPP-oriented management.119 However, a

ore recent small randomized controlled trial suggested hat a modified Lund approach (to include mannitol), uided by microdialysis monitoring, had less mortality han an aggressive CPP-oriented approach (70 to 80 mm g) in a patient group equally distributed between TBI

nd SAH.120 Although the study design had significant aws, the possible benefit is worthy of further explora-ion. Some subsets of disorders may possibly respond dif-erentially to each approach, determined in part by lesion olume, inflammatory burden, and blood-brain barrier ntegrity.


Currently, ICP/Pbo2 and ventriculostomy are fre-quently used in the management of patients with severe TBI. However, these invasive monitors are contraindi-cated if coagulopathy is present. The occurrence of coag-ulopathy in TBI is associated with a poor prognosis and should be vigorously treated with clotting factors, fresh frozen plasma, and platelets.

Hyperglycemia is associated with poor outcome in multiple retrospective studies.26 Meta-analysis of tight glycemic control on outcome in patients with TBI indi-cates no benefit,121 whereas Vespa and associates, in a crossover study, demonstrated increased metabolic cri-sis associated with its use.28 More moderate targets seem prudent.

Corticosteroids had an adverse effect on mortality and morbidity in a multicenter evaluation of more than 10,000 patients with brain injury, and these drugs cannot be recommended for use.122

Hypothermia still may have a role in controlling ICP in patients withTBI.123 Early prophylactic use may also be beneficial.124 Finally, after an initial failure to improve outcome, subsequent reanalysis of previous multicenter studies suggested a differential benefit of modest hypo-thermia in those patients undergoing surgical evacua-tion of a mass lesion, as compared with those without hypothermia.125

The timing of prophylaxis against deep vein thrombo-sis (DVT) has been an issue of controversy. Investigators generally agree on the need for prophylaxis because up to 25% of patients with isolated TBI develop DVT,126 and most clinicians agree with implementation of prophy-laxis 48 hours after injury. The immediate postoperative use of heparin prophylaxis is probably safe and does not confer additional risk of bleeding.127

SUBARACHNOID HEMORRHAGE

Most cases of SAH are aneurysmal in origin (aSAH). The incidence of aSAH in the United States has been esti-mated at 9.7 per 100,000 per year, but it may be as high as 14.5 per 100,000.128 As much as a 10-fold variability by ethnicity and geography is noted, with the incidence in Finland and Japan more than double that in the United States.129 Women have a greater risk than men by a fac-tor of 1.24.129 Most aneurysms occur in persons who are more than 50 years old, but gender differences exist, with peaks in men aged 25 to 45 years, women aged 55 to 85 years, and men older than 85 years.129 aSAH has a rela-tively severe morbidity and mortality. Between 12% and 15% of patients will die before hospitalization, and 25% will die within the first 48 hours, with initial hemorrhage the primary cause of death, followed by rebleeding.128,130 Subsequent morbidity and death are attributable to neu-rologic deficits secondary to ischemia.128

Significant improvements in mortality and morbidity have occurred in recent decades.129 This finding suggests that further reductions may be achievable with contin-ued changes in surgical practice and further concentra-tion of expertise in regional centers. Paralleling this has been the development of neuroimaging and endovascular technologies, which have played a large part in improved outcome.131,132


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Early Versus Late TreatmentMortality and morbidity from SAH in those who survived the initial hemorrhage are mostly secondary to rebleed-ing of unsecured aneurysms or onset of delayed cerebral ischemia. Delayed cerebral ischemia has long been con-sidered secondary to vasospasm, but some emerging evi-dence indicates dissociation between vasospasm and final ischemic deficit, a finding suggesting other etiologies of ischemia (e.g., microthrombosis).133 This information has discouraged the use of vasospasm as an independent out-come measure in clinical trials,127 but vasospasm remains an important cause of ischemia. Rebleeding peaks within the first 24 hours after the initial hemorrhage and declines progressively thereafter, reaching a plateau of 2% by 6 months.130 In contrast, vasospasm tends to develop by the third day, peaks between 5 and 7 days, and gener-ally wanes by 14 days. This pattern led to some debate on the timing of treatment—in which rebleeding may be averted by early intervention but at a risk of an increased risk of vasospasm, which may induce devastating neuro-logic ischemic deficit. Surgically, early treatment is also associated with less optimal brain relaxation conditions. Although no difference in outcome was reported, aggres-sive vasopressor therapy and endovascular support have tipped the balance in the favor of early clipping in the first 72 hours after bleeding.134 Since publication of the International Subarachnoid Aneurysm Trial, endovascu-lar coiling is increasingly the treatment of choice, particu-larly in posterior fossa aneurysms and in patients in poor medical condition.135

In addition to rebleeding and vasospasm, acute hydro-cephalus develops in 25% to 30% of patients after SAH, and emergency ventriculostomy may be lifesaving as well as offering a more accurate prognosis.136

AntifibrinolyticsAlthough antifibrinolytics were previously associated with increased incidence of stroke,137 their transient use before clipping may offer some advantage, and although some concern exists for increased rates of hydrocepha-lus, studies are under way.138 Many clinicians, however, control arterial blood pressure with the use of vasoactive infusions (e.g., nicardipine) to reduce the risk of rebleed-ing until the aneurysm is secured.139

VasospasmVasospasm is thought to derive from the attenuation of nitric oxide–induced vasodilation, with an associated enhanced production of endothelin production and con-sequent vasoconstriction. The extravascular heme mol-ecule is the leading candidate in a long list of possible culprits.140 Seventy percent of patients with SAH develop angiographic vasospasm, although only 30% to 40% of patients will become symptomatic. Patients with a large amount of subarachnoid blood are at higher risk for the development of vasospasm. The Fisher grade is frequently used clinically to prognosticate the risk of vasospasm,80 and the highest incidence of vasospasm is observed in patients with modified Fisher grade 4.82 A meta-analysis of treatment techniques suggested no difference in the incidence of vasospasm among treatment modalities,141 whereas more recent studies suggested that the incidence

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nd severity of vasospasm are less following endovascular reatment compared with surgical clipping, but that dif-erence had little effect on outcome.142,143

The components of “triple H” therapy (hypervol-mia, hypertension, and hemodilution) have been dvocated in varying forms for the treatment of vaso-pasm since the 1950s and as a consistent package since he 1980s.144 Despite a significant anecdotal history of ffect, little evidence of benefit has been noted in ran-omized control trials and meta-analysis.145,146 Triple therapy may also be associated with an increased fre-uency of complications,147 probably because of the use f hypervolemia.146,148

Current recommendations center on augmentation of rterial blood pressure with vasopressors, in the context f euvolemia rather than hypervolemia.128,129

Hemodilution is largely a passive result of hypervol-mia, thus reducing its relevance; more importantly, a igher admission hemoglobin level is associated with

ess cerebral infarction and better outcome.149 The use f deliberate transfusion to increase oxygen delivery is ontroversial, however, with some evidence of increased asospasm and poor outcome to counter assertions of enefit.149,150 The general critical care literature reinforces hese deleterious effects of transfusion.151 A prospective rial is awaited.

Studies on the use of nimodipine provide the only level evidence from randomized control trials in SAH. This gent, when administered prophylactically from diagno-is for 21 days, offers modest improvement in outcome ith reduction in the incidence of ischemic deficit.128,130

t does not have a readily apparent effect on the incidence f angiographic vasospasm,152 thereby lending weight to he argument for alternative explanation of its beneficial ffects.133 Nimodipine is known to have fibrinolytic activ-ty that may be of benefit in microthrombosis.153

Management of vasospasm is facilitated by the appro-riate use of imaging, including the use of transcranial oppler monitoring, SPECT, and cerebral angiography hen indicated. Institution of triple H therapy necessi-

ates the use of invasive monitoring, including that for rterial blood pressure and central venous pressure (or ther indices of preload).

The use of mechanical balloon dilation of blood essels—angioplasty—has added a major weapon to the rmamentarium against vasospasm.154,155 Angioplasty is imited by the caliber of blood vessels, as well as their ccessibility, and it carries a risk of catastrophic rupture.155

Pharmacologic angioplasty with intraarterial injection f a vasodilator is an accepted technique. First established sing papaverine, the use of calcium channel block-rs such as nicardipine and verapamil is being increas-ngly reported and has fewer adverse effects. All current gents are limited by the transient nature of their effects <24 hours).156 Vasodilators may be used in vessels too mall to be accessible by balloons.

Other therapeutic approaches have proven disappoint-ng to date. Trials of endothelin antagonists and statins rovided further evidence of some dissociation between asospasm and clinical outcomes, but neither drug class howed any effect on outcome despite a decrease in the ncidence of vasospasm.157,158

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Cardiac DysfunctionSignificant autonomic disturbance may arise with SAH, thus resulting in changes in the electrocardiogram and myocardial performance. Electrocardiographic changes are frequent but do not appear to relate to outcome.159 However, one series described a 32% incidence of abnor-mal perfusion scans, independent of the clinical history, electrocardiogram pattern, or neurologic condition.160

Abnormal echocardiography has been described in up to 8% of patients with SAH, mostly in patients with blood in basal cisterns, frequently accompanied by hypo-tension and pulmonary edema; this feature is associated with a poor neurologic grade. A typical pattern of sym-metric T-wave inversion and severe QTc prolongation was described, although multiple electrocardiographic patterns had been observed.161

The phenomenon of neurogenic stunned myocardium is a definite clinical entity, with what can be a severe lim-itation of cardiac contractility. It is, however, a revers-ible condition, in contrast to myocardial infarction, and it has a good recovery profile. Obvious abnormalities of function start to recede within 72 hours, but when stunning is severe, endovascular management rather than surgical treatment may be indicated (if the aneu-rysm is suitable). Cardiac dysfunction may complicate and limit the active treatment options for vasospasm and may render early mechanical angioplasty more appropri-ate.162 Unlike atherosclerotic ischemic cardiac myopa-thy, stunned myocardium often exhibits apical sparing on echocardiographic examination.163 Conversely, patients with SAH develop cardiac dysfunction similar to takotsubo cardiomyopathy, which is an acute transient dysfunction resulting from sympathetic overactivity in postmenopausal women.164 Troponins are frequently increased in acute SAH, and high levels are associated with increased hemorrhage, hemodynamic manipula-tions, and worse outcomes.165 Whether this release of troponin represents a frank cardiac injury or a “myocar-dial leak” remains unknown. Adrenoreceptor polymor-phism was implicated in myocardial stunning, in which different receptor genotypes denoted an increased sensi-tivity to and release of catecholamines, in turn associated with a 3- to 4.8-fold increase in risk of cardiac injury and dysfunction.166

A typical strategy for cardiovascular management is given in Box 105-4. Comprehensive consensus guidelines have been published.128,130

Respiratory DysfunctionPulmonary injury is a frequent complication in the clinical course of the patient with SAH; nearly 17% of patients will experience severe dysfunction. This finding is associated with a poor neurologic outcome.167 Blood transfusion can increase the risk of lung injury (transfu-sion-related acute lung injury [TRALI]), which, in turn, affects mortality168 (see Chapter 61). Acute pulmonary edema can also occur in patients with poor-grade SAH, and this edema can be either neurogenic or cardiogenic.

Endocrine and Metabolic DerangementsHyperglycemia is a risk factor for poor outcome, espe-cially in SAH.169,170 However, aggressive glucose control

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is not useful in SAH and may worsen outcome.171 As in TBI, no basis exists for the use of corticosteroids.172

Hyponatremia is observed in 30% to 40% of patients with SAH.173 Whether cerebral salt-wasting syndrome (CSWS) or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is the dominant mecha-nism is debated.174

In CSWS, sodium is actively excreted from the body in high concentration, and accompanying diuresis occurs despite ongoing hyponatremia.175 Berendes and col-leagues demonstrated an associated increase in brain natriuretic peptide (BNP) release, thought at that time to derive exclusively from the brain.176 Given the increas-ing evidence for the ventricle as the main source of pro-duction of BNP, it is unclear whether BNP arises from a stressed ventricle at the time of the hemorrhage and asso-ciated sympathetic discharge or from a brain experiencing abnormal perfusion states of homeostatic areas. Hypona-tremia is also associated with cerebral infarction,177 in keeping with the clinical observation that hyponatre-mia predicts the onset of vasospasm by approximately 24 hours.178

SIADH is the more common etiology of hyponatremia in general, but it should not induce reduction in circulat-ing blood volume. That such a reduction does occur after SAH persuades many (including us) to consider CSWS the

GENERAL 1. Manage hypertension in unsecured aneurysms (with nicar-

dipine titrated to systolic BP < 140 mm Hg. 2. Maintain euvolemia prophylactically; no role for prophylac-

tic hypervolemia. 3. Administer nimodipine (possibly statins).CARDIOVASCULAR INSTABILITY 1. BP and cardiac output goals will alter as aneurysm is

secured. 2. ECGIf abnormal (QTc prolongation, ST-segment changes): check troponins.If troponins elevated: perform echocardiography. 3. Perform echocardiography if any manifested hypotension

or heart failure is suspected. 4. Monitor cardiac output. 5. Support on dobutamine for cardiac output and norepi-

nephrine for blood pressure. 6. Consider coiling as soon as practicable. 7. Reserve coronary catheterization for isolated wall motion

deficit and rising troponins (coil first if possible). 8. Avoid β-blockers unless the patient has active coronary

artery disease. 9. Vasospasm: treat with euvolemia/mild hypervolemia,

pressors, and cardiac output monitoring: adjust targets as perfusion tests suggest.

10. Transfusion: maintain hematocrit >25%. Avoid use of stored blood if possible.

BOX 105-4 Suggested Cardiovascular Management Strategies in Subarachnoid Hemorrhage

BP, Blood pressure; ECG, electrocardiogram.

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3113

drome;

Chapter 105: Neurocritical Care

Serum Na+

�135 mEq/L

Assessextracellular

volume

NormalLow High

Urineosmolality

Urinesodium

�20 �20

Adrenalinsufficiency,

CSWS

Diarrhea

�20 �20

Renalfailure

Heart failureCirrhosis

�100 �100

Psychogenicpolydipsia

SIADH,CSWS

(compensated)

Urinesodium

Figure 105-8. Algorithm for the differential diagnosis of hyponatremia in the neurosurgical patient. CSWS, Cerebral salt-wasting synSIADH, syndrome of inappropriate secretion of antidiuretic hormone.

more relevant etiology.179 Profound differences exist in the subsequent management of hyponatremia in these two conditions. CSWS indicates replacement with sodium and fluids, whereas SIADH may indicate fluid restriction, which may aggravate vasospasm and ischemic deficit. The situation is rendered all the more complex by the consid-eration that volume loading itself induces natriuresis.180 Both disorders are associated with SAH, and the main dis-tinguishing feature is the state of intravascular volume; CSWS is associated with depletion, whereas SIADH is associated with elevation. Because of the adversely com-bined effects of hyponatremia and decreased blood vol-ume on delayed ischemic deficits, many clinicians have advocated the use of hypertonic saline as the primary treatment for hyponatremia in patients with SAH. 181 A suggested algorithm for resolving diagnostic uncertainty is given in Figure 105-8.

Feeding and NutritionSAH induces a profound stress response in which the hypercatabolic state relates to the severity of the neu-rologic insult. Resting energy expenditure may reach a peak of 172% that of normal on day 10 after hemor-rhage. This change, coupled with the tendency to suffer from headache, nausea, and vomiting, leads to relative hypoalbuminemia that may compound the tendency for hypovolemia.182

ISCHEMIC STROKE

Stroke is the fourth leading cause of death in the United States after heart disease, cancer, and chronic lower respi-ratory disease. It is a major source of disability, with 795,000 cases per year and a prevalence of 3%.183

The deprivation of oxygen and nutrients to the brain beyond the combined thresholds of severity and time

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induces cellular death in neuronal tissue. In complete occlusion, this process starts within minutes. Around the dead tissue, an area of marginally sufficient blood sup-ply exists in which the probability of cell death is related to ischemic time. This is the ischemic penumbra and is potentially salvageable with aggressive intervention. Just as cardiologists say “time is muscle,” it can also be said that “time is neurons.”

Thus, the goals of treatment have moved away from physiologic stabilization and risk factor avoidance toward accelerated reperfusion and retrieval of threatened brain tissue.

Paralleling aggressive cardiac management in threat-ened infarction, treatment should start in the emergency department but continue into the ICU. Intravenous thrombolytics were initially deployed, followed by intraarterial and mechanical thrombolysis and, more recently, varying combinations of each modality. Cur-rent recommendations for treatment windows are 4.5 hours for intravenous therapy or 8 hours for the intra-arterial route, but this regimen may be adjusted in the light of perfusion- and diffusion-weighted MRI mis-match.184 No evidence suggests the benefit of one strat-egy over another on the most recent systematic review of anterior circulation stroke. The addition of stents to support subsequent vessel patency is a fast-growing practice with ongoing studies exploring efficacy.184 Ver-tebrobasilar occlusion may benefit from the more recent techniques.185

Vigorous perfusion should be maintained until throm-bolysis has been attempted. Consequently, hypertension should not be treated unless it is inducing myocardial damage or unless intracerebral hemorrhage (ICH) has already occurred (hemorrhagic conversion). This latter circumstance also precludes thrombolysis. Hypotension should be actively avoided.

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Once thrombolysis has been attempted, this increases the risks of hemorrhage, and hypertension should be moderated.186 Unwanted side effects obviously center around hemorrhage, which is associated with higher thrombolytic doses and later treatment.187 Keen atten-tion should be paid to postprocedural CT scans and any signs of systemic hemorrhage such as lower abdominal pain, which may indicate retroperitoneal bleeding. Areas of brain that cannot be salvaged will swell, causing com-pressive ischemia in adjacent regions. Just as the effects of TBI and SAH may vary by anatomic site, so, too, will the effects of ischemic stroke vary with the particular vascular area of occlusion.

In addition to control of cerebral volume, interest has revived in the early use of decompressive surgery in cir-cumstances of “malignant” swelling. Edema can induce ICP in excess of 30 mm Hg, with a correspondingly high mortality. Studies to date suggest treatment benefit if decompressive craniectomy is carried out in the first 24 hours after onset of symptoms, with aggressively sized bone flaps.188 Increasing age and CT hypodensity have adverse effects, but hemispheric dominance is less impor-tant. However, efficacy remains a concern because good functional outcomes are in the minority.189

POSTOPERATIVE NEUROSURGICAL CARE

Many neurosurgical procedures are lengthy and involve significant insult to the brain (see Chapter 70). Thus, postoperative admission to the ICU for avoidance of sec-ondary insult and a more graduated withdrawal of ven-tilatory support is common, although most significant events after craniotomy happen in the immediate post-operative period.190 ICU care particularly entails careful control of arterial blood pressure to minimize edema formation, by taking into account potential compromise of autoregulation and cerebrovascular compliance. How-ever, the importance of neurologic examination cannot be overemphasized, and early withdrawal or intermit-tent interruption of sedation to allow appropriate clini-cal examination is a prudent approach to follow these patients.

Patients with vascular lesions such as arteriovenous malformations and vascular tumors predisposed to the development of hyperemia benefit from careful attention to blood pressure management, as do patients undergoing carotid endarterectomy. In both arteriovenous malforma-tion and carotid disease, areas of the brain adjacent to the malformation or ipsilateral to the tight carotid stenosis may have absent autoregulatory control or may autoregu-late only at a significantly lesser range of arterial blood pressure. Until the autoregulatory mechanism returns to normal, blood pressure should be carefully and tightly controlled to prevent what has been termed normal pres-sure perfusion breakthrough. This can be accomplished with intravenous nicardipine or esmolol infusion, or both, to allow titratable adjustment of the blood pressure.

Aneurysmal clipping is not in this category, except in cases of vascular graft bypass procedures, in which atten-tion should be paid to minimum as well as maximum pressure targets. This is known as the Goldilocks approach. If arterial blood pressure is maintained too low, then

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his may risk graft thrombosis. If arterial blood pressure s too high, then the graft may rupture, or hemorrhage

ay occur. Although the range maintained is arbitrary, nd no supporting data are available, systolic blood pres-ure probably should be maintained in a narrow range etween 100 and 120 mm Hg.

Although not common, patients treated with lumbar SF drainage may develop central herniation syndrome. he diagnosis is not always apparent, and the sudden ecline in mental status, with a history of CSF drainage, hould prompt appropriate imaging of the brainstem. reatment is with fluid hydration and maintenance of he patient in the Trendelenburg position.

NTRACEREBRAL HEMORRHAGE

ontraumatic ICH may arise from ruptured aneurysm, uptured arteriovenous malformation, hemorrhagic troke (amyloid angiopathy, hypertension), conversion rom ischemic stroke, tumor, substance abuse (alcohol, ocaine, methamphetamines), and the use of warfarin Coumadin). This wide range of differential diagnoses an swiftly be refined by the CT scan, with accompany-ng clinical signs aiding localization and the assessment f pathophysiologic effect. Angiography may be required o rule out aneurysmal rupture.

Management is to avoid secondary insult by reducing he incidence of rebleeding, hypoxemia, hypercarbia, or dema.191,192 Essential care is directed toward the airway nd circulation. If the initial CT or MRI appearance sug-ests arteriovenous malformation, then care should be aken to limit blood pressure to reduce the risk of rebleed-ng. The addition of ICP monitoring allows one to set the PP target and provide a more physiologic approach to

he management of systemic blood pressure. If the ICH is n the posterior fossa or midbrain, consideration should e given to the insertion of a ventriculostomy to reduce he risk of hydrocephalus. Patients with lesions in these egions are prone to airway and respiratory problems and ay need early tracheal intubation to protect their air-ay and prevent aspiration.Nimodipine does not have an established role in these

ircumstances. Corticosteroids are also not indicated. If he patient is receiving warfarin, it should be reversed ith fresh frozen plasma and vitamin K.Most intracranial hematomas expand in volume dur-

ng the first 24 hours, and the volume of expansion is cor-elated with outcome. Although recombinant factor VIIa ed to a reduction in hemorrhage volume, outcome is not mproved. The role of recombinant factor VIIa in ICH is herefore uncertain, although it may be useful for rapid eversal of patients receiving warfarin.

The management of intracranial hemorrhage is gen-rally medical and supportive, with control of arterial lood pressure to less than 180 mm Hg. Ongoing clinical rials are targeting a systolic blood pressure of 140 mm Hg o decrease the risk of ICH volume expansion.193,194

Surgery is rarely indicated.192 However, in patients with erebellar hemorrhage, and brainstem compression, or in hose showing acute neurologic deterioration or obstruc-ive hydrocephalus, surgical evacuation of clots may be ndicated.191,192 Although patients with other types of

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stroke have experienced improved morbidity and mortal-ity in recent years, no significant change in outcome after ICH has occurred.

BRAIN INJURY AFTER CARDIAC ARREST

Although the therapeutic cerebroprotective value of induced moderate hypothermia has been disappointing in both TBI and SAH, its efficacy in improving neurologic outcome has been demonstrated in patients who suffered global hypoxia secondary to ventricular fibrillation (see also Chapter 108). Neurologic morbidity is common in those patients experiencing global cerebral ischemia as a consequence of cardiac arrest and is related to the genera-tion of free radicals and cellular injury on reperfusion of the ischemic brain.

Two studies reported improved neurologic outcome and reduced mortality in patients with ventricular fibril-lation who were resuscitated but remained in coma and were immediately treated with mild hypothermia in the range of 32° to 34° C.195,196 These results were con-firmed in a wider population, and a regimen of 12 to 24 hours of mild hypothermia is now recommended treat-ment for all post–cardiac arrest patients with neurologic dysfunction.197

Whereas initial studies induced hypothermia using cooled intravenous solutions, more sophisticated meth-ods and devices have since been introduced. These include noninvasive methods such as forced air cooling with limb and trunk blankets, topical adhesive cooling pads, and invasive methods deploying intravascular heat exchange catheters. Water-cooled adhesive pads connected to heat exchange units are the most commonly used methods at present.

Some clinicians consider the use of somatosensory evoked potentials (particularly the N20 and N70 laten-cies) to be helpful in the prognosis of coma after cardiac arrest.198

STATUS EPILEPTICUS

This condition has been defined as “repeated seizures occurring frequently without recovery between attacks” and has a significant morbidity and mortality, with approximately 50,000 deaths per year for an estimated annual incidence of 126,000 to 195,000 cases.199 Some clinicians have attempted to refine this condition by using a stricter definition of continuous seizure lasting at least 30 minutes. Irrespective of the definition of sta-tus epilepticus, prompt treatment of seizure should be instituted because a seizure lasting beyond 5 minutes is unlikely to stop spontaneously. Variants of seizure type are seen, but all may present in status epilepticus, includ-ing nonconvulsive types, which present their own par-ticular diagnostic challenges.200

Seizure activity may arise from any major insult affect-ing the cerebral cortex, whether infectious, mechanical, metabolic, or toxic. Even mild insults may provoke sta-tus epilepticus in which the seizure threshold is reduced by preexisting parenchymal disease or comorbidity (e.g., alcohol withdrawal). Given the previously outlined emphasis on the avoidance and termination of secondary



insult to the brain, the metabolic disadvantage of statuepilepticus is readily apparent. Management guidelinehave been published.201 Goals of treatment include seizure termination, physiologic support, and preventionof recurrence. This approach may involve intubationand ventilation, in which long-term paralytic agentshould not be used for fear of masking ongoing or recurrent seizure. Electroencephalographic control is highlrecommended. Preferred anticonvulsants for acute termination include lorazepam and midazolam, in view otheir relatively benign cardiovascular profile. Phenytoinremains a commonly used agent but takes time to administer because it can provoke hypotension and bradycardia if given rapidly. Hypotensive effects may also limithe usefulness of thiopental, pentobarbital, and propofol.201 In some patients refractory to treatment with usuaantiepileptics, inhaled anesthetics have been used withsuccess.202

GUILLAIN-BARRÉ SYNDROME

Guillain-Barré syndrome (GBS) occurs at a rate of 1 t4 cases per 100,000 population per year. The incidencincreases with age, and this disorder is one of the moscommon neurologic causes of admission to critical carunits.203,204

The classic form of GBS is acute inflammatory demyelinating polyneuropathy that appears as progressivelascending muscle weakness. This can manifest as flacciparalysis and respiratory failure. Several clustered conditions are associated with the syndrome, including acutinflammatory demyelinating polyneuropathy (AIDP)acute motor axonal neuropathy (AMAN), acute motorsensory axonal neuropathy (AMSAN), and Miller-Fishesyndrome (MFS), with MFS affecting the cranial nervefirst. AIDP is the most common variant seen in the UniteStates, and more than 50% of all patients have a recenhistory of bacterial or viral infection. Campylobacter jejunis the most frequently observed pathogen, along withcytomegalovirus, Epstein-Barr virus, and herpes simplex. GBS may display sensory and autonomic featuresdepending on the subtype, and some variation in speeof onset and offset is noted. Commonly, symptoms progress over several days to reach their peak at 2 weeks, witha plateau thereafter. In approximately 5% of patients, GBprogresses more rapidly, with maximal loss of functionwithin 72 hours of symptom onset. At 4 weeks, most havprogressed to the limit of their symptoms, and improvement is observed to start soon thereafter. Recovery mabe protracted for up to 6 months, however. Whether thspeed of onset relates to a slower rate of recovery and outcome limitation is debated.203,204

Loss of ventilatory efficacy is the main reason foadmission to the ICU. A forced vital capacity of less than20 mL/kg is a sensitive indicator of need for observationand 15 mL/kg for probable intubation, along with clinical signs of fatigue and airway compromise. Hypercarbiis a relatively late sign, and the clinician should not relon it.

Bulbar dysfunction, albeit less common, may appeabefore ventilatory compromise, particularly in patientwith the MFS variant.



Dysautonomia is seen in up to 20% of patients and is a source of morbidity.205 It should be monitored care-fully, because of the significant mortality of arrhythmia in older patients. Dysautonomia can vary from urinary retention to fixed tachycardia to both severe hypotension and paroxysmal hypertension.

Investigations should include electrocardiography, CSF protein (for acellular protein elevation), electromy-ography (axonal degeneration is associated with poorer recovery), and antibody status or screening for possible causative pathogens and also prognosis. GM1 antibody is associated with worsened recovery, whereas MFS is associ-ated with anti-GQ1b antibody.204

Particular challenges to management are the problems of deafferentation pain and psychiatric depression. The pain can be severe, is truncal in distribution, and may respond to anticonvulsants more than to opiates. It cer-tainly contributes to the frequently observed depression. This pain is often worsened by immobility, boredom, and the limited ability of busy staff to engage actively with a (relatively unusual for the neurocritical care unit) cogni-tively intact patient. Early tracheostomy in identifiably prolonged cases is appropriate.

Both symptom limitation and recovery from GBS have been improved with the use of plasmapheresis or the intravenous administration of gamma globulin. No advantage is seen with one treatment approach over the other or in combination. However, many physicians try them sequentially in cases of treatment failure. Persis-tence of foot drop at the conclusion of immunotherapy is an indicator of longer-term ventilation.206

Neither interferon nor corticosteroid use has been shown to improve outcome, either alone or in combina-tion with immunotherapy.203

SPINAL CORD INJURY

In contrast to GBS, spinal cord injury is much more com-mon (11,000 cases/year), is intractable to treatment, and almost inevitably has permanent effects. The num-ber afflicted in the United States is estimated to exceed 270,000. The degree of dysfunction is similar to GBS in that as the level of injury ascends, the patient has a high level of motor paralysis of the lower limbs, trunk, upper limbs, and diaphragm. Additionally, traumatic sympa-thectomy also occurs, producing bradycardia, hypoten-sion, and gastrointestinal paralysis. This gastrointestinal aspect is often overlooked, and subsequent abdominal distention can embarrass an already compromised dia-phragm into inefficacy. The cardiovascular effects of sympathectomy, particularly above T5, manifest as bra-dycardia and hypotension.207 This patient can be sup-ported by fluid and pressor therapy, and the tachycardic effect of dopamine may be a useful attribute. Unopposed vagal stimuli, as well as hypoxia, may induce bradycar-dia.207 Resuscitation targets are controversial, with more recent interest in maintaining spinal perfusion analogous to the CPP of TBI. Patients with injuries below T5 may still manifest hypotension but usually only on the provo-cation of posture, hypovolemia, or comorbidities.

Ventilatory support depends on the level of injury. If the injury is below C5, although the diaphragm remains


functional, in the acute stage respiratory embarrassment secondary to abdominal and intercostal paralysis can still occur because flaccidity in these muscles significantly decreases the functional efficiency of the diaphragmatic contraction. Thus, paradoxic respiration with chest indrawing during inspiration occurs. This can be allevi-ated in part with the use of an abdominal binder. With complete cervical spinal cord injury, acute respiratory fail-ure is common, secondary to the sudden loss of functional residual capacity and the inability of the sternocleidomas-toid muscle to stabilize the chest wall. With time, many patients can regain the ability to breathe spontaneously, except those with high cervical lesions. Controversy exists regarding the ventilatory pattern used for spinal patients. Some investigators suggest that a larger tidal volume should be used, with an aim of opening more alveoli, reducing atelectasis, and treating air hunger. No randomized clini-cal trials are available to support this, and it would seem contrary to more recent insights into lung stretch injury. Air hunger may be more a consequence of disordered pro-prioception than an indication to hyperventilate.208

Lower limb blood flow is reduced with increased arterial and venous pooling. This is associated with a higher inci-dence of thromboembolic disease, and early prophylaxis with low-molecular-weight heparin is recommended.

As with GBS, the patient with spinal cord injury is commonly aware, and this constitutes an additional burden of psychological stress. Consequently, the best approach taken is truly holistic, tending to psychologi-cal needs, as well as to cardiopulmonary, gastrointestinal, renal, and integumentary support. Significant advances have been made in the critical care and rehabilitation support afforded to these patients, and 2-year survival has increased significantly since the 1980s. Unfortunately, this improvement has not translated to increased long-term survival.209

MYASTHENIA GRAVIS

Although myasthenia gravis is a relatively uncommon disease (prevalence of 10 to 20 per 100,000), it is relevant to neurocritical care in that patients can present acutely with rapid deterioration of muscle function, predisposing to ventilatory failure—the myasthenic crisis. Myasthenia itself has a strong association with various autoimmune conditions (e.g., thyroid disease, pernicious anemia, rheumatoid arthritis), as well as being linked to women with certain human leukocyte antigen (HLA) types.210,211

The myasthenic crisis can be precipitated by a progres-sion in severity of the disease state or often by amplifica-tion by another factor. This factor can include infection, recent surgery, or interruption of immunosuppressants. Many drugs can exacerbate myasthenic crisis, includ-ing aminoglycosides, fluoroquinolones, anticonvulsants (including phenytoin), steroids, β-blockers, calcium antagonists, ketamine, lidocaine, neuromuscular block-ers, and anticholinergic agents.211

The diagnosis should exclude GBS, brainstem stroke, organophosphate poisoning, and botulism. Tests should include electrophysiology, CSF protein, edrophonium response, and antibodies to acetylcholine and muscle tyrosine kinase receptors.


The presentation is typically that of acutely worsening weakness of either respiratory or pharyngeal muscles, or both. The patient should be observed closely for signs of impending respiratory failure. Forced vital capacity is again useful with 15 mL/kg being a useful trigger for intubation.211

The other mainstay of therapy is by immunomodu-lation. Typically, intravenous immunoglobulin or plas-mapheresis is started quickly to limit progression of symptoms and avert frank crisis. Corticosteroids do have a role in establishing longer-term control of immu-nosuppression because immunoglobulin G (IgG) and plasmapheresis have limited duration of efficacy. Corti-costeroids alone are associated with a transient worsening of symptoms, before improvement, so they are best used concurrently with or immediately after plasmapheresis or IgG.212

MENINGITIS

Meningitis is a serious condition producing inflam-mation of the leptomeninges covering the CNS. The causative pathogens differ among different patient popu-lations. Community infections are frequently caused by Streptococcus pneumoniae, Haemophilus influenzae, Listeria monocytogenes, Neisseria meningitidis, and group B strep-tococci. N. meningitidis is particularly evident in teenag-ers. Since the advent of a childhood vaccination program, H. influenzae affects chiefly adults, but the other organ-isms tend to affect all age groups. Nosocomial infection, in contrast, predominantly arises in the neurosurgical patient, especially with the use of ventricular devices, and the pathogens here comprise gram-negative rods and staphylococci. Diagnostic features include fever almost invariably with the classic nuchal rigidity and change in mental status; less often, photophobia, papilledema, and new-onset seizures may be seen. A rash is typical of meningococcal infection, whereas arthritis occurs in a significant minority. Tests should include CSF Gram stain and culture by lumbar puncture, but any previous antibi-otic dosing can diminish sensitivity. Under this circum-stance, polymerase chain reaction (PCR) testing is the method of choice, thus displacing the more variable latex agglutination test. A CT scan should delay the lumbar puncture only when the patient’s history suggests a previ-ous mass lesion, stroke, or focal infection, recent seizures, or immunocompromise. Similarly, signs of papilledema, depressed level of consciousness, or focal deficit indicate a need for a CT examination to avoid herniation. Cere-bral edema not infrequently develops in patients with meningitis and can lead to acute deterioration in mental status. ICP monitoring may be indicated.

Treatment should be delivered swiftly, pausing only to obtain emergency samples for Gram stain and culture. If no identification is possible on Gram stain, empiric anti-biotic therapy should be delivered with third-generation cephalosporins (e.g., ceftriaxone or cefotaxime), along with vancomycin until organism and sensitivities are obtained. This approach covers the community-acquired pathogens. Nosocomial or trauma-associated infections can be effectively treated with cefepime and vancomycin. Steroids are useful adjuncts in bacterial meningitis and have been shown to reduce mortality.213

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The outcome of meningitis is a function of patient-related factors, the pathogenicity of the organism, and the time to effective treatment. An interesting study examined admission hypotension, altered mental status, or seizures for an effect on outcome. A 9% mortality rate occurred when one factor was present, and it increased to 33% for two factors and to 57% for all three.214

ENCEPHALITIS

Encephalitis manifests with fever, headache, and altera-tion of consciousness. Patients may also have delirium, focal deficit, and, commonly, seizures. Nuchal rigidity may be present in a mixed meningoencephalitis picture but should be absent in isolated encephalitis. Accompa-nying identifiers may be a vesicular rash associated with herpes zoster (although its absence does not remove zos-ter from suspicion), bilateral paralysis typical of West Nile disease, parotitis if mumps is suspected, and, of course, the hyperactivity, hydrophobia, and pharyngeal spasm of rabies. West Nile neuroinvasive disease has increased its incidence from 62 cases in 1999 to 438 in 2011, over 43 states, with estimates of up to 34,000 non-neurologic infections per year.215 Many nonviral and noninfectious causes of encephalitis may confound the diagnosis. These include vasculitis, systemic lupus ery-thematosus, stroke, rickettsial and parasitic infection, and drug-induced meningitis (e.g., IgG). Careful exami-nation of clinical features, history, and laboratory data is necessary. CSF should be drawn for viral DNA poly-merase chain reaction, as well as the routine biochemis-try, culture, and cell count. MRI is useful in identifying the demyelination and edema that can be difficult to see on CT. Serum serology is helpful for the diagnosis of Epstein-Barr virus, mumps, and West Nile disease as sources of encephalitis. Paired samples are recommended to allow later comparison if CSF PCR is unhelpful. Brain biopsy was considered the gold standard but is now a last option after CSF PCR, culture, and serology have proven negative.

Herpes simplex type 1 infection carries a very poor outlook if it is not treated expeditiously, and a course of intravenous acyclovir is recommended as soon as samples are drawn.

The pathogen remains unidentified more often than not, and outcome usually then depends on classification of the clinical features, with intractable seizure and cere-bral edema carrying a poor prognosis. Self-limiting sei-zure usually indicates a swift recovery.

BRAIN DEATH

It is crucially important that the physician understand the principles of the diagnosis of brain death and be able to apply them assiduously and without compromise (see Chapter 76). Many unfortunate instances of poor under-standing have led to imperfect examination, misdiagno-sis, and considerable distress to all concerned.

Declaration of brain death was originally codified by the Harvard criteria in 1968, with subsequent modifica-tion to allow separation of cerebral death from death of the entire nervous system including the spinal cord.216

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The diagnosis is built on a solid clinical examination of nervous system function, by examining the reflex response of the brain and cranial nerves to varying stim-uli of hypercarbia, pain, light, temperature change, atti-tudinal change of the middle ear, and detection of the blink, cough, and gag reflexes. The mechanisms for the cause of neurologic dysfunction should be clear. As with the operation of the GCS scale, the examination must be done in circumstances of adequate systemic oxygenation and perfusion. Confounders, such as hypothermia, meta-bolic or endocrine compromise, and persistent sedative or neuromuscular drugs, should be avoided, corrected, or removed. Although guidelines allow a single examiner in adults,217 many clinicians believe that two examiners are preferable, and this is mandatory in pediatric cases218 (see also Chapter 95). At least one of the testing physicians should have had training in neurology, neurosurgery, or neurocritical care. Time between tests is less important for diagnosis than for the opportunity to start commu-nicating with and preparing the family. One of the tests should include an appropriately conducted apnea trial in the presence of the physician, with confirmation of adequate changes in Pco2. Two apnea trials are required in pediatric cases.218 If for any reason any test cannot be completed in a safe manner, or to the satisfaction of either physician, then an ancillary test of CBF should be performed.

The hospital should have an institutionally approved protocol for the conduct of these tests and mechanisms in place for review and quality improvement.

ETHICAL CONSIDERATIONS

Ethical issues are frequently encountered in a neuro-logic ICU setting (see Chapter 10). Unfortunately, as well as the mortality described previously, significant life- altering morbidity occurs, to the extent that many patients and families would not desire aggressive ther-apy.219 This can be a difficult concept to accept for the physician, whose aim is to heal and preserve life. How-ever, the ethical imperative in Western culture is to pre-serve the autonomy of the individual (along with the principles of nonmaleficence, beneficence, and justice), and this has been extended to health care decision mak-ing. This situation may lead to uncomfortable choices and communication within the health care team, whose members may have differing opinions on goals, and from there to the patient and relatives, who, again, may think very differently.

Certain strategies can avoid or minimize these difficulties:

• Prognosis should be made on the basis of the best available evidence. This may involve planning and discussion among the team members in advance of meeting with families. The personal anecdote should be avoided, even if solicited.

• The relationship within the team should be open and collegial, with mutual respect given to the principle of open discussion. This approach avoids misperception of goals and attitudes and enables more


consistent communication with families, who often find dissonance among members of the ICU team disturbing.

• The presence of an advance directive offers major benefits, and the neurocritical care unit should have an admissions protocol that includes asking all competent, conscious patients to consider making their attitudes or wishes known.

• Regular family and patient conferences allow communication of prognosis as it is appropriate and offer the opportunity for correction of any misconceptions, as well as progressive education of the family to anticipated problems.

• Internal institutional mechanisms for raising concerns and conducting reviews should be in place. This is often facilitated by the presence of an institutional ethics committee, whose members can examine the issues, promote educational discussion, and help achieve a consensus.

• All decision making should be documented carefully and completely.

• Orders for limitation or withdrawal of therapy should be written explicitly, and institutional protocols should be used wherever possible.

Other important areas of possible conflict exist that are not possible to address within the confines of this text, but readers are advised to educate themselves on the following:

• The issues surrounding organ donation from the brain dead and the non–heart-beating donor

• Withdrawal of care for the incompetent patient without family

• Hospital bylaws and state legislation on the certification of death, whether that be by neurologic or cardiovascular criteria

CONCLUSION

Neurocritical care demands a thorough comprehension of the physiology, pharmacology, and pathology of the ner-vous system, as well as for the organ systems supporting it. The best care is provided in circumstances that allow multidisciplinary collaboration and appropriate atten-tion to detail of often complex and demanding patho-logic processes, but integrating them optimally under the direction of the critical care physician.

Complete references available online at expertconsult.com

RefeRences

1. Zygun D: Curr Opin Crit Care 11:139, 2005. 2. Suarez JI, et al: Crit Care Med 32:2311, 2004. 3. Maramattom BV, et al: Neurology 63:2142, 2004. 4. Kalmar AF, et al: Br J Anaesth 94:791, 2005. 5. Klatzo I: Acta Neuropathol (Berl) 72:236, 1987. 6. Jones PA, et al: J Neurosurg Anesthesiol 6:4, 1994. 7. Beaumont A, et al: J Neurotrauma 18:1359, 2001. 8. Faraci FM, Heistad DD: Physiol Rev 78:53, 1998. 9. Wartenberg KE, et al: Crit Care Med 34:617, 2006. 10. McKeating EG, et al: Anesth Analg 86:759, 1998. 11. Stocchetti NC, et al: J Neurotrauma 24:1339, 2007.


http://expertconsult.com

http://refhub.elsevier.com/B978-0-7020-5283-5.00105-3/ref0010











12. Muench E, et al: Crit Care Med 33:2367, 2005. 13. Manley G, et al: Arch Surg 136:1118, 2001. 14. Chesnut RM, et al: J Trauma 34:216, 1993. 15. Rosner MJ, et al: J Neurosurg 83:949, 1995. 16. Karanjia N, et al: Neurocrit Care 15:4, 2011. 17. McKeating EG, et al: Br J Anaesth 78:520, 1997. 18. Malham GM, Souter MJ: Br J Neurosurg 15:381, 2001. 19. Mascia L, et al: Crit Care Med 35:1815, 2007. 20. Wolf S, et al: Acta Neurochir Suppl 81:99, 2002. 21. Diringer MN, Zazulia AR: Neurocrit Care 1:219, 2004. 22. Xiao F: Acad Emerg Med 9:933, 2002. 23. Claydon VE, et al: Spinal Cord 44:341, 2006. 24. Orpello JM, Benjamin E: Critical care of patients with subarach-

noid hemorrhage. In Bederson JB, editor: Subarachnoid hemor-rhage: pathophysiology and management, Park Ridge, Ill, 1997, American Association of Neurological Surgeons, p 173.

25. Perel P, et al: Cochrane Database Syst Rev(4)CD001530, 2006. 26. Rovlias A, Kotsou S: Neurosurgery 46:335, 2000. 27. NICE-SUGAR Study Investigators: N Engl J Med 360:1283, 2009. 28. Vespa P, et al: Crit Care Med 40:1923, 2012. 29. Kilpatrick MM, et al: Neurosurgery 47:850, 2000. 30. Gungor E, et al: Neurol Sci 22:261, 2001. 31. Greer DM, et al: Stroke 39:3029, 2008. 32. Clifton GL, et al: N Engl J Med 344:556, 2001. 33. Todd MM, et al: N Engl J Med 352:135, 2005. 34. Badjatia N: Crit Care Med 37(Suppl):S250, 2009. 35. Cremer OL, et al: Crit Care Med 33:2207, 2005. 36. Chesnut RM, et al: New Engl J Med 367:2471, 2012. 37. Sahuquillo J, et al: J Neurosurg 90:16, 1999. 38. Lozier AP, et al: Neurosurgery 51:170, 2002. 39. Piper I, et al: Neurosurgery 49:1158, 2001. 40. Lundberg N: Acta Psychiatr Scand Suppl 36:1, 1960. 41. Symon L, et al: Adv Exp Med Biol 94:775, 1977. 42. Kety SS: Keio J Med 43:9, 1994. 43. Sioutos PJ, et al: Neurosurgery 36:943, 1995. 44. Melot C, et al: J Cereb Blood Flow Metab 16:1263, 1996. 45. Aaslid R, et al: J Neurosurg 57:769, 1982. 46. Eden A: Stroke 19:1445, 1988. 47. Aaslid R, et al: J Neurosurg 60:37, 1984. 48. Lindegaard KF, et al: Acta Neurochir Suppl (Wien) 42:81, 1988. 49. Sviri GE, et al: Neurosurgery 59:360-366, 2006. 50. Kincaid MS, et al: J Neurosurg 110:67, 2009. 51. Tiecks FP, et al: Stroke 26:1014, 1995. 52. Mascia L, et al: Intensive Care Med 26:202, 2002. 53. Aaslid R: Front Neurol Neurosci 21:216, 2006. 54. Kirkness CJ, et al: Biol Res Nurs 2:175, 2001. 55. Vavilala MS, et al: Pediatr Crit Care Med 5:257, 2004. 56. Souter MJ, Andrews PJ: Br J Anaesth 76:744, 1996. 57. Coplin WM, et al: Neurosurgery 42:533, 1998. 58. Gopinath SP, et al: J Neurol Neurosurg Psychiatry 57:717, 1994. 59. Macmillan CS, et al: J Neurol Neurosurg Psychiatry 70:101, 2001. 60. Stocchetti N, et al: Anesth Analg 99:230, 2004. 61. Robertson CS, et al: J Neurosurg 67:361, 1987. 62. Artru F, et al: J Neurosurg Anesthesiol 16:226, 2004. 63. Stiefel MF, et al: J Neurosurg 105:568, 2006. 64. Oddo M, et al: Neurosurgery 69:1037, 2011. 65. Gupta AK, et al: J Neurosurg 96:263, 2002. 66. Kett-White R, et al: Neurosurgery 50:1213, 2002. 67. Brain Tissue Oxygen Monitoring in Traumatic Brain Injury (TBI)

(BOOST 2). <http://clinicaltrials.gov/ct2/show/NCT00974259/> (Accessed 20.10.12.)

68. Hillered L, et al: J Neurotrauma 22:3, 2005. 69. Bellander BM, et al: Intensive Care Med 30:2166, 2004. 70. Little AS, et al: J Neurosurg 106:805, 2007. 71. Claassen J, et al: Stroke 33:1225, 2002. 72. Al-Rawi PG: Acta Neurochir Suppl 95:453, 2005. 73. Buchner K, et al: Zentralbl Neurochir 61:69, 2000. 74. McQuillen PS, et al: Stroke 38:736, 2007. 75. Moritz S, et al: Anesthesiology 107:563, 2007. 76. Lopez JA, Elliot JP: When should follow-up computed tomogra-

phy scans be obtained?. In Valadka AB, Andrews BT, editors: Neu-rotrauma: evidence-based answers to common questions, New York, 2005, Thieme, p 105.

77. Servadei F, et al: Neurosurgery 46:70, 2000. 78. Marshall LF, et al: J Neurotrauma 9(Suppl 1):S287, 1992.

Downloaded from ClinicalKey.com at Buddhist TzuFor personal use only. No other uses without permission


79. Vos PE, et al: J Neurotrauma 18:649, 2001. 80. Fisher CM, et al: Neurosurgery 6:1, 1980. 81. Grosset DG, et al: Neuroradiology 36:418, 1994. 82. Frontera JA, et al: Neurosurgery 59:21, 2006. 83. Citerio G, et al: Acta Neurochir (Wien) 142:769, 2000. 84. Degos V, et al: Anesth Analg 114:1026, 2012. 85. Teasdale G, Jennett B: Lancet 2:81, 1974. 86. Hunt WE, Hess RM: J Neurosurg 28:14, 1968. 87. Teasdale GM, et al: J Neurol Neurosurg Psychiatry 51:1457, 1988. 88. Tisdall MM, Smith M: Br J Anaesth 99:61, 2007. 89. Langlois JA, et al: Traumatic brain injury in the United States: emer-

gency department visits, hospitalizations, and deaths, Atlanta, 2006, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.

90. Hicks RR, et al: J Trauma 68:1257, 2010. 91. Winqvist S, et al: Brain Inj 21:1079, 2007. 92. Stuke L, et al: Ann Surg 245:651, 2007. 93. Provenzale J: Emerg Radiol 14:1, 2007. 94. Kim KA, et al: Neurosurgery 57:737, 2005. 95. Zafonte RD, et al: Brain Inj 11:403, 1997. 96. Lee EJ, et al: J Trauma 45:946, 1998. 97. Jones NR, et al: Br J Neurosurg 7:465, 1993. 98. Woertgen C, et al: J Clin Neurosci 13:718, 2006. 99. Wu HM, et al: Neurosurgery 55:1306, 2004. 100. Mattioli C, et al: J Neurosurg 98:37, 2003. 101. Murray GD, et al: J Neurotrauma 24:329, 2007. 102. Collier BR, et al: J Neurosurg Anesthesiol 16:196, 2004. 103. Cooper DJ, et al: N Engl J Med 364:1493, 2011. 104. Ravussin P, et al: J Neurosurg 64:104, 1986. 105. Kamel H, et al: Crit Care Med 39:554, 2011. 106. Battison C, et al: Crit Care Med 33:196, 2005. 107. Himmelseher S: Curr Opin Anaesthesiol 20:414, 2007. 108. Lescot T, et al: Crit Care Med 34:3029, 2006. 109. Finfer S, et al: N Engl J Med 350:2247, 2004. 110. Myburgh J, et al: N Engl J Med 357:874, 2007. 111. Ginsberg MD, et al: Biochem Soc Trans 34:1323, 2006. 112. Brain Trauma Foundation: J Neurotrauma 24:S87, 2007. 113. Davis DP: Resuscitation 76:333, 2008. 114. Brain Trauma Foundation: J Neurotrauma 24:S59, 2007. 115. Robertson CS, et al: Crit Care Med 27:2086, 1999. 116. Balestreri M, et al: Neurocrit Care 4:8, 2006. 117. Nordstrom CH: Neurocrit Care 2:83, 2005. 118. Grande PO, et al: J Trauma 42:S23, 1997. 119. Naredi S, et al: Acta Anaesthesiol Scand 45:402, 2001. 120. Dizdarevic K, et al: Clin Neurol Neurosurg 114:142, 2012. 121. Zafar SN, et al: J Neurotrauma 28:1307, 2011. 122. Edwards P, et al: Lancet 365:1957, 2005. 123. Sadaka F, Veremakis C: Brain Inj 26:899, 2012. 124. Fox JL, et al: CJEM 12:355, 2010. 125. Clifton GL, et al: J Neurosurg 117:714, 2012. 126. Denson K, et al: Am J Surg 193:380, 2007. 127. Macdonald RL, et al: Surg Neurol 59:363, 2003. 128. Connolly Jr ES, et al: Stroke 43:1711, 2012. 129. de Rooij NK, et al: J Neurol Neurosurg Psychiatry 78:1365, 2007. 130. Diringer MN, et al: Neurocrit Care 15:211, 2011. 131. Berman MF, et al: Stroke 34:2200, 2003. 132. Hop JW, et al: Stroke 28:660, 1997. 133. Vergouwen MD, et al: J Cereb Blood Flow Metab 28:1761, 2008. 134. Haley Jr EC, et al: Stroke 23:205, 1992. 135. Molyneux AJ, et al: Lancet 366:809, 2005. 136. Ransom E, et al: Neurocritical Care 6:174, 2007. 137. Roos Y, et al: Stroke 34:2308, 2003. 138. Gaberel T, et al: Acta Neurochir (Wien) 154:1, 2012. 139. Aiyagari V, et al: Cerebrovascular disease. In Schmidt GA, Hall

JB, Wood LDH, editors: Principles of critical care, ed 3, New York, 2005, McGraw-Hill Professional, p 985.

140. Suhardja A: Nat Clin Pract Cardiovasc Med 1:110, 2004. 141. de Oliveira JG, et al: Neurosurg Rev 30:22, 2007. 142. Suzuki H, Taki W: Acta Neurochir Suppl 115:99, 2013. 143. Dumont AS, et al: Stroke 41:2519, 2010. 144. Kassell NF, et al: Neurosurgery 11:337, 1982. 145. Treggiari MM, et al: J Neurosurg 98:978, 2003. 146. Rinkel GJ, et al: Cochrane Database Syst Rev(4)CD000483, 2004. 147. Egge A, et al: Neurosurgery 49:593, 2001. 148. Muench E, et al: Crit Care Med 35:1844, 2007.

Chi General Hospital JC September 20, 2016.. Copyright ©2016. Elsevier Inc. All rights reserved.



























































http://clinicaltrials.gov/ct2/show/NCT00974259/



























































































149. Naidech AM, et al: Crit Care Med 35:2383, 2007. 150. Levine J, et al: Neurosurgery 66:312, 2010. 151. Vincent JL, et al: JAMA 288:1499, 2002. 152. Dorhout Mees SM, et al: Cochrane Database Syst Rev(3)CD000277,

2007. 153. Roos YB, et al: Stroke 32:1860, 2001. 154. Eskridge JM, et al: Neurosurgery 42:510, 1998. 155. Bejjani GK, et al: Neurosurgery 42:979, 1998. 156. Elliott JP, et al: J Neurosurg 88:277, 1998. 157. Macdonald RL, et al: Lancet Neurol 10:618, 2011. 158. Sanchez-Peña P, et al: Crit Care Med 40:594, 2012. 159. Manninen PH, et al: J Neurosurg Anesthesiol 7:12, 1995. 160. Szabo MD, et al: Anesth Analg 76:253, 1993. 161. Mayer SA, et al: Stroke 30:780, 1999. 162. Jain R, et al: AJNR Am J Neuroradiol 25:126, 2004. 163. Zaroff JG, et al: J Am Soc Echocardiogr 13:774, 2000. 164. Lee VH, et al: J Neurosurg 105:264, 2006. 165. Hravnak M, et al: Stroke 40:3478, 2009. 166. Zaroff JG, et al: Stroke 37:1680, 2006. 167. Gruber A, et al: J Neurosurg 88:28, 1998. 168. Kahn JM, et al: Crit Care Med 34:196, 2006. 169. Frontera JA, et al: Stroke 37:199, 2006. 170. Charpentier C, et al: Stroke 30:1402, 1999. 171. Schmutzhard E, Rabinstein AA: Neurocrit Care 15:281, 2011. 172. Feigin VL, et al: Cochrane Database Syst Rev(3)CD004583, 2005. 173. Harrigan MR: Neurosurgery 38:152, 1996. 174. Hannon MJ, et al: J Clin Endocrinol Metab 97:1423, 2012. 175. Qureshi AI, et al: Neurosurgery 50:749, 2002. 176. Berendes E, et al: Lancet 349:245, 1997. 177. Wijdicks EF, et al: Ann Neurol 17:137, 1985. 178. Igarashi T, et al: Neurol Res 29:835, 2007. 179. Kasuya H, et al: Stroke 34:956, 2003. 180. Cowley Jr AW, Roman RJ: Baillieres Clin Endocrinol Metab 3:331,

1989. 181. Sterns R, Silver S: J Am Soc Nephrol 19:194, 2008. 182. Kasuya H, et al: Neurosurgery 42:1268, 1998. 183. Roger VL, et al: Circulation 125:e2, 2012. 184. Mullen MT, et al: Stroke 43:2350, 2012.

Downloaded from ClinicalKey.com at BuddhistFor personal use only. No other uses without permiss

185. Kansara A, et al: J Neurointerv Surg 4:274, 2012. 186. Wityk RJ: Neurologist 13:171, 2007. 187. Wardlaw JM, et al: Cochrane Database Syst Rev(2)CD000213, 2000. 188. Wagner S, et al: J Neurosurg 94:693, 2001. 189. Huang P, et al: Br J Neurosurg 26:504, 2012. 190. Rhondali O, et al: J Neurosurg Anesthesiol 23:118, 2011. 191. Broderick J, et al: Stroke 38:2001, 2007. 192. Mendelow AD, et al: Lancet 365:387, 2005. 193. INTERACT Investigators: Lancet Neurol 7:391, 2008. 194. Qureshi AI, Palesch YY: Neurocrit Care 15:559, 2011. 195. Bernard SA, et al: N Engl J Med 346:557, 2002. 196. Hypothermia After Cardiac Arrest Study Group: N Engl J Med

346:549, 2002. 197. Arrich J, et al: Cochrane Database Syst Rev(9)CD004128, 2012. 198. Madl C, et al: Crit Care Med 28:721, 2000. 199. DeLorenzo RJ, et al: Neurology 46:1029, 1996. 200. Walker MC: Int Rev Neurobiol 81:287, 2007. 201. Brophy GM, et al: Neurocrit Care 17:3, 2012. 202. Kofke WA, et al: Anesthesiology 71:653, 1989. 203. Cosi V, Versino M: Neurol Sci 27(Suppl 1):S47, 2006. 204. Hughes RA, Cornblath DR: Lancet 366:1653, 2005. 205. Hughes RAC, et al: Arch Neurol 62:1194, 2005. 206. Fourrier F, et al: Crit Care 15:R65, 2011. 207. Bilello JF, et al: Arch Surg 138:1127, 2003. 208. Brown R, et al: Respir Care 51:853, 2006. 209. Strauss DJ, et al: Arch Phys Med Rehabil 87:1079, 2006. 210. Phillips LH: Neurol 24:17, 2004. 211. Juel VC: Semin Neurol 24:75, 2004. 212. Jani-Acsadi A, Lisak RP: J Neurol Sci 261:127-133, 2007. 213. van de Beek D, et al: Lancet Infect Dis 4:139, 2004. 214. Aronin SI, et al: Ann Intern Med 129:862, 1998. 215. Centers for Disease Control and Prevention: MMWR Morb Mortal

Wkly Rep 61:510, 2012. 216. Wijdicks EFM: Neurology 61:970, 2003. 217. Wijdicks EF, et al: Neurology 74:1911, 2010. 218. Nakagawa TA, et al: Pediatrics 128:e720, 2011. 219. Buchanan KM, et al: Neurosurgery 46:831, 2000.

Tzu Chi General Hospital JC September 20, 2016.ion. Copyright ©2016. Elsevier Inc. All rights reserved.












































































RefeRences

1. Zygun D: Non-neurological organ dysfunction in neurocritical care: impact on outcome and etiological considerations, Curr Opin Crit Care 11:139-143, 2005.

2. Suarez JI, Zaidat OO, Suri MF, et al: Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team, Crit Care Med 32:2311-2317, 2004.

3. Maramattom BV, Bahn MM, Wijdicks EF: Which patient fares worse after early deterioration due to swelling from hemispheric stroke? Neurology 63:2142-2145, 2004.

4. Kalmar AF, Van AJ, Caemaert J, et al: Value of Cushing reflex as warning sign for brain ischaemia during neuroendoscopy, Br J Anaesth 94:791-799, 2005.

5. Klatzo I: Pathophysiological aspects of brain edema, Acta Neuro-pathol (Berl) 72:236-239, 1987.

6. Jones PA, Andrews PJ, Midgley S, et al: Measuring the burden of secondary insults in head-injured patients during intensive care, J Neurosurg Anesthesiol 6:4-14, 1994.

7. Beaumont A, Hayasaki K, Marmarou A, et al: Contrasting effects of dopamine therapy in experimental brain injury, J Neurotrauma 18:1359-1372, 2001.

8. Faraci FM, Heistad DD: Regulation of the cerebral circulation: role of endothelium and potassium channels, Physiol Rev 78:53-97, 1998.

9. Wartenberg KE, Schmidt JM, Claassen J, et al: Impact of medical complications on outcome after subarachnoid hemorrhage, Crit Care Med 34:617-623, 2006.

10. McKeating EG, Andrews PJ, Mascia L: The relationship of soluble adhesion molecule concentrations in systemic and jugular venous serum to injury severity and outcome after traumatic brain injury, Anesth Analg 86:759-765, 1998.

11. Stocchetti N, Colombo A, Ortolano F, et al: Time course of intra-cranial hypertension after traumatic brain injury, J Neurotrauma 24:1339-1346, 2007.

12. Muench E, Bauhuf C, Roth H, et al: Effects of positive end- expiratory pressure on regional cerebral blood flow, intracranial pressure, and brain tissue oxygenation, Crit Care Med 33:2367-2372, 2005.

13. Manley G, Knudson MM, Morabito D, et al: Hypotension, hypoxia, and head injury: frequency, duration, and conse-quences, Arch Surg 136:1118-1123, 2001.

14. Chesnut RM, Marshall LF, Klauber MR, et al: The role of second-ary brain injury in determining outcome from severe head injury, J Trauma 34:216-222, 1993.

15. Rosner MJ, Rosner SD, Johnson AH: Cerebral perfusion pressure: management protocol and clinical results, J Neurosurg 83:949-962, 1995.

16. Karanjia N, Nordquist D, Stevens R, Nyquist P: A clinical descrip-tion of extubation failure in patients with primary brain injury, Neurocrit Care 15(1):4-12, 2011.

17. McKeating EG, Andrews PJ, Signorini DF, Mascia L: Transcranial cytokine gradients in patients requiring intensive care after acute brain injury, Br J Anaesth 78:520-523, 1997.

18. Malham GM, Souter MJ: Systemic inflammatory response syn-drome and acute neurological disease, Br J Neurosurg 15:381-387, 2001.

19. Mascia L, Zavala E, Bosma K, et al: High tidal volume is associ-ated with the development of acute lung injury after severe brain injury: an international observational study, Crit Care Med 35:1815-1820, 2007.

20. Wolf S, Schurer L, Trost HA, Lumenta CB: The safety of the open lung approach in neurosurgical patients, Acta Neurochir Suppl 81:99-101, 2002.

21. Diringer MN, Zazulia AR: Osmotic therapy: fact and fiction, Neu-rocrit Care 1:219-233, 2004.

22. Xiao F: Bench to bedside: brain edema and cerebral resuscitation: the present and future, Acad Emerg Med 9:933-946, 2002.

23. Claydon VE, Steeves JD, Krassioukov A: Orthostatic hypotension following spinal cord injury: understanding clinical pathophysi-ology, Spinal Cord 44:341-351, 2006.

24. Orpello JM, Benjamin E: Critical care of patients with subarach-noid hemorrhage. In Bederson JB, editor: Subarachnoid hemor-rhage: pathophysiology and management, Park Ridge, Ill, 1997, American Association of Neurological Surgeons, pp 173-188.

Downloaded from ClinicalKey.com at Buddhist Tz
For personal use only. No other uses without permission
3120.e1

25. Perel P, Yanagawa T, Bunn F, et al: Nutritional support for head-injured patients, Cochrane Database Syst Rev(4)CD001530, 2006.

26. Rovlias A, Kotsou S: The influence of hyperglycemia on neuro-logical outcome in patients with severe head injury, Neurosurgery 46:335-342, 2000.

27. NICE-SUGAR Study Investigators: Intensive versus conven-tional glucose control in critically ill patients, N Engl J Med 360: 1283-1297, 2009.

28. Vespa P, McArthur DL, Stein N, et al: Tight glycemic control increases metabolic distress in traumatic brain injury: a ran-domized controlled within-subjects trial, Crit Care Med 40(6): 1923-1929, 2012.

29. Kilpatrick MM, Lowry DW, Firlik AD, et al: Hyperthermia in the neurosurgical intensive care unit, Neurosurgery 47:850-855, 2000.

30. Gungor E, Alli N, Comoglu S, Comcuoglu C: Phenytoin hypersen-sitivity syndrome, Neurol Sci 22:261-265, 2001.

31. Greer DM, Funk SE, Reaven NL, et al: Impact of fever on outcome in patients with stroke and neurologic injury: a comprehensive meta-analysis, Stroke 39:3029-3035, 2008.

32. Clifton GL, Miller ER, Choi SC, et al: Lack of effect of induction of hypothermia after acute brain injury, N Engl J Med 344:556-563, 2001.

33. Todd MM, Hindman BJ, Clarke WR, Torner JC: Mild intraopera-tive hypothermia during surgery for intracranial aneurysm, N Engl J Med 352:135-145, 2005.

34. Badjatia N: Hyperthermia and fever control in brain injury, Crit Care Med 37(Suppl):S250-S257, 2009.

35. Cremer OL, van Dijk GW, van Wensen E, et al: Effect of intracra-nial pressure monitoring and targeted intensive care on functional outcome after severe head injury, Crit Care Med 33:2207-2213, 2005.

36. Chesnut RM, Temkin N, Carney N, et al: A trial of intracranial-pressure monitoring in traumatic brain injury, New Engl J Med 367:2471-2481, 2012.

37. Sahuquillo J, Poca MA, Arribas M, et al: Interhemispheric supra-tentorial intracranial pressure gradients in head-injured patients: are they clinically important? J Neurosurg 90:16-26, 1999.

38. Lozier AP, Sciacca RR, Romagnoli MF, Connolly Jr ES: Ventric-ulostomy-related infections: a critical review of the literature, Neurosurgery 51:170-181, 2002.

39. Piper I, Barnes A, Smith D, Dunn L: The Camino intracranial pres-sure sensor: is it optimal technology? An internal audit with a review of current intracranial pressure monitoring technologies, Neurosurgery 49:1158-1164, 2001.

40. Lundberg N: Continuous recording and control of ventricular fluid pressure in neurosurgical practice, Acta Psychiatr Scand Suppl 36:1-193, 1960.

41. Symon L, Lassen NA, Astrup J, Branston NM: Thresholds of isch-aemia in brain cortex, Adv Exp Med Biol 94:775-782, 1977.

42. Kety SS: The measurement of cerebral blood flow by means of inert diffusible tracers, Keio J Med 43:9-14, 1994.

43. Sioutos PJ, Orozco JA, Carter LP, et al: Continuous regional cere-bral cortical blood flow monitoring in head-injured patients, Neu-rosurgery 36:943-949, 1995.

44. Melot C, Berre J, Moraine JJ, Kahn RJ: Estimation of cerebral blood flow at bedside by continuous jugular thermodilution, J Cereb Blood Flow Metab 16:1263-1270, 1996.

45. Aaslid R, Markwalder TM, Nornes H: Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries, J Neurosurg 57:769-774, 1982.

46. Eden A: Transcranial Doppler ultrasonography and hyperostosis of the skull, Stroke 19:1445-1446, 1988.

47. Aaslid R, Huber P, Nornes H: Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound, J Neurosurg 60:37-41, 1984.

48. Lindegaard KF, Nornes H, Bakke SJ, et al: Cerebral vasospasm after subarachnoid haemorrhage investigated by means of transcranial Doppler ultrasound, Acta Neurochir Suppl (Wien) 42:81-84, 1988.

49. Sviri GE, Ghodke B, Britz GW, et al: Transcranial Doppler grad-ing criteria for basilar artery vasospasm, Neurosurgery 59:360-366, 2006.

50. Kincaid MS, Souter MJ, Treggiari MM, et al: Accuracy of tran-scranial Doppler ultrasonography and single-photon emission computed tomography in the diagnosis of angiographically dem-onstrated cerebral vasospasm, J Neurosurg 110:67-72, 2009.

u Chi General Hospital JC September 20, 2016.
. Copyright ©2016. Elsevier Inc. All rights reserved.




















































































































































References3120.e2

51. Tiecks FP, Lam AM, Aaslid R, Newell DW: Comparison of static and dynamic cerebral autoregulation measurements, Stroke 26:1014-1019, 1995.

52. Mascia L, Andrews PJ, McKeating EG, et al: Cerebral blood flow and metabolism in severe brain injury: the role of pressure auto-regulation during cerebral perfusion pressure management, Inten-sive Care Med 26:202-205, 2002.

53. Aaslid R: Cerebral autoregulation and vasomotor reactivity, Front Neurol Neurosci 21:216-228, 2006.

54. Kirkness CJ, Mitchell PH, Burr RL, Newell DW: Cerebral autoregu-lation and outcome in acute brain injury, Biol Res Nurs 2:175-185, 2001.

55. Vavilala MS, Lee LA, Boddu K, et al: Cerebral autoregulation in pediatric traumatic brain injury, Pediatr Crit Care Med 5:257-263, 2004.

56. Souter MJ, Andrews PJ: Validation of the Edslab dual lumen oximetry catheter for continuous monitoring of jugular bulb oxy-gen saturation after severe head injury, Br J Anaesth 76:744-746, 1996.

57. Coplin WM, O’Keefe GE, Grady MS, et al: Accuracy of continu-ous jugular bulb oximetry in the intensive care unit, Neurosurgery 42:533-539, 1998.

58. Gopinath SP, Robertson CS, Contant CF, et al: Jugular venous desaturation and outcome after head injury, J Neurol Neurosurg Psychiatry 57:717-723, 1994.

59. Macmillan CS, Andrews PJ, Easton VJ: Increased jugular bulb satu-ration is associated with poor outcome in traumatic brain injury, J Neurol Neurosurg Psychiatry 70:101-104, 2001.

60. Stocchetti N, Canavesi K, Magnoni S, et al: Arterio-jugular differ-ence of oxygen content and outcome after head injury, Anesth Analg 99:230-234, 2004.

61. Robertson CS, Grossman RG, Goodman JC, Narayan RK: The predictive value of cerebral anaerobic metabolism with cerebral infarction after head injury, J Neurosurg 67:361-368, 1987.

62. Artru F, Dailler F, Burel E, et al: Assessment of jugular blood oxy-gen and lactate indices for detection of cerebral ischemia and prognosis, J Neurosurg Anesthesiol 16:226-231, 2004.

63. Stiefel MF, Udoetuk JD, Spiotta AM, et al: Conventional neuro-critical care and cerebral oxygenation after traumatic brain injury, J Neurosurg 105:568-575, 2006.

64. Oddo M, Levine JM, Mackenzie L, et al: Brain hypoxia is associ-ated with short-term outcome after severe traumatic brain injury independently of intracranial hypertension and low cerebral per-fusion pressure, Neurosurgery 69:1037-1045, 2011.

65. Gupta AK, Hutchinson PJ, Fryer T, et al: Measurement of brain tissue oxygenation performed using positron emission tomogra-phy scanning to validate a novel monitoring method, J Neurosurg 96:263-268, 2002.

66. Kett-White R, Hutchinson PJ, Al-Rawi PG, et al: Adverse cerebral events detected after subarachnoid hemorrhage using brain oxy-gen and microdialysis probes, Neurosurgery 50:1213-1221, 2002.

67. Brain Tissue Oxygen Monitoring in Traumatic Brain Injury (TBI) (BOOST 2). <http://clinicaltrials.gov/ct2/show/NCT00974259/> (Accessed 20.10.12.)

68. Hillered L, Vespa PM, Hovda DA: Translational neurochemical research in acute human brain injury: the current status and potential future for cerebral microdialysis, J Neurotrauma 22:3-41, 2005.

69. Bellander BM, Cantais E, Enblad P, et al: Consensus meeting on microdialysis in neurointensive care, Intensive Care Med 30: 2166-2169, 2004.

70. Little AS, Kerrigan JF, McDougall CG, et al: Nonconvulsive status epilepticus in patients suffering spontaneous subarachnoid hem-orrhage, J Neurosurg 106:805-811, 2007.

71. Claassen J, Carhuapoma JR, Kreiter KT, et al: Global cerebral edema after subarachnoid hemorrhage: frequency, predictors, and impact on outcome, Stroke 33:1225-1232, 2002.

72. Al-Rawi PG: Near-infrared spectroscopy in brain injury: today’s perspective, Acta Neurochir Suppl 95:453-457, 2005.

73. Buchner K, Meixensberger J, Dings J, Roosen K: Near-infrared spectroscopy: not useful to monitor cerebral oxygenation after severe brain injury, Zentralbl Neurochir 61:69-73, 2000.

74. McQuillen PS, Barkovich AJ, Hamrick SE, et al: Temporal and ana-tomic risk profile of brain injury with neonatal repair of congeni-tal heart defects, Stroke 38:736-741, 2007.

Downloaded from ClinicalKey.com at BuddhFor personal use only. No other uses without permi

75. Moritz S, Kasprzak P, Arlt M, et al: Accuracy of cerebral monitor-ing in detecting cerebral ischemia during carotid endarterectomy: a comparison of transcranial Doppler sonography, near-infrared spectroscopy, stump pressure, and somatosensory evoked poten-tials, Anesthesiology 107:563-569, 2007.

76. Lopez JA, Elliot JP: When should follow-up computed tomogra-phy scans be obtained?. In Valadka AB, Andrews BT, editors: Neu-rotrauma: evidence-based answers to common questions, New York, 2005, Thieme, pp 105-108.

77. Servadei F, Murray GD, Penny K, et al: The value of the “worst” computed tomographic scan in clinical studies of moderate and severe head injury: European Brain Injury Consortium, Neurosur-gery 46:70-75, 2000.

78. Marshall LF, Marshall SB, Klauber MR, et al: The diagnosis of head injury requires a classification based on computed axial tomogra-phy, J Neurotrauma 9(Suppl 1):S287-S292, 1992.

79. Vos PE, van Voskuilen AC, Beems T, et al: Evaluation of the trau-matic coma data bank computed tomography classification for severe head injury, J Neurotrauma 18:649-655, 2001.

80. Fisher CM, Kistler JP, Davis JM: Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomo-graphic scanning, Neurosurgery 6:1-9, 1980.

81. Grosset DG, McDonald I, Cockburn M, et al: Prediction of delayed neurological deficit after subarachnoid haemorrhage: a CT blood load and Doppler velocity approach, Neuroradiology 36:418-421, 1994.

82. Frontera JA, Claassen J, Schmidt JM, et al: Prediction of symp-tomatic vasospasm after subarachnoid hemorrhage: the modified fisher scale, Neurosurgery 59:21-27, 2006.

83. Citerio G, Stocchetti N, Cormio M, Beretta L: Neuro-Link, a com-puter-assisted database for head injury in intensive care, Acta Neu-rochir (Wien) 142:769-776, 2000.

84. Degos V, Lescot T, Icke C, et al: Computed tomography-estimated specific gravity at hospital admission predicts 6-month outcome in mild-to-moderate traumatic brain injury patients admitted to the intensive care unit, Anesth Analg 114:1026-1033, 2012.

85. Teasdale G, Jennett B: Assessment of coma and impaired con-sciousness: a practical scale, Lancet 2:81-84, 1974.

86. Hunt WE, Hess RM: Surgical risk as related to time of interven-tion in the repair of intracranial aneurysms, J Neurosurg 28:14-20, 1968.

87. Teasdale GM, Drake CG, Hunt W, et al: A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies, J Neurol Neurosurg Psychiatry 51:1457, 1988.

88. Tisdall MM, Smith M: Multimodal monitoring in traumatic brain injury: current status and future directions, Br J Anaesth 99:61-67, 2007.

89. Langlois JA, Rutland-Brown W, Thomas KE: Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths, Atlanta, 2006, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.

90. Hicks RR, Fertig SJ, Desrocher RE, et al: Neurological effects of blast injury, J Trauma 68:1257-1263, 2010.

91. Winqvist S, Jokelainen J, Luukinen H, Hillbom M: Parental alco-hol misuse is a powerful predictor for the risk of traumatic brain injury in childhood, Brain Inj 21:1079-1085, 2007.

92. Stuke L, az-Arrastia R, Gentilello LM, Shafi S: Effect of alcohol on Glasgow Coma Scale in head-injured patients, Ann Surg 245: 651-655, 2007.

93. Provenzale J: CT and MR imaging of acute cranial trauma, Emerg Radiol 14:1-12, 2007.

94. Kim KA, Wang MY, McNatt SA, et al: Vector analysis correlating bullet trajectory to outcome after civilian through-and-through gunshot wound to the head: using imaging cues to predict fatal outcome, Neurosurgery 57:737-747, 2005.

95. Zafonte RD, Mann NR, Millis SR, et al: Functional outcome after violence related traumatic brain injury, Brain Inj 11:403-407, 1997.

96. Lee EJ, Hung YC, Wang LC, et al: Factors influencing the func-tional outcome of patients with acute epidural hematomas: anal-ysis of 200 patients undergoing surgery, J Trauma 45:946-952, 1998.

97. Jones NR, Molloy CJ, Kloeden CN, et al: Extradural haematoma: trends in outcome over 35 years, Br J Neurosurg 7:465-471, 1993.

ist Tzu Chi General Hospital JC September 20, 2016.ssion. Copyright ©2016. Elsevier Inc. All rights reserved.




















































http://clinicaltrials.gov/ct2/show/NCT00974259/

































































































98. Woertgen C, Rothoerl RD, Schebesch KM, Albert R: Comparison of craniotomy and craniectomy in patients with acute subdural haematoma, J Clin Neurosci 13:718-721, 2006.

99. Wu HM, Huang SC, Hattori N, et al: Subcortical white matter metabolic changes remote from focal hemorrhagic lesions suggest diffuse injury after human traumatic brain injury, Neurosurgery 55:1306-1315, 2004.

100. Mattioli C, Beretta L, Gerevini S, et al: Traumatic subarachnoid hemorrhage on the computerized tomography scan obtained at admission: a multicenter assessment of the accuracy of diagno-sis and the potential impact on patient outcome, J Neurosurg 98: 37-42, 2003.

101. Murray GD, Butcher I, McHugh GS, et al: Multivariable prognos-tic analysis in traumatic brain injury: results from the IMPACT study, J Neurotrauma 24:329-337, 2007.

102. Collier BR, Miller SL, Kramer GS, et al: Traumatic subarach-noid hemorrhage and QTc prolongation, J Neurosurg Anesthesiol 16:196-200, 2004.

103. Cooper DJ, Rosenfeld JV, Murray L, et al: Decompressive cra-niectomy in diffuse traumatic brain injury, N Engl J Med 364: 1493-1502, 2011.

104. Ravussin P, Archer DP, Tyler JL, et al: Effects of rapid mannitol infusion on cerebral blood volume: a positron emission tomo-graphic study in dogs and man, J Neurosurg 64:104-113, 1986.

105. Kamel H, Navi BB, Nakagawa K, et al: Hypertonic saline versus mannitol for the treatment of elevated intracranial pressure: a meta-analysis of randomized clinical trials, Crit Care Med 39: 554-559, 2011.

106. Battison C, Andrews PJ, Graham C, Petty T: Randomized, con-trolled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury, Crit Care Med 33:196-202, 2005.

107. Himmelseher S: Hypertonic saline solutions for treatment of intracranial hypertension, Curr Opin Anaesthesiol 20:414-426, 2007.

108. Lescot T, Degos V, Zouaoui A, et al: Opposed effects of hypertonic saline on contusions and noncontused brain tissue in patients with severe traumatic brain injury, Crit Care Med 34:3029-3033, 2006.

109. Finfer S, Bellomo R, Boyce N, et al: A comparison of albumin and saline for fluid resuscitation in the intensive care unit, N Engl J Med 350:2247-2256, 2004.

110. Myburgh J, Cooper J, Finfer S, et al: Saline or albumin for fluid resuscitation in patients with traumatic brain injury, N Engl J Med 357:874-884, 2007.

111. Ginsberg MD, Palesch YY, Hill MD: The ALIAS (ALbumin In Acute Stroke) phase III randomized multicentre clinical trial: design and progress report, Biochem Soc Trans 34:1323-1326, 2006.

112. Brain Trauma Foundation: Guidelines for the management of severe traumatic brain injury. XIV. Hyperventilation, J Neurotrauma 24:S87-S90, 2007.

113. Davis DP: Early ventilation in traumatic brain injury, Resuscitation 76:333-340, 2008.

114. Brain Trauma Foundation: Guidelines for the management of severe traumatic brain injury. IX. Cerebral perfusion thresholds, J Neurotrauma 24:S59-S64, 2007.

115. Robertson CS, Valadka AB, Hannay HJ, et al: Prevention of sec-ondary ischemic insults after severe head injury, Crit Care Med 27:2086-2095, 1999.

116. Balestreri M, Czosnyka M, Hutchinson P, et al: Impact of intracra-nial pressure and cerebral perfusion pressure on severe disability and mortality after head injury, Neurocrit Care 4:8-13, 2006.

117. Nordstrom CH: Physiological and biochemical principles under-lying volume-targeted therapy: the “Lund concept.”, Neurocrit Care 2:83-95, 2005.

118. Grande PO, Asgeirsson B, Nordstrom CH: Physiologic principles for volume regulation of a tissue enclosed in a rigid shell with application to the injured brain, J Trauma 42:S23-S31, 1997.

119. Naredi S, Olivecrona M, Lindgren C, et al: An outcome study of severe traumatic head injury using the “Lund therapy” with low-dose prostacyclin, Acta Anaesthesiol Scand 45:402-406, 2001.

120. Dizdarevic K, Hamdan A, Omerhodzic I, Kominlija-Smajic E: Modified Lund concept versus cerebral perfusion pressure-tar-geted therapy: a randomised controlled study in patients with sec-ondary brain ischaemia, Clin Neurol Neurosurg 114:142-148, 2012.

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Downloaded from ClinicalKey.com at Buddhist Tzu Chi For personal use only. No other uses without permission. Copy

References 3120.e3

21. Zafar SN, Iqbal A, Farez MF, Kamatkar S, de Moya MA: Intensive insulin therapy in brain injury: a meta-analysis, J Neurotrauma 28:1307-1317, 2011.

22. Edwards P, Arango M, Balica L, et al: Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticoste-roid in adults with head injury: outcomes at 6 months, Lancet 365:1957-1959, 2005.

23. Sadaka F, Veremakis C: Therapeutic hypothermia for the man-agement of intracranial hypertension in severe traumatic brain injury: a systematic review, Brain Inj 26:899-908, 2012.

24. Fox JL, Vu EN, Doyle-Waters M, et al: Prophylactic hypothermia for traumatic brain injury: a quantitative systematic review, CJEM 12:355-364, 2010.

25. Clifton GL, Coffey CS, Fourwinds S, et al: Early induction of hypothermia for evacuated intracranial hematomas: a post hoc analysis of two clinical trials, J Neurosurg 117:714-720, 2012.

26. Denson K, Morgan D, Cunningham R, et al: Incidence of venous thromboembolism in patients with traumatic brain injury, Am J Surg 193:380-383, 2007.

27. Macdonald RL, Amidei C, Baron J, et al: Randomized, pilot study of intermittent pneumatic compression devices plus dalteparin versus intermittent pneumatic compression devices plus heparin for prevention of venous thromboembolism in patients undergo-ing craniotomy, Surg Neurol 59:363-372, 2003.

28. Connolly Jr ES, Rabinstein AA, Carhuapoma JR, et al: Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association, Stroke 43:1711-1737, 2012.

29. de Rooij NK, Linn FH, van der Plas JA, et al: Incidence of subarach-noid haemorrhage: a systematic review with emphasis on region, age, gender and time trends, J Neurol Neurosurg Psychiatry 78: 1365-1372, 2007.

30. Diringer MN, Bleck TP, Claude Hemphill 3rd J, et al: Critical care management of patients following aneurysmal subarach-noid hemorrhage: recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference, Neurocrit Care 15:211-240, 2011.

31. Berman MF, Solomon RA, Mayer SA, et al: Impact of hospital-related factors on outcome after treatment of cerebral aneurysms, Stroke 34:2200-2207, 2003.

32. Hop JW, Rinkel GJ, Algra A, van GJ: Case-fatality rates and func-tional outcome after subarachnoid hemorrhage: a systematic review, Stroke 28:660-664, 1997.

33. Vergouwen MD, Vermeulen M, Coert BA, et al: Microthrombosis after aneurysmal subarachnoid hemorrhage: an additional expla-nation for delayed cerebral ischemia, J Cereb Blood Flow Metab 28:1761-1770, 2008.

34. Haley Jr EC, Kassell NF, Torner JC: The International Cooperative Study on the Timing of Aneurysm Surgery: the North American experience, Stroke 23:205-214, 1992.

35. Molyneux AJ, Kerr RS, Yu LM, et al: International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascu-lar coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion, Lancet 366:809-817, 2005.

36. Ransom E, Mocco J, Komotar R, et al: External ventricular drain-age response in poor grade aneurysmal subarachnoid hemor-rhage: effect on preoperative grading and prognosis, Neurocritical Care 6:174-180, 2007.

37. Roos Y, Rinkel G, Vermeulen M, et al: Antifibrinolytic therapy for aneurysmal subarachnoid hemorrhage: a major update of a Cochrane review, Stroke 34:2308-2309, 2003.

38. Gaberel T, Magheru C, Emery E, Derlon JM: Antifibrinolytic therapy in the management of aneurismal subarachnoid hemor-rhage revisited: a meta-analysis, Acta Neurochir (Wien) 154:1-9, 2012.

39. Aiyagari V, Powers WJ, Diringer MN: Cerebrovascular disease. In Schmidt GA, Hall JB, Wood LDH, editors: Principles of critical care, ed 3, New York, 2005, McGraw-Hill Professional, pp 985-996.

40. Suhardja A: Mechanisms of disease: roles of nitric oxide and endothelin-1 in delayed cerebral vasospasm produced by aneurys-mal subarachnoid hemorrhage, Nat Clin Pract Cardiovasc Med 1: 110-116, 2004.

General Hospital JC September 20, 2016.right ©2016. Elsevier Inc. All rights reserved.























































































































































References3120.e4

141. de Oliveira JG, Beck J, Ulrich C, et al: Comparison between clip-ping and coiling on the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis, Neurosurg Rev 30:22-30, 2007.

142. Suzuki H, Taki W: Prospective Registry of Subarachnoid Aneu-rysms Treatment (PRESAT) Group: effect of aneurysm treatment modalities on cerebral vasospasm after aneurysmal subarachnoid hemorrhage, Acta Neurochir Suppl 115:99-105, 2013.

143. Dumont AS, Crowley RW, Monteith SJ, et al: Endovascular treat-ment or neurosurgical clipping of ruptured intracranial aneu-rysms: effect on angiographic vasospasm, delayed ischemic neurological deficit, cerebral infarction, and clinical outcome, Stroke 41(11):2519-2524, 2010.

144. Kassell NF, Peerless SJ, Durward QJ, et al: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension, Neurosurgery 11:337-343, 1982.

145. Treggiari MM, Walder B, Suter PM, Romand JA: Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy follow-ing subarachnoid hemorrhage, J Neurosurg 98:978-984, 2003.

146. Rinkel GJ, Feigin VL, Algra A, van Gijn J: Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage, Cochrane Database Syst Rev(4)CD000483, 2004.

147. Egge A, Waterloo K, Sjoholm H, et al: Prophylactic hyperdynamic postoperative fluid therapy after aneurysmal subarachnoid hem-orrhage: a clinical, prospective, randomized, controlled study, Neurosurgery 49:593-605, 2001.

148. Muench E, Horn P, Bauhuf C, et al: Effects of hypervolemia and hypertension on regional cerebral blood flow, intracranial pres-sure, and brain tissue oxygenation after subarachnoid hemor-rhage, Crit Care Med 35:1844-1851, 2007.

149. Naidech AM, Jovanovic B, Wartenberg KE, et al: Higher hemo-globin is associated with improved outcome after subarachnoid hemorrhage, Crit Care Med 35:2383-2389, 2007.

150. Levine J, Kofke A, Cen L, et al: Red blood cell transfusion is asso-ciated with infection and extracerebral complications after sub-arachnoid haemorrhage, Neurosurgery 66:312-318, 2010.

151. Vincent JL, Baron JF, Reinhart K, et al: Anemia and blood transfu-sion in critically ill patients, JAMA 288:1499-1507, 2002.

152. Dorhout Mees SM, Rinkel G, Feigin V, et al: Calcium antagonists for aneurysmal subarachnoid haemorrhage, Cochrane Database Syst Rev(3)CD000277, 2007.

153. Roos YB, Levi M, Carroll TA, et al: Nimodipine increases fibrino-lytic activity in patients with aneurysmal subarachnoid hemor-rhage, Stroke 32:1860-1862, 2001.

154. Eskridge JM, McAuliffe W, Song JK, et al: Balloon angioplasty for the treatment of vasospasm: results of first 50 cases, Neurosurgery 42:510-516, 1998.

155. Bejjani GK, Bank WO, Olan WJ, Sekhar LN: The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage, Neurosurgery 42:979-986, 1998.

156. Elliott JP, Newell DW, Lam DJ, et al: Comparison of balloon angio-plasty and papaverine infusion for the treatment of vasospasm following aneurysmal subarachnoid hemorrhage, J Neurosurg 88:277-284, 1998.

157. Macdonald RL, Higashida RT, Keller E, et al: Clazosentan, an endo-thelin receptor antagonist, in patients with aneurysmal subarach-noid haemorrhage undergoing surgical clipping: a randomised, double-blind, placebo-controlled phase 3 trial (CONSCIOUS-2), Lancet Neurol 10:618-625, 2011.

158. Sanchez-Peña P, Nouet A, Clarençon F, et al: Atorvastatin decreases computed tomography and S100-assessed brain isch-emia after subarachnoid aneurysmal hemorrhage: a comparative study, Crit Care Med 40:594-602, 2012.

159. Manninen PH, Ayra B, Gelb AW, Pelz D: Association between elec-trocardiographic abnormalities and intracranial blood in patients following acute subarachnoid hemorrhage, J Neurosurg Anesthesiol 7:12-16, 1995.

160. Szabo MD, Crosby G, Hurford WE, Strauss HW: Myocardial per-fusion following acute subarachnoid hemorrhage in patients with an abnormal electrocardiogram, Anesth Analg 76:253-258, 1993.

161. Mayer SA, Lin J, Homma S, et al: Myocardial injury and left ventricular performance after subarachnoid hemorrhage, Stroke 30:780-786, 1999.


162. Jain R, Deveikis J, Thompson BG: Management of patients with stunned myocardium associated with subarachnoid hemorrhage, AJNR Am J Neuroradiol 25:126-129, 2004.

163. Zaroff JG, Rordorf GA, Ogilvy CS, Picard MH: Regional patterns of left ventricular systolic dysfunction after subarachnoid hem-orrhage: evidence for neurally mediated cardiac injury, J Am Soc Echocardiogr 13:774-779, 2000.

164. Lee VH, Connolly HM, Fulgham JR, et al: Tako-tsubo cardiomy-opathy in aneurysmal subarachnoid hemorrhage: an underappre-ciated ventricular dysfunction, J Neurosurg 105:264-270, 2006.

165. Hravnak M, Frangiskakis JM, Crago EA, et al: Elevated cardiac tro-ponin I and relationship to persistence of electrocardiographic and echocardiographic abnormalities after aneurysmal subarach-noid hemorrhage, Stroke 40:3478-3484, 2009.

166. Zaroff JG, Pawlikowska L, Miss JC, et al: Adrenoceptor polymor-phisms and the risk of cardiac injury and dysfunction after sub-arachnoid hemorrhage, Stroke 37:1680-1685, 2006.

167. Gruber A, Reinprecht A, Gorzer H, et al: Pulmonary function and radiographic abnormalities related to neurological outcome after aneurysmal subarachnoid hemorrhage, J Neurosurg 88:28-37, 1998.

168. Kahn JM, Caldwell EC, Deem S, et al: Acute lung injury in patients with subarachnoid hemorrhage: incidence, risk factors, and out-come, Crit Care Med 34:196-202, 2006.

169. Frontera JA, Fernandez A, Claassen J, et al: Hyperglycemia after SAH: predictors, associated complications, and impact on out-come, Stroke 37:199-203, 2006.

170. Charpentier C, Audibert G, Guillemin F, et al: Multivariate analy-sis of predictors of cerebral vasospasm occurrence after aneurys-mal subarachnoid hemorrhage, Stroke 30:1402-1408, 1999.

171. Schmutzhard E, Rabinstein AA: Spontaneous subarachnoid hem-orrhage and glucose management, Neurocrit Care 15:281-286, 2011.

172. Feigin VL, Anderson N, Rinkel GJ, et al: Corticosteroids for aneu-rysmal subarachnoid haemorrhage and primary intracerebral haemorrhage, Cochrane Database Syst Rev(3)CD004583, 2005.

173. Harrigan MR: Cerebral salt wasting syndrome: a review, Neurosurgery 38:152-160, 1996.

174. Hannon MJ, Finucane FM, Sherlock M, et al: Clinical review: dis-orders of water homeostasis in neurosurgical patients, J Clin Endo-crinol Metab 97:1423-1433, 2012.

175. Qureshi AI, Suri MF, Sung GY, et al: Prognostic significance of hypernatremia and hyponatremia among patients with aneurys-mal subarachnoid hemorrhage, Neurosurgery 50:749-755, 2002.

176. Berendes E, Walter M, Cullen P, et al: Secretion of brain natri-uretic peptide in patients with aneurysmal subarachnoid haemor-rhage, Lancet 349:245-249, 1997.

177. Wijdicks EF, Vermeulen M, Hijdra A, van Gijn J: Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful? Ann Neurol 17:137-140, 1985.

178. Igarashi T, Moro N, Katayama Y, et al: Prediction of symptomatic cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage: relationship to cerebral salt wasting syndrome, Neu-rol Res 29:835-841, 2007.

179. Kasuya H, Onda H, Yoneyama T, et al: Bedside monitoring of circulating blood volume after subarachnoid hemorrhage, Stroke 34:956-960, 2003.

180. Cowley Jr AW, Roman RJ: Control of blood and extracellular vol-ume, Baillieres Clin Endocrinol Metab 3:331-369, 1989.

181. Sterns R, Silver S: Cerebral salt wasting versus SIADH: what differ-ence? J Am Soc Nephrol 19:194-196, 2008.

182. Kasuya H, Kawashima A, Namiki K, et al: Metabolic profiles of patients with subarachnoid hemorrhage treated by early surgery, Neurosurgery 42:1268-1274, 1998.

183. Roger VL, Go AS, Lloyd-Jones DM, et al: Heart disease and stroke statistics—2012 update: a report from the American Heart Asso-ciation, Circulation 125:e2-e220, 2012.

184. Mullen MT, Pisapia JM, Tilwa S, et al: Systematic review of out-come after ischemic stroke due to anterior circulation occlusion treated with intravenous, intra-arterial, or combined intravenous + intra-arterial thrombolysis, Stroke 43:2350-2355, 2012.

185. Kansara A, Pandey P, Tiwari A, et al: Stenting of acute and sub-acute intracranial vertebrobasilar arterial occlusive lesions, J Neu-rointerv Surg 4:274-280, 2012.
























































































































































186. Wityk RJ: The management of blood pressure after stroke, Neurologist 13:171-181, 2007.

187. Wardlaw JM, del Zoppo G, Yamaguchi T: Thrombolysis for acute ischaemic stroke, Cochrane Database Syst Rev(2)CD000213, 2000.

188. Wagner S, Schnippering H, Aschoff A, et al: Suboptimum hemicraniectomy as a cause of additional cerebral lesions in patients with malignant infarction of the middle cerebral artery, J Neurosurg 94:693-696, 2001.

189. Huang P, Lin FC, Su YF, et al: Predictors of in-hospital mortality and prognosis in patients with large hemispheric stroke receiving decompressive craniectomy, Br J Neurosurg 26:504-509, 2012.

190. Rhondali O, Genty C, Halle C, et al: Do patients still require admission to an intensive care unit after elective craniotomy for brain surgery? J Neurosurg Anesthesiol 23:118-123, 2011.

191. Broderick J, Connolly S, Feldmann E, et al: Guidelines for the man-agement of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Inter-disciplinary Working Group, Stroke 38:2001-2023, 2007.

192. Mendelow AD, Gregson BA, Fernandes HM, et al: Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Sur-gical Trial in Intracerebral Haemorrhage (STICH): a randomised trial, Lancet 365:387-397, 2005.

193. INTERACT Investigators: Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial, Lancet Neurol 7:391-399, 2008.

194. Qureshi AI, Palesch YY: Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) II: design, methods, and rationale, Neurocrit Care 15:559-576, 2011.

195. Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypother-mia, N Engl J Med 346:557-563, 2002.

196. Hypothermia After Cardiac Arrest Study Group: Mild therapeu-tic hypothermia to improve the neurologic outcome after cardiac arrest, N Engl J Med 346:549-556, 2002.

197. Arrich J, Holzer M, Havel C, et al: Hypothermia for neuroprotec-tion in adults after cardiopulmonary resuscitation, Cochrane Data-base Syst Rev(9)CD004128, 2012.

198. Madl C, Kramer L, Domanovits H, et al: Improved outcome prediction in unconscious cardiac arrest survivors with sensory evoked potentials compared with clinical assessment, Crit Care Med 28:721-726, 2000.

199. DeLorenzo RJ, Hauser WA, Towne AR, et al: A prospective, pop-ulation-based epidemiologic study of status epilepticus in Rich-mond, Virginia, Neurology 46:1029-1035, 1996.

200. Walker MC: Treatment of nonconvulsive status epilepticus, Int Rev Neurobiol 81:287-297, 2007.

201. Brophy GM, Bell R, Claassen J, et al: Guidelines for the evaluation and management of status epilepticus, Neurocrit Care 17:3-23, 2012.

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2

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2

2

2

2

2

2

2

2

2

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Downloaded from ClinicalKey.com at Buddhist Tzu ChFor personal use only. No other uses without permission. Cop

References 3120.e5

02. Kofke WA, Young RS, Davis P, et al: Isoflurane for refractory status epilepticus: a clinical series, Anesthesiology 71:653-659, 1989.

03. Cosi V, Versino M: Guillain-Barré syndrome, Neurol Sci 27(Suppl 1): S47-S51, 2006.

04. Hughes RA, Cornblath DR: Guillain-Barré syndrome, Lancet 366:1653-1666, 2005.

05. Hughes RAC, Wijdicks EFM, Benson E, et al: Supportive care for patients with Guillain-Barré syndrome, Arch Neurol 62:1194-1198, 2005.

06. Fourrier F, Robriquet L, Hurtevent JF, Spagnolo S: A simple func-tional marker to predict the need for prolonged mechanical venti-lation in patients with Guillain-Barré syndrome, Crit Care 15:R65, 2011.

07. Bilello JF, Davis JW, Cunningham MA, et al: Cervical spinal cord injury and the need for cardiovascular intervention, Arch Surg 138:1127-1129, 2003.

08. Brown R, DiMarco AF, Hoit JD, Garshick E: Respiratory dys-function and management in spinal cord injury, Respir Care 51: 853-868, 2006.

09. Strauss DJ, DeVivo MJ, Paculdo DR, Shavelle RM: Trends in life expectancy after spinal cord injury, Arch Phys Med Rehabil 87:1079-1085, 2006.

10. Phillips LH: The epidemiology of myasthenia gravis, Semin Neurol 24:17-20, 2004.

11. Juel VC: Myasthenia gravis: management of myasthenic crisis and perioperative care, Semin Neurol 24:75-81, 2004.

12. Jani-Acsadi A, Lisak RP: Myasthenic crisis: guidelines for preven-tion and treatment, J Neurol Sci 261:127-133, 2007.

13. van de Beek D, de Gans J, McIntyre P, Prasad K: Steroids in adults with acute bacterial meningitis: a systematic review, Lancet Infect Dis 4:139-143, 2004.

14. Aronin SI, Peduzzi P, Quagliarello VJ: Community-acquired bacte-rial meningitis: risk stratification for adverse clinical outcome and effect of antibiotic timing, Ann Intern Med 129:862-869, 1998.

15. Centers for Disease Control and Prevention: West Nile virus dis-ease and other arboviral diseases: United States, 2011, MMWR Morb Mortal Wkly Rep 61:510-514, 2012.

16. Wijdicks EFM: The neurologist and Harvard criteria for brain death, Neurology 61:970-976, 2003.

17. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM: Evidence-based guideline update: determining brain death in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology, Neurology 74:1911-1918, 2010.

18. Nakagawa TA, Ashwal S, Mathur M, et al: Clinical report—guide-lines for the determination of brain death in infants and children: an update of the 1987 task force recommendations, Pediatrics 128:e720-e740, 2011.

19. Buchanan KM, Elias LJ, Goplen GB: Differing perspectives on out-come after subarachnoid hemorrhage: the patient, the relative, the neurosurgeon, Neurosurgery 46:831-838, 2000.

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Chapter 105 - Neurocritical Care - Anesthesiamiller8e:... · margin. 3. This is typically seen in severe lateral herniation (”midline shift”) when the anterior cerebral vasculature