Introduction

Neural function is essential to human existence. Thus, loss of any neural element in the course of a critical illness represents a major loss to a given individual. Neurons or supporting elements may be lost in a small, virtually unnoticeable manner, perhaps manifest as cognitive or behavioral deficit, or there may be widespread selective neuronal loss or tissue infarction with more apparent and disabling deficits. Based on the notion that neural function is the essence of acceptable survival from critical illness, it is crucial for perioperative management to include considerations of neural viability and the impact and interactions of the primary diseases and therapeutics on the nervous system.

There are numerous perioperative scenarios where a patient may present with neurologic dysfunction. In a general sense, these scenarios often involve ischemia, trauma, or neuroexcitation. Each of these, as they progressively worsen, at some point typically involve a period of decreased cerebral perfusion pressure (CPP), usually resulting from elevated intracranial pressure, eventually compromising cerebral blood flow sufficiently to produce permanent neuronal loss, infarction, and possibly brain death. A variety of biochemical pathways play a major role. In this chapter we review the important physiologic factors, and intracranial pressure (ICP) considerations and therapeutic options critical to contemporary perioperative care of the patient with injury to the central nervous system (CNS).

Monitoring Neurologic Examination

The neurologic examination of the patient with an acute neurologic condition is a process that requires the physician to have a specialized anatomic and physiologic knowledge of the nervous system and the anesthesiologist should be familiar with the most basic components of the neurologic examination to identify promptly life-threatening conditions that may require urgent action. The majority of the information necessary to localize a lesion in the patient with neurologic disease can be obtained through a careful history and physical examination. Although a detailed description of neurologic examination is beyond the scope of this chapter, a rapid 5-min neurologic assessment may be sufficient to establish baseline conditions and to detect subsequent changes in neurologic status. Therefore, for the nonneurologist it is important to focus on the components of the neurologic examination described in the following sections.

Mental Status, Cranial Nerves, Motor and Sensorial Function, and Reflexes

Intracranial Hypertension

Physiology

The brain, spinal cord, cerebrospinal fluid (CSF), and blood are encased in the skull and vertebral canal, thus constituting a nearly incompressible system ( Fig. 24.1 ). In a totally incompressible system pressure would vary linearly with increased volume. However, there is capacitance in the system, thought to be provided by the intervertebral spaces and the vasculature. Once this capacitance is exhausted, the ICP increases dramatically with increased intracranial volume ( Fig. 24.2 ).

The brain, spinal cord, and blood are encased in the skull and vertebral canal, thus constituting a nearly incompressible system. System capacitance is thought to be provided via intervertebral spaces.

(Reprinted with permission of Kofke, WA. Neurologic Intensive Care. In: Albin MS, ed. Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives . 1247–1347.)

Nonlinear relationship between intracranial pressure (ICP) and intracranial volume. At normal ICP, small changes in intracranial volume produce small changes in the ICP. However, as ICP progressively increases, the ICP increases per unit change in volume become progressively larger and more dramatic.

Based on the relation:

<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax_Error style="POSITION: relative" data-mathml='CBF=MAP−ICP/CVR’>[Math Processing Error]CBF=MAP−ICP/CVR
CBF=MAP−ICP/CVR

where CBF is cerebral blood flow, MAP is mean arterial pressure, and CVR is cerebrovascular resistance.

The concern arises that increasing ICP is necessarily associated with decrements in CBF. However, the effect of increasing ICP on CBF is not straightforward as MAP may increase with ICP elevations, and CVR adjusts with decreasing CPP (increasing cerebral blood volume) to maintain CBF until maximal vasodilatation occurs. This is thought to occur at CPP < 50 mmHg although considerable interindividual heterogeneity in this value exists and the lower limit has been nicely critiqued by Drummond. Thus, increasing ICP is often associated with cerebral vasodilatation and/or reflexly increased MAP to maintain CBF.

Normal ICP is < 10 mmHg. ICP > 20 mmHg is generally associated with escalation of ICP-reducing therapy. However, this is an epidemiologically derived number. Head trauma studies have indicated that patients with ICP > 20 mmHg generally do not do well. However, physiologically, simply elevating ICP to > 20 mmHg is not necessarily associated with decrements in CBF, provided the above-noted compensatory mechanisms occur. Recent guidelines recommend treatment of intracranial pressure when it is > 22 mmHg because values above this level are associated with increased mortality.

Nonetheless, increasing ICP because of mass lesions or obstruction of CSF outflow can exhaust compensatory mechanisms. When this occurs, compromise of CBF does eventually occur. Initially, abnormality arises in distal runoff of the cerebral circulation. As the process continues, compromise of diastolic perfusion arises. With this the normally continuous (through systole and diastole) cerebral perfusion becomes discontinuous ( Fig. 24.3 ). Further compromise of cerebral perfusion pressure results in anaerobic metabolism, exacerbation of edema, and ultimately intracranial circulatory arrest. Thus, when ICP increases it is important to detect it and ascertain whether this lethal sequence of events may be occurring.

Progression of transcranial Doppler (TCD) waveforms after head injury from intact cerebral blood flow (CBF) and normal appearing TCD waveform to intracranial hypertension sufficient to induce intracerebral circulatory arrest. Schematic of decreasing cerebral perfusion pressure (CPP) indicated in the lower panel. ICP , intracranial pressure.

(Reproduced by permission from Hassler W, Steinmetz H, Gawlowski J. Transcranial Doppler ultrasonography in raised intracranial pressure and in intracranial circulatory arrest. J Neurosurg 1988;68:745–751.)

Factors That Exacerbate Intracranial Hypertension

Under normal conditions, the intracranial volume is occupied by the brain parenchyma (80%), CSF (10%) and blood (10%). Pathologic structures, including masses caused by blood (hematoma), neoplasia, or abscesses, may also occupy space. Since the volume of the intracranial vault is somehow fixed, when the volume of one or more of these compartments enlarges sufficiently to exhaust normal capacitive compensatory mechanisms, ICP begins to rise. Further increases in volume of one or more of these compartments then leads to the sequence of events associated with increasing ICP described previously.

Two Types of Intracranial Hypertension

In a general sense, there are two types of intracranial hypertension, categorized according to CBF as hyperemic or oligemic ( Fig. 24.4 ). Although conceptualized here as a dichotomous process, undoubtedly the real physiology is more of a continuum between the two.

Two types of intracranial hypertension. From a baseline condition, intracranial pressure (ICP) can increase in two ways. One is via an increase in cerebral blood volume associated with reflex vasodilation as a result of moderate blood pressure decreases or hyperemia. The second mechanism of intracranial hypertension is via malignant brain edema or other expanding masses encroaching on the vascular bed to produce intracranial ischemia.

(Reprinted with permission of Kofke, WA. Neurologic Intensive Care. In: Albin MS, ed. Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives . 1247–1347.)

In the normal state, increases in CBF are not associated with increased ICP, as the normal capacitive mechanisms absorb the increased intracranial blood volume. However, in the situation of disordered intracranial compliance, small increases in intracranial volume resulting from increased CBF produce increases in ICP. When cerebral blood volume (CBV) increases, intracranial contents increase hence increasing ICP in a noncompliant system.

This, however, raises questions about an important issue. Elevated ICP has traditionally been considered to be a concern because it indicates that cerebral perfusion might be jeopardized. It is, however, unclear whether it is appropriate to be concerned about high ICP inducing intracranial oligemia when the cause of the high ICP is intracranial hyperemia. There have been no detailed examinations of this question although there have been some studies that allow reasonable inferences about the significance of hyperemic intracranial hypertension.

For many years, it has been known that brief noxious stimuli briefly increase ICP in the setting of decreased intracranial compliance. Studies have reported that such situations are associated with hyperemia, strongly suggesting that hyperemic intracranial hypertension is not a dangerous situation. However, it is reasonable to be concerned, at least theoretically, about such hyperemia for three reasons. First, elevated ICP caused by hyperemia in one portion of the brain may increase ICP to compromise CBF in other areas of the brain in which rCBF is marginal. Second, increased pressure in one area of the brain may produce gradients that might lead to a herniation syndrome. Third, there is theoretical concern that inappropriate hyperemia may predispose the brain to worsened edema or hemorrhage as occurs with other hyperperfusion syndromes. Thus, hyperemic intracranial hypertension has a theoretical potential to be deleterious but this has yet to be conclusively demonstrated. For brief periods, as may occur during intubation or other limited noxious stimuli, it is suggested that it might not be problematic.

In contrast, oligemic intracranial hypertension is associated with compromised cerebral perfusion. This is supported by the high mortality observed in head trauma patients in whom ICP rises as a result of brain edema after head injury with decrements in CBF. Transcranial Doppler (TCD) and CBF studies on these patients have demonstrated that CBF is low and perfusion is discontinuous during the cardiac cycle (see Fig. 24.3 ). Moreover, jugular venous bulb data indicates that O ₂ extraction is markedly increased, suggesting anaerobic metabolism. In this setting, noxious stimuli can further increase the ICP, thus producing the situation of hyperemic or oligemic intracranial hypertension. Presumably in this setting the hyperemic rise in ICP acts to compromise rCBF further in areas of brain edema.

Presentation

Although frequently linked, intracranial hypertension is not a synonym of brain herniation. These events can occur both independently or in association. Intracranial hypertension is currently defined as a sustained elevation for more than 5 minutes of ICP > 22 mmHg, and its accurate identification requires placement of an invasive intracranial monitoring. However, intracranial monitors are usually absent during the acute phase of the traumatized brain management, therefore, anesthesiologists should be familiar with clinical signs and symptoms suggestive of elevated ICP. These signs and symptoms include headache, nausea, or vomiting, altered mental status, and the Cushing triad (bradycardia, hypertension, and irregular respirations or apnea).

On the other hand, herniation syndromes are the result of differences in pressure gradients across the intracranial compartments ultimately leading to the shifting or compression of vital neural and vascular structures. Common sites of brain herniation are the medial temporal lobe (uncal), cingulum (subfalcine), and inferior cerebellum (tonsillar herniation). The classic signs of uncal herniation include loss of consciousness associated with ipsilateral pupillary dilatation and contralateral hemiparesis resultant from compression of the ascending arousal pathways, oculomotor nerve (CN III), and corticospinal tract ( Table 24.3 ).

ICP Monitoring

The purpose of monitoring ICP is to improve reliably the clinician’s ability to maintain adequate CPP and cerebral oxygenation. The only way to determine CPP reliably is to monitor both ICP and MAP continuously. This combined approach has been associated with the potential to improve patients’ outcomes after closed head injury.

Despite its widespread application, supporting evidence from randomized clinical trials (RCTs) is lacking or insufficient and indications outside TBI management are somewhat ill-defined. In 2012, Chestnut et al. conducted a multicenter, controlled trial in 324 patients who suffered from severe TBI. Patients were randomly assigned to one of two specific protocols: guidelines-based management of ICP in which a parenchymal monitor was used or a treatment protocol based on clinical and imaging findings. The primary outcome was survival time, impaired consciousness, and functional status at 3 and 6 months after initial injury. Intracranial ICP monitoring failed to show superiority to care based on imaging and clinical findings. A large body of level II evidence exist with regard to ICP monitoring in TBI. Management of severe TBI patients using information from ICP monitoring is recommended to reduce in-hospital and 2-week postinjury mortality. Thus, the current recommendations are to monitor ICP in all salvageable patients with a TBI (GCS 3–8 after resuscitation) and an abnormal CT scan that reveals hematomas, contusions, swelling, herniation, or compressed basal cisterns. Also, ICP monitoring is indicated in patients with severe TBI with a normal CT scan if more than two of the following features are noted at admission: age > 40 years, unilateral or bilateral motor posturing, or SBP < 90 mmHg.

The current gold standard for ICP monitoring is the ventriculostomy catheter or external ventricular drain (EVD), where a catheter is inserted in either lateral ventricle, usually via a small right frontal burr hole. This ventricular catheter is connected to a standard pressure transducer via fluid-filled tubing ( Fig. 24.5 ). The external transducer must be maintained at a specific level to ensure adequate CPP. The reference point for ICP is the foramen of Monro, although in practical terms, the external auditory meatus is often used as a landmark ( Fig. 24.6 ). EVDs allow the clinician to measure global ICP and have some useful advantages over other ICP monitors, including the ability to perform periodic in vivo external calibration and therapeutic CSF drainage and sampling. The primary disadvantage of intraventricular catheters is the associated increased rate of infection and accidental overdrainage. This infectious risk increases the longer the EVD is in place, and prophylactic catheter changes do not appear to reduce the risk of infection. Another potential disadvantage of intraventricular systems includes a small risk of hemorrhage during placement; this risk is greater in patients taking anticoagulants or antiplatelets and misplacement ( Fig. 24.7 ). In addition, when intracranial mass lesions or ventricular effacement caused by swelling are present, EVD placement may be difficult even for the most experienced neurosurgeon.

Standard intracranial pressure (ICP) transducer composed of (1) a flushless transducer next to a three-way stopcock thats allows intermittent or continuous ICP monitoring and CSF drainage, and (2) a collecting chamber to accurately quantify CSF drained.

External ventricular drainage system.

(Reprinted with permission from Kofke WA et al. Neurologic Intensive Care. In: Albin MS, ed. Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives. New York: McGraw-Hill; 1997.)

Development of subdural hematoma (SDH) after external ventricular drain (EVD) placement in a patient taking oral anticoagulation. (A) Initial head CT after EVD placement demonstrates a small SDH. (B) Follow-up head CT at 6 hours after EVD placement with significant expansion requiring decompressive surgery.

In addition to intraventricular catheters, there is intraparenchymal, subarachnoid, and epidural ICP monitoring catheters. Intraparenchymal catheters consist of a thin wire with a fiberoptic transducer at the tip (fiberoptic Camino system, Natus Medical Inc., Middleton, WI), inserted into the brain parenchyma via a small skull burr hole. They have a lower risk of infection and hemorrhage than EVDs. Disadvantages include the inability to drain CSF for therapeutic or diagnostic purposes and the potential to lose accuracy or development of “zero drift” (degree of difference relative to zero atmosphere) over the course of days.

Noninvasive ICP monitoring devices have been developed to reduce the complications associated with invasive devices. Tympanic membrane displacement, TCD pulsatility index, intraocular pressure, optic nerve sheath diameter, and magnetic resonance imaging (MRI) of the optic nerve sheath have been used to provide a noninvasive estimate of ICP. So far, none of these methods has provided accuracy sufficient to replace invasive ICP monitors.

Waveform Analysis

Normal ICP waveform consists of three arterial components superimposed on the respiratory rhythm. The first arterial wave is the percussion wave (P1), which reflects the ejection of blood from the heart transmitted through the choroid plexus in the ventricles. The second wave is the tidal wave (P2), which reflects brain compliance; and finally, the third wave is the dicrotic wave (P3), which reflects aortic valve closure. Under physiologic conditions, the percussion wave is the tallest, with the tidal and dicrotic waves having progressively smaller amplitudes. When intracranial hypertension is present, cerebral compliance is diminished. This is reflected by an increase in the peak of the tidal and dicrotic waves exceeding that of the percussion wave ( Fig. 24.8 ).

Intracranial pressure (ICP) waveform. Upper tracing: Components of a normal ICP waveform: P1, percussion wave; P2, tidal wave; P3, dicrotic wave. Lower tracing: Typical noncompliant ICP waveform seen in intracranial hypertension. As ICP increases, a distinctive elevation of the P2 wave above P1 occurs.

Pathologic waveforms include A, B, and C described by Lundberg in the 1960s. Pathologic A or plateau waves are abrupt, marked elevations in ICP of 50 to 100 mmHg, which usually last for 5–20 minutes and represent the loss of intracranial compliance and autoregulatory mechanisms. Moreover, they can lead to development of a positive feedback cycle that eventually leads to continuous reduction in CPP with subsequent cerebral ischemia. Thus, the presence of A waves should suggest the need for urgent intervention to help control ICP. Type B waves occur at a frequency of 0.5 to 2 waves/min with elevations of ICP of 20–30 mmHg, reflecting change in vascular tone that occurs when the CPP is at the lower limit of normal autoregulation. C waves occur at a frequency of 4–8/min; they reflect changes in systemic vasomotor tone and have little pathologic significance.

Treatment of Intracranial Hypertension

The main goal in treating intracranial hypertension is to prevent the development of secondary injuries by maintaining adequate CPP, oxygenation, and glucose supply (without hyperglycemia) to promote adequate oxygen and nutrient supplies. The best clinical strategy is to diagnose and to treat the underlying cause(s), avoid exacerbating factors, and reduce ICP ( Table 24.4 ). Current management of acute brain injury is aimed to maintain ICP < 22 mmHg, CPP between 60 and 70 mmHg, and SBP at ≥ 100 mmHg for patients 50 to 69 years old or at ≥ 110 mmHg for patients 15 to 49 or > 70 years. CPP augmentation to higher perfusing pressures may elevate the risk of systemic complications, including the development of acute respiratory distress syndrome (ARDS). More recent evidence has failed to show such association. This can be explained in part to the development of better lung-protective strategies to treat ARDS. In addition, as the Lund group has suggested in the past, hypertension-induced exacerbation of brain edema can further increase ICP. This increase in ICP leads to reduced venous outflow and increased venous pressure, which in turn act to worsen the brain edema, constituting a positive feedback cycle initially started by arterial hypertension.

Therapy of intracranial hypertension is primarily directed at removing the cause as far as possible. This is not always possible. In such cases, therapy is aimed at controlling ICP, hoping that the primary cause of the intracranial hypertension will resolve. Controlling ICP is thus a supportive maneuver, intended to preserve viable neuronal tissue until the high ICP situation resolves. In general, therapeutic maneuvers to reduce ICP involve one of six classes of therapy: (1) decrease cerebral blood volume, (2) decrease CSF volume, (3) induce serum hyperosmolarity, (4) resect dead or injured brain tissue or resect viable but less important brain tissue (e.g., anterior temporal lobe), (5) resect non-neural masses or hematomas, and (6) remove the calvarium to permit unopposed outward brain swelling (decompressive craniectomy). For purposes of this chapter, we will categorize interventions based on current tiered therapy algorithms ( Fig. 24.9 ). Recent advances in the use of brain tissue oxygen monitors occasionally affect the manner in which these maneuvers are used to ensure continued optimal PbrO ₂ . However, their use is somewhat limited in the operating room given the invasive nature and obstruction of the surgical field.

Tiered algorithm for management of elevated intracranial pressure.

Intracranial Hypertension/Cerebral Herniation Treatment Algorithm

Hyperventilation

Hyperventilation is a quick and efficient method to lower ICP transiently in acute emergencies. In normal adults, CBV is 3–4 mL per 100 g of cerebral tissue and 70% of the total volume corresponds to venous blood. Veins and capillaries do not react to fluctuations in PaCO _2; therefore, hyperventilation-related changes in CBV are a result of arterial reactivity to changes in PaCO ₂ . Hyperventilation has been utilized for almost a century and the earliest documented use was reported by Lundberg in 1959. Because CBF is largely dependent on PaCO ₂ , as PaCO ₂ decreases with hyperventilation, there is an associated cerebral vasoconstriction leading to a subsequent reduction in cerebral blood volume and ICP. CBF decreases by 3% for every 1 mmHg reduction in PaCO ₂ and this effect is mediated by extracellular fluid (ECF) pH changes. Thus, PaCO ₂ levels between 20 and 25 mmHg are associated with a reduction of CBF up to 40%–50%. However, CBF returns to its original state over 6–24 hours as the brain adapts by adjusting the bicarbonate levels in the ECF to normalize the pH. At the level of the proximal renal tubule, bicarbonate reabsorption is inhibited and excretion of H ⁺ is stimulated. These responses initiate minutes after the onset of alkalosis and persist for hours or days allowing normalization of CSF and perivascular pH. It is important to recognize that acute discontinuation of hyperventilation can cause a rebound increase in CBF leading to an ICP crisis and hyperventilation should therefore be discontinued gradually.

Hyperventilation is performed in the intubated patient by increasing tidal volume or rate, and it is commonly used to facilitate neurosurgical exposure as it provides “brain relaxation” in the surgical field. A prior multicenter randomized trial showed that hyperventilation to PaCO ₂ = 25 ± 2 mmHg) was effective at reducing ICP and improving the surgical exposure during craniotomy. However, current consensus is to maintain normocapnia during intracranial surgery and to consider transient hyperventilation as a temporary measure when the “tight brain” is resistant to other means of treatment.

Cerebral and Systemic Effects of Hyperventilation

Multiple cerebral and systemic effects have been identified that can affect all organ systems, not only the cerebral vasculature. It decreases perfusion to kidneys, gastrointestinal tissue, skin, and muscle. Respiratory effects include hypocapnia-induced bronchoconstriction, reduced hypoxic pulmonary vasoconstriction, and increased permeability of the alveolo-arterial membrane. Moreover, respiratory alkalosis complicates tissue hypoxia by shifting the oxygen-dissociation curve to the left and compromises coronary blood flow, thus increasing the risk of coronary spasm. Hyperventilation has also been found to increase extracellular lactate and glutamate levels, which may contribute to secondary brain injury.

Hyperventilation introduces a risk of decreasing CBF to a dangerous level ( Fig. 24.10 ). A study in trauma patients showed that routine hyperventilation was associated with worse neurologic outcome at 3 and 6 months after the injury ( Fig. 24.11 ). The reason for this is uncertain as no-one has demonstrated that anaerobic metabolism occurs with hyperventilation in this setting. Possible causes are: (a) HV produces alkalemia and increased affinity of oxygen for hemoglobin, (b) it decreases seizure threshold, (c) the potential exists for hyperventilation to produce only a transient effect or to produce a paradoxical increase in ICP ( Fig. 24.12 ), and (d) upon discontinuation of hyperventilation, a paradoxical CSF acidosis can occur.

Effects of hyperventilation on cerebral blood flow (CBF) . Two examples of disparate effects of hyperventilation on CBF. Both figures are stable xenon CBFs in head trauma patients with and without hyperventilation. CBF scale is indicated on the right in mL/100 g/min and is indicated above each study. CT images are indicated in the lower figures and CBF maps in the upper figures. (A) PaCO ₂ was decreased from 39 to 29 mmHg. The baseline scan (right) shows hyperemia and the hyperventilated scan (left) shows CBFs of approximately 30 mL/100 g per minute, which are probably acceptable flows. (B) PaCO ₂ was decreased from 46 to 30 mmHg. The baseline CBF ( right ) had only marginally acceptable CBF. The effect of hyperventilation ( left ) was to produce widespread areas of CBF less than 20 mL/100 g per minute, which are probably unacceptable flows.

(Reprinted with permission from Kofke WA et al. Neurologic intensive care. In Albin MS, ed. Textbook of Neuroanesthesia with Neurosurgical and Neuroscience Perspectives. New York: McGraw-Hill; 1997.)

Head trauma patients were randomized to receive hyperventilation or normoventilation. Outcome was worse in hyperventilated patients. D, Death; G/MD, good recovery/moderate disability; GCS, Glasgow Coma Scale; SD/V, severe disability/vegetative state.

Paradoxical rise in intracranial pressure (ICP) induced by mechanical hyperventilation, presumably a result of mechanical pressure effects predominating over hypocarbic cerebral vasoconstriction. It is likely that hyperventilation induced a decrease in blood pressure, which resulted in an opposing reflex increase in cerebral blood volume. “Bolt” refers to subarachnoid screw, “vent” to ventricular catheter.

(Reproduced with permission from Ropper A, Kennedy S: Postoperative neurosurgical care. In: Ropper A, ed. Neurological and Neurosurgical Intensive Care . New York: Raven Press; 1993: 185–191.)

Multiple clinical studies in TBI have confirmed that hyperventilation can cause significant reductions in CBF. Jugular bulb venous oxygen saturation (SjvO ₂ ) and partial brain tissue oxygen pressure (PbtO ₂ ) values can be dramatically reduced by continuous hyperventilation. Hypocapnia increases the likelihood of detecting brain tissue hypoxia when using PbtO ₂ monitors. This effect is more pronounced during the first few days post-TBI and it is associated with poor outcomes. Using a modified PET scan, Coles et al. evaluated CBF, CBV and oxygen extraction factor (OEF) in patients within 10 days of trauma. Hypocapnia was found to cause a decrease in CBF, and an increase in volume of ischemic areas and OEF.

The presence of hyperemia can be determined by the use of direct brain CBF determination or via jugular bulb oximetry. Brain tissue PbrO ₂ may be helpful in this determination but this remains to be definitively demonstrated. High ICP associated with a low A-VDO ₂ across the brain (3–4 vol%) is thought to indicate that hyperventilation can be safely used. In an emergency situation, even if the nature of the high ICP (oligemic vs hyperemic) is not known, acutely administered hyperventilation should be used to keep ICP down or to reverse a herniation syndrome or plateau wave until more definitive diagnosis or therapy can be performed.

Hyperosmolar Therapy

The intravascular administration of hyperosmolar agents such as mannitol and/or hypertonic saline (HTS) creates an osmolar gradient that facilitates water transport across the BBB into the circulation, where it is excreted by the kidneys. The net effect is a reduction of the interstitial fluid and a decrease in ICP. For acute elevation in ICP, therapy with either mannitol or HTS have shown similar efficacy in decreasing ICP.

Mannitol remains a commonly used hyperosmolar agent. It is an osmotic diuretic freely filtered by the renal glomerulus and does not undergo tubular reabsorption. It lowers ICP through two main effects; first, through hypoviscosity-mediated autoregulatory vasoconstriction, also called the “rheological effect,” and second, it may induce a further decrease in ICP through brain dehydration in areas with intact blood brain barrier. However, this may be limited through generation of intracellular idiogenic osmoles equalizing transmembrane osmolar gradients.

Mannitol is administered as 0.5–1 g/kg as intravenous (IV) bolus through either peripheral or central line and can be repeated every 4–6 hours. Reduction in ICP is usually achieved within minutes, peaks at about 1 hour, and last 4 to 6 hours. Fluid balance, renal function, and plasma osmolality must be monitored because no therapeutic effect is seen with osmolality > 320 mOsm/kg. If plasma osmolality is > 320 mOsm/kg, osmolar gap (measured osm – calculated osm) should be calculated and if < 20 mOsm/kg, mannitol should be administered. If > 20 mOsm/kg, HTS should be considered, because the risk of renal dysfunction is higher. Patients with known renal disease may be poor candidates for osmotic diuresis. Another frequent complication related to mannitol is hypotension because of its diuretic effect. Acute hypotension is most commonly seen after rapid infusions and can be minimized by prolonged infusions (15–30 minutes).

Unfortunately, mannitol can have delayed effects to increase ICP. This can occur by four mechanisms. First, as a potent osmotic diuretic, mannitol can have a secondary effect to decrease systemic blood volume, thus decreasing cardiac output and blood pressure. This can result in normal reflex autoregulatory increases in CBV, which can increase ICP. Second, the increased urine output, if not replaced with commensurate IV fluid therapy, can elevate hematocrit, thus opposing the initial mannitol-induced decrease in viscosity. Third, mannitol can cross the BBB in an unpredictable manner with the possibility introduced of rebound increase in ICP, similar to that observed with urea. This is partly related to the reflection coefficient of 0.9 indicating that it can even slowly diffuse into the normal brain. Fourth, there is a theoretical possibility of generation of increased intracellular osmolarity, via so-called idiogenic osmoles, which may predispose to rebound increase in brain volume with discontinuation of mannitol. These complications of mannitol are probably lessened if urine output is replaced with balanced crystalloid infusion and if, once blood osmolarity is increased, it is not allowed to decrease rapidly to the prior level unless clinical improvement indicates that weaning of ICP-reducing therapy is appropriate. This certainly should be considered in any patient demonstrating periodic abrupt increases in ICP.

HTS has increasingly been used for treatment of acute elevated ICP, replacing mannitol as a first-line agent in multiple institutions. With a reflection coefficient of 1.0 and no potential to produce deleterious diuresis and undesired hypovolemia, it has properties that made it the most attractive hyperosmolar agent.

The ability of HTS to lower ICP was initially described in 1919 by McKesson and it is available in different concentrations ranging from 2% to 23.4%. HTS can be given as a bolus alone or in addition to mannitol. HTS 2% and 3% boluses can be given via a peripheral line and concentrations > 5% should be given via a central venous catheter because of elevated osmolarity ( Table 24.5 ). However, in acute emergencies 3%–7.5% HTS should be administered regardless of the presence of central venous access. Two prior prehospital trials using HTS 3% and 7.5% via peripheral lines did not show any negative effects. Administration of HTS through intraosseous access should be done carefully and with concentrations of < 7% because of the potential risk of myonecrosis.

The mechanism of action behind HTS involves many theories, with the most common involving the creation of an osmotic shift of fluid from the intracellular space to the intravascular and interstitial space. In addition, HTS shrinks red blood cells, making them more deformable and enhancing their passage across capillaries. A recent study shows that HTS can reverse brain oxygenation and metabolism dysfunction through vasodilatory, mitochondrial, and anti-edema effects. The combination of these effects result in a biphasic reduction in ICP by improving rheologic properties and then by osmotic activity through aquaporins across the BBB. Aquaporins are water channels present in the brain responsible for CSF production and water distribution; its downregulation after TBI is associated with development of cerebral edema. In addition, prior evidence suggests that HTS modulates the innate immune response by diminishing the neutrophil and endothelial cell activation leading to a reduction in microvascular injury and permeability.

HTS has been studied in animal models of ICH, subarachnoid hemorrhage (SAH), and TBI. In a notable prior related canine ICH study, HTS was associated with decreased intraparenchymal pressure throughout the brain, including the perihematomal region. More recently, Schreibman et al. described an experimental ICH model in which hyperosmolar therapy shows reduction of neuroinflammation by causing a reduced activation of microglia/macrophages in perihematomal tissues. Yin et al. suggest that HTS ameliorates TBI-induced cerebral edema by suppressing brain edema, proinflammatory cytokine expression and apoptosis via downregulation of aquaporin 4 in a rat TBI model. In dogs with ICH treated with either mannitol or HTS, both drugs effectively decreased ICP although HTS duration of action was longer.

In humans, the effect of HTS has been reported in ischemic stroke, ICH, SAH, TBI, and hepatic encephalopathy. All studies show that HTS effectively and reproducibly reduces ICP with concomitant improvement in CPP. Indeed, Suarez et al. showed one important effect of 23.4% HTS in eight patients as a therapy that effectively decreases ICP when all other medical therapies do not work ( Fig. 24.13 ). Tseng et al. reported that in 10 patients with poor grade SAH, ICP was found to decrease by around 75% and CBF was enhanced in the face of decreased cerebrovascular resistance, indicating potential rheologic and cerebral vasodilatory of HTS 23.5%. Al-Rawi et al. demonstrated that an increase in CBF is followed by improvement in tissue oxygenation and metabolism when poor-grade SAH patients are treated with 23.5%. More importantly, this increment in tissue oxygenation was found to correlate with improved neurologic outcomes.

This stacked-bar chart shows the mean pretreatment intracranial pressure (ICP) and the mean ICP 1 hour after treatment with 23.4% saline for every episode of refractory intracranial hypertension (RIH). Patient distribution is as follows: 1 , spontaneous basal ganglia hemorrhage; 2 , subarachnoid hemorrhage; 3 , subarachnoid hemorrhage; 4–6 , traumatic head injury; 7–8 , subarachnoid hemorrhage; ˆ, subarachnoid hemorrhage; 10–12 , subarachnoid hemorrhage; 13–20 , brain tumor.

(Reproduced with permission of Suarez JI, Qureshi AI, Bhardwaj A, et al: Crit Care Med 1998;26:1118–1122.)

Ware et al. assessed the effects of 23.4% HTS in TBI patients with elevated ICP refractory to mannitol. They found HTS to have a longer effect on ICP reduction than mannitol and to be effective in patients with Na > 150 mEq/L. Paredes-Andrade et al. studied HTS 23.4% on ICP in the setting of different serum and CSF osmolarities. HTS was found to decrease ICP irrespective of serum or CSF osmolarity, possibly indicating a nonosmotic mechanism of action. More recently, a 30% HTS concentration was tested in TBI and no associated harmful or hematologic abnormalities were observed. In 2013, Eskandari et al. tested HTS 14.6% after TBI and showed that patients who exhibited refractory intracranial hypertension can be treated effectively and safely with repeated boluses of 14.6% with no significant change in renal function or hemodynamics. Oxidative stress processes play an important role in secondary brain injury. In a study of 33 adults with TBI, HTS showed antioxidant effects by decreasing the amount of serum total antioxidant power, reactive oxygen species and nitric oxide. Diringer et al. studied the effects of HTS 23.4% and mannitol 20% on CBF, CBV, OEF, and cerebral metabolic rate (CMR) O ₂ in nine patients who developed cerebral edema with midline shift from acute ischemic stroke. They found that increased CBF on the contralateral unaffected hemisphere was dependent on mean arterial pressure. No effect on CBV was observed, arguing against the compensatory cerebral vasoconstriction previously proposed as a mechanism for ICP reduction.

Efficacy of HTS for Reduction of ICP

Several small studies in humans have assessed the ability of HTS to reduce ICP. A retrospective study by Qureshi et al. showed that HTS decreases ICP in head trauma in postoperative brain edema but not nontraumatic ICH or ischemic stroke. Schatzman et al. performed a prospective nonrandomized evaluation of HTS in severe head injury and found that it effectively reduced ICP. A subsequent prospective randomized study by Vialet et al. in TBI patients found better ICP control compared with mannitol. Another prospective randomized study did not show better ICP control with HTS compared with standard therapy. However, in this study the sample size was relatively small and the HTS patients were sicker on entry into the study. Three studies report that HTS can be safely and effectively used in children to decrease ICP after TBI. Suarez et al. studying severe SAH patients reported that HTS therapy effectively decreased ICP while concomitantly increasing CBF (see Fig. 24.13 ). Schwartz et al. evaluated HTS/hetastarch therapy in ischemic stroke patients with high ICP, compared with mannitol. Both therapies decreased ICP, but the HTS group had better control.

Patients with intracranial hypertension associated with hepatic encephalopathy have also been demonstrated by Murphy et al. to sustain ICP decrements after HTS. Moreover, HTS and mannitol have been reported as a useful bridge therapy while awaiting liver transplant in patients who suffer from cerebral edema.

Although many studies show the efficacy of HTS in improving ICP and other parameters, the effect of this intervention on long-term clinical outcomes remains unclear. In 1991, Vassar et al. evaluated this hypothesis showing a trend for better outcomes in HTS-treated patients. One controlled trial randomly assigned 226 patients with TBI to prehospital resuscitation with 250 mL HTS 7.5% or the same volume of Ringer lactate. Survival until hospital discharge, 6-month survival, and neurologic function 6 months after injury were not different. This study did not assess the impact of systematic use of HTS throughout the hospital course. Koenig et al. evaluated the effect of 23.4% HTS on reversal of transtentorial herniation in 68 patients who suffered from various intracranial pathologies. HTS reversed transtentorial herniation quickly and reduced ICP, but clinical outcomes remained poor.

Overall, mannitol and HTS have been compared in some randomized trials of patients with intracranial hypertension derived from a variety of causes (traumatic brain injury, stroke, tumors). Meta-analyses of these trials have found that HTS appears to have greater efficacy in managing elevated ICP, but clinical outcomes have not been systematically examined. Further clinical trials are required to clarify the appropriate role of hypertonic saline infusion versus mannitol in the acute management of intracranial hypertension.

HTS clearly has the potential to exert a positive impact in the management of intracranial hypertension. However, there are concerns expressed about possible deleterious effects. Perhaps one of the most worrisome concerns is renal failure. This was mentioned in a report by Peterson wherein 2 of 10 children developed reversible renal failure, also, however, related to multiorgan failure and sepsis. Nonetheless, the issues were further underscored in editorials by Valadka et al. and Dominquez et al. but with disagreement about this as a significant risk expressed by Bratton et al. Other potential adverse effects were reviewed by Suarez and include:

CSF Drainage

CSF volume is reduced by removal via ventricular drain (see Figs. 24.5 and 24.6 ). This can be affected by setting the drainage at a prescribed level above the midbrain or prescribing that the drain be opened anytime ICP exceeds 20–25 mmHg. Leaving a drain open risks excessive CSF drainage when the patient coughs or with drain manipulation in the course of routine nursing procedures and can contribute to collapse of the ventricles or subdural hemorrhage. Excessive and abrupt decrease in local pressure around the drain can produce intracranial gradients, leading to a herniation syndrome. Leaving the drain clamped and monitored, however, risks the development of untreated intracranial hypertension.

CBV Decreasing Drugs

CBF decreasing (and therefore CBV decreasing) drugs that can decrease ICP include barbiturates, benzodiazepines, etomidate, and propofol. Notably, all are CNS depressants and become ineffective once the EEG become isoelectric. Thus, their use indicates acceptance on the part of the clinician to lose any reliable neurologic examination. Unlike hyperventilation, these agents decrease CBF coupled to CMR. Thus, the CBF decreases should not provide a milieu for anaerobic metabolism. Lidocaine also decreases CBF and CMR to decrease ICP although with a less pronounced decrement in neurologic function. Mannitol’s immediate effects are also thought to be mediated by reduction in cerebral blood volume, although this is undoubtedly minor and temporary as a mechanism. Barbiturates are discussed as a tier-3 therapy in the next section.

Decompressive Craniectomy

First described by Thomas Kocher in 1901 and subsequently by Cushing in 1908, decompressive craniectomy (DC) is a surgical procedure in which part of the skull uni- or bilaterally is removed and the underlying dura opened. DC removes the rigid confines of the cranial vault, allowing further expansion of the intracranial contents with subsequent reduction of intracranial hypertension and brain herniation risk. Although intravascular arterial blood accounts for the majority of the intracranial blood volume, venous contribution to ICP is commonly overlooked. Diffuse brain edema can lead to generalized venous compression and a cycle of venous hypertension. In a recent study after TBI, alleviation of venous sinus compression might have contributed to the ICP-reducing effect of DC.

Although DC has been investigated in a number of neurological conditions, RCTs have only been evaluated in TBI and stroke. DC can be a primary or secondary procedure. A cohort study of patients with traumatic subdural hematoma (SDH), demonstrated lower mortality in patients undergoing primary DC compared with conventional craniotomy where the bone flap is replaced. However, there is no high-quality evidence to support this approach. The Randomized Evaluation of Surgery with Craniectomy for patients Undergoing Evacuation of Acute Subdural Haematoma (RESCUE-ASDH) trial is a multicenter, randomized trial comparing the effectiveness of primary DC versus craniotomy and bone-flap replacement after evacuation of an ASDH in adult head-injured patients ( http://www.rescueasdh.org/ ); subjects recruitment was completed in 2019. Results of trial are still pending. Secondary DC is most commonly undertaken as a last-tier (life-saving) intervention in a patient with severe intracranial hypertension refractory to tiered escalation of interventions to control ICP. There are three main approaches to DC (bifrontal, uni- or bilateral hemicraniectomy, suboccipital). The craniectomy must be of sufficient size to allow effective ICP control.

Airway Evaluation and Management

Therapeutic Options

The main options to consider in airway management have to do with whether and how deeply to produce CNS depression and which tool will be used to effect intubation of the trachea. There are pros and cons to each approach and considerable clinical judgment is needed to match the spectrum of benefits and risks to the underlying disease processes.

Awake Versus Asleep

There is a continuum of anesthetic states that may be used, varying from awake and unsedated to fully anesthetized with neuromuscular blockade. In the context of possible intracranial hypertension or hemorrhage, the side effects of anesthetic drugs can be usefully used to control systemic and intracranial hypertension. The full spectrum of effects of anesthetic drugs is beyond the scope of this chapter. But, briefly, thiopental, propofol, and etomidate have direct ICP-reducing qualities that can be of use during intubation, a procedure well-known to produce intracranial hypertension. Attenuation of systemic hypertension can be augmented with judicious use of an opioid such as fentanyl in addition to a blood pressure–reducing drug such as thiopental or propofol. Neuromuscular blockade can be achieved with vecuronium or rocuronium, neither of which has any reported cerebrovascular effects. Succinylcholine can also be used although concerns remain about it causing increased ICP, probably related to increased cerebral blood flow inducing afferent spindle stimulation. However, after a large bolus of one of the usual aforementioned induction drugs, succinylcholine seems to be associated with no significant problems. Moreover, its use is theoretically safe with hyperacute onset paraplegia or quadriplegia (i.e., before nicotinic receptor upregulation) but Dr. Cruz and Dr. Kofke refrain from its use at any time with spinal cord injury patients because of concern about the speed of receptor upregulation or inaccurate history leading to fatal hyperkalemia.

Awake endotracheal intubation is an option for cooperative patients with acute spinal cord injury (SCI). However, its use has advantages and disadvantages ( Table 24.6 ). Retrospective studies have not shown differences in neurologic outcome with awake versus asleep fiberoptic intubation in acute SCI. Thus, the choice of technique should be based on clinical situation, patient cooperation, and clinical expertise.

Table 24.6

Awake fiberoptic intubation.

Advantages	Disadvantages
▪ Neurologic evaluation can be performed after airway management. ▪ Spontaneous ventilation is maintained throughout the procedure. ▪ Head and neck are maintained in neutral position while airway is secured.	▪ Time consuming. ▪ Even with adequate air topicalization, coughing and gagging may still occur with potential for C-spine motion. ▪ Visualization may be difficult with excessive secretions, presence of blood and vomitus. ▪ Sedation is commonly required and might obscure clinical assessment. ▪ Requires technical expertise. ▪ Risk of local anesthesia systemic toxicity.

 

Cricoid or No Cricoid Pressure?

It has been hypothesized that any unidirectional force applied to the cervical vertebrae during cricoid pressure may cause excessive neck movement and exacerbate preexisting lesions. Studies have demonstrated that cricoid pressure causes cervical spine displacement of different degrees when the posterior aspect of the neck is not supported. The clinical implication of these movements was assessed retrospectively in patients who had C-spine injuries and they were found to be free of neurologic impairment. However, it would be sensible to avoid movements of the potentially fractured cervical spine, if at all possible. The double-handed maneuver, which is popular in trauma patients to provide support to the posterior cervical spine and to provide stabilization to the posterior aspect of the neck, seems to be a safer alternative to the single-handed maneuver. The assistant performing bimanual CP should not be assigned to other duties until intubation has been completed. If the bimanual technique is obstructing the glottic view, it may need to be switched back to a single-handed maneuver to improve laryngoscopic visualization. Cricoid pressure utilization is controversial in SCI because forceful pressure over the site of the C-spine fracture can cause displacement. Moreover, the efficacy of cricoid pressure to prevent regurgitation has been questioned. These authors do not routinely use cricoid pressure during rapid sequence induction for patients with acute cervical SCI; a gentle BURP maneuver could be utilized to improve glottic view.

Cervical Spine Distraction During Airway Instrumentation

Although neurologic impairment during airway manipulation is very uncommon, all airway maneuvers are associated with some degree of C-spine mobilization. However, this is based only on retrospective evidence and expert opinion. In patients with cervical cord injuries, it is generally better to use little or no anesthetic drugs, except as needed for safe conscious sedation and then to use fiberoptic bronchoscopy with good topicalization. This does require cooperation of the patient and if that is not possible or the intubation needs to be done in an emergency, direct laryngoscopy with in-line immobilization has not been associated with apparent neurologic complications, although its anatomic efficacy has been questioned. Notably, Lennarsen et al. reported in fresh cadavers that neither traction nor in-line immobilization prevented distraction nor angulation of the C4–5 injured cervical spine with laryngoscopy by Macintosh blade. Because concern persists about this approach producing or exacerbating cervical spine injury, it remains reserved for emergencies or for the uncooperative patient in whom general anesthesia with rapid intubation by laryngoscopy is the only viable option. In fact, direct laryngoscopy with manual in-line stabilization is the most commonly used technique for emergency endotracheal intubation in patients with acute cervical SCI, and it is recommended according to Advanced Trauma Life Support guidelines. In a survey of 122 physician anesthesiologists, indirect techniques were preferred for elective intubation of patients with cervical spine injury (CSI) and direct laryngoscopy was preferred for emergency intubation.

There have been many reports of various approaches to endotracheal intubation with various endpoints. Some are simply case reports indicating that a given technique worked in a given patient with cervical vertebral instability. However, a prospective randomized study that provides conclusive outcome data favoring a given approach remains unpublished. Nonetheless, there are some studies that used other reasonable surrogate endpoints that can provide an element of evidentiary support for some approaches.

Basic airway maneuvers such as mask ventilation, chin lift, and jaw thrust have the potential for displacement of the cervical spine even when a cervical collar is in place. The sniffing position entails flexion of the lower neck and extension of the head on the upper neck. In anesthetized normal patients, the majority of cervical movement during classic Macintosh laryngoscopy occurs at the occipitoatlantal and atlantoaxial articulations (C1–C2). Lower cervical segments are displaced only minimally with direct laryngoscopy. In cadaver studies with cervical instability, chin lift and jaw thrust were found to result in more C-spine displacement and increase in disc space than either oral or nasal intubation, but jaw thrust without chin lift or neck extension resulted in significantly reduced displacement.

Turkstra et al. in normal anesthetized patients carried out a fluoroscopic evaluation of neck extension produced by bag-valve-mask ventilation (BVM), Macintosh blade laryngoscopy, light wand, and GlideScope. They found minimal movement during BVM, with the most extension noted by Macintosh blade laryngoscopy. Both light wand and GlideScope produced much less neck extension than Macintosh blade laryngoscopy with the light wand taking an equivalent time and the GlideScope taking longer.

Rudolph et al. compared Macintosh laryngoscopy with a rigid Bonvil fiberoptic scope reporting less cervical spine motion with the rigid fiberoptic scope but it was not zero. Hastings et al. evaluating external extension without fluoroscopy reported very little neck extension with the Bullard laryngoscope compared with Miller and Macintosh blades.

Robitaille et al. reported that during intubation under general anesthesia with neuromuscular blockade and manual in-line stabilization, the use of GlideScope produced better glottic visualization but did not significantly decrease movement of the nonpathologic C-spine when compared with direct laryngoscopy.

Brimacombe et al. in cadavers with C3 instability compared the effects of facemask application, esophageal/tracheal Combitube, laryngoscopy guided intubation, flexible fiberoptic-guided intubation, intubating laryngeal mask airway (LMA), and maximal head/neck flexion and extension. Displacement was negligible with the fiberscope, moderate with LMA and with facemask/chin lift, worse with laryngoscopy, and worst with Combitube. Extension of the neck data as a percentage of the maximum seen with purposeful neck extension are presented in Fig. 24.14 .

Summary of effects of various airway maneuvers on fresh cadavers with experimentally induced cervical instability. LMA , laryngeal mask airway.

(From data of Brimacombe J, Keller C, Kunzel K, et al: Anesth Analg 2000;91:1274–1278.)

In another fluoroscopic study of C-spine injured cadavers, Gerling et al. compared laryngoscope blades combined with in-line immobilization, reporting that the Miller blade produced less cervical vertebral displacement than the Macintosh blade and that manual immobilization is superior to cervical collar during intubation.

The use of video laryngoscopes such as GlideScope, C-MAC, McGrath, Airtraq, etc., has been associated with improvement in glottis visualization when manual in-line stabilization is used and probably less C-spine displacement. However, procedural time may be longer for inexperienced clinicians. Ruetzler et al. reported that in a simulated setting of difficult intubation, GlideScope and C-MAC were superior compared with conventional direct laryngoscopy. In a recent systematic review and meta-analysis of RCTs comparing any intubation device with the Macintosh laryngoscope in humans with C-spine immobilization, Suppan et al. reported that the Airtraq was associated with a significant reduction of intubation failure at the first attempt, a higher rate of Cormack-Lehane grade 1, reduction of operational time, and oropharyngeal complications. Brück et al. compared C-MAC and GlideScope in patients with C-spine disorders and reported that both devices provide an excellent glottic view, but tracheal intubation was more successful on the first attempt with the GlideScope. Yumul et al. compared the C-MAC video laryngoscope with the standard fiberoptic scope with an eye piece for intubation in patients with C-spine immobilization. The glottic view at the time of intubation did not differ significantly with the two devices; however, the C-MAC facilitated more rapid tracheal intubation compared with the fiberoptic scope. The peak heart rate response following insertion of the tracheal tube was also lesser in the C-MAC group. Holmes et al. reported that among patients with acute CSI at a high-volume academic trauma center, video laryngoscopy was the most commonly used initial intubation technique. Awake fiberoptic bronchoscopy (FOB) and direct laryngoscopy were performed infrequently and no cases of neurological deterioration secondary to airway management occurred with any method.

Fiberoptic intubation, either asleep or awake, causes little motion of the cervical spine. However, coughing and/or gagging can occur during awake intubation if not adequately topically anesthetized, resulting in motion of the injured spine. In fact, fiberoptic scope in an emergency situation with providers who are inexperienced with this device has a high failure rate and can be very challenging if the patient is uncooperative or with excessive blood or secretions in the airway.

In summary, airway management in the presence of acute CSI is probably the most challenging scenario for the anesthesiologist. Traditionally, awake fiberoptic has been recommended because it limits cervical spine motion during tracheal intubation and allows neurological examination after the procedure. However, in the real world the brain-injured patient typically is not cooperative such that the agitation that might ensue with fiberoptic attempts can produce unacceptable patient-induced neck movement. This then results in the need for increasing amounts of sedation, in the context of a full stomach. This may or may not produce sufficient sedation while putting the patient in an unacceptable in-between state of pharmacologically depressed sensorium with persisting agitation and an unprotected airway. The situation may be enough of an emergency that the use of a fiberoptic technique, in a setting of developing hypoxemia, full stomach, possible airway injury with associated secretions, means the planned nonexpeditious intubation has an unacceptable risk of hypoxemia and/or aspiration. For these reasons, in such situations many clinicians advocate direct laryngoscopy with appropriate doses of CNS depressants and neuromuscular blockade with immobilization or in-line traction. If a difficult airway problem arises in this situation, there should be no extreme laryngoscopy attempts that will clearly risk quadriplegia. Rather the algorithm should move quickly to LMA to at least establish oxygenation followed by securing the airway via LMA and then by intubation, or by tracheostomy.

Currently, with the widespread availability of video laryngoscopy, fiberoptic use is declining dramatically. Assuming care is taken to limit neck movement, providers should use the intubation technique with which they have the most experience and skill. In applying these data to an individual patient, considerable judgement may be needed. Often the best evidence-based method may not fit your individual patient situation. Nonetheless, video laryngoscopy of the airway with intubation of the trachea seems to be the new gold standard and certainly should be associated with near zero risk of exacerbation of spinal cord injury.

Oxygenation

PaO ₂ Physiology

The conceptual relationship of CBF to PaO ₂ is depicted in Fig. 24.15 . Hypoxemia, usually below a PaO ₂ of approximately 50–60 mmHg, is associated with vasodilation. At the opposite extreme, Floyd et al. in a group of healthy volunteers demonstrated the vasoconstrictive effect of hyperoxemia and its accompanying hypocapnea ( Fig. 24.16 ). Nakajima et al. evaluated this phenomenon in patients with cerebrovascular disease, finding that areas of the brain with impaired cerebrovascular reserve were not adversely affected by hyperoxia.

Hyperoxia vasoconstricts the brain and hypoxemia produces significant vasodilation. CBF , Cerebral blood flow.

Colorized continuous arterial spin labeled (CASL)-perfusion MRI images with scale depicting cerebral blood flow (CBF) changes in response to air: air 4% CO ₂ , air 6% CO ₂ , 100% O ₂ , 96% O ₂ /4% CO ₂ , and 94% O ₂ /6% CO ₂ .

(Reproduced from Floyd T, Clark J, Gelfand R, et al: J App Physiol 2003;95:2453–2461 with permission.)

Outcome Data

The optimal PaO ₂ to seek in a brain injured patient is presently unclear. There are data that support hyperoxic therapy along with data that suggest such an approach is deleterious. In addition, the bedside decision about PaO ₂ management is further coupled to cerebrovascular reserve issues previously discussed. Thus, a low PaO ₂ that would normally be tolerated through vasodilation may not be so well tolerated if vasodilatory reserve is compromised with, for example, carotid occlusion, brain edema, or anemia.

Fiskum et al. among others have reported in laboratory studies that hyperoxic therapy promotes generation of free radicals and that such oxidative stress causes mitochondrial injury, which will act to impair neurologic recovery. This notion from in vitro considerations is supported by in vivo studies in rodents and dogs, which demonstrated worse neurologic outcomes when hyperoxia is used before or after an ischemic insult.

Conversely, with the advent of reports supporting the feasibility and reliability of brain tissue PO ₂ monitoring, data regarding increased brain tissue oxygen monitoring show that normoxemic therapy, in the context of cerebral hypoxia, may promote ischemic injury. Indeed, many recent reports have described in nonrandomized retrospective and prospective series of both traumatic and SAH patients that brain tissue PO ₂ less than 20–30 mmHg is associated with worsened neurologic outcome ( Fig. 24.17 ). Notably, however, these studies did not examine effects of hyperoxia, which is the negative situation identified by Fiskum et al. These studies point out the value of avoiding tissue hypoxia, perhaps at the cost of systemic hyperoxia but not intracranial hyperoxia. However, one side observation made by these studies is the impact of avoiding hyperoxia because brain tissue oxygen monitoring allows the provision of minimal FiO ₂ that permits the optimal (not too high not too low) brain tissue oxygen level.

Restricted cubic spline functions of the relative risk of death as related to initial low values categorized into < 5, < 10, and < 15 mmHg. The ordinal characterization follows from the layering of the curves, < 5 being worse than < 10, which is worse than < 15. Note that the curves stabilize at long durations of hypoxia.

(Redrawn from van den Brink W, van Santbrink H, Steyerberg E, et al: Neurosurgery 2000;46:876–878.)

Given these potentially conflicting therapeutic priorities, it seems that the most sensible approach at this time is as follows: In the presence of a brain tissue PO ₂ monitor, adjust physiologic parameters to keep PbrO ₂ > 20 mmHg. This may entail use of FiO ₂ > 60% with concomitant risk of pulmonary oxygen toxicity. It seems that this risk can be incurred for 1 to 2 days but that continued dependence on pulmonary toxic oxygen concentrations should produce a time-dependent increase in pressure on the caregivers to decrease FiO2, even if this means use of higher airway pressure or allowing PbrO ₂ to decrease after a few days.

In the absence of a PbrO ₂ monitor, the clinician is left basing therapy on assumptions about brain oxygenation. If it is felt that many brain areas are well perfused and at risk for hyperoxia, pulmonary management should aim for PaO ₂ just sufficient to produce SaO ₂ > 95%. Conversely, if there is elevated ICP and/or areas of brain hypoperfusion then a reasonable empiric approach would be to utilize an FiO ₂ of 0.60. This will maximize PaO ₂ and PbrO ₂ but without significant risk of acute pulmonary injury.

PEEP and Intracranial Hypertension

Positive end expiratory pressure (PEEP) can increase ICP ( Fig. 24.18 ), and this relationship has been the subject of clinical research for decades. Two mechanisms can be posited. The first is through impedance of cerebral venous return to increase cerebral venous pressure and ICP. The second is through decreased blood pressure and reflex increase in cerebral blood volume to increase ICP. Huseby’s data suggest that cerebral venous effects only occur with very high PEEP.

Intracranial pressure (ICP) and arterial blood pressure (BP) before and with the application of positive end-expiratory pressure (PEEP) (4 to 8 cmH ₂ O) in severely head-injured patients. The patients are arbitrarily divided into two groups: those with an ICP increase equal to or above 10 mmHg and those with ICP gains below 10 mmHg. Note that PEEP-induced blood pressure decreased appear to be more marked in patients sustaining larger ICP increases. (Reproduced by permission from Battison C, Andrews PJ, Graham C, et al: Randomized, controlled trial on the effect of a 20% mannitol solution and a 7.5% saline/6% dextran solution on increased intracranial pressure after brain injury.

(Redrawn from Shapiro H, Marshall L: J Trauma 1978;18:254–256.)

Frost demonstrated that applying PEEP between 5 and 12 cm H ₂ O (and even transiently up to 40 cm H ₂ O improved arterial oxygenation without increasing ICP. Shapiro et al. demonstrated increases in ICP in head-injured humans with intracranial hypertension with application of PEEP (see Fig. 24.18 ). Examination of their data indicates that the most profound decreases in CPP occurred in patients with PEEP-induced decrements in mean arterial pressure consistent with the notion put forth by Rosner that decreases in blood pressure increase CBV to increase ICP Aidinis et al. Studies in cats confirmed these observations in a more controlled setting. In addition, they assessed the role of pulmonary compliance, finding that decreased pulmonary compliance with oleic acid injections results in less of an effect of PEEP to increase ICP. Such observations indicate in situations where PEEP is likely to be needed, often accompanied by decrements in pulmonary compliance, that any adverse effects on ICP are less likely to manifest. This may be related to observations that hemodynamic effects of PEEP are less apparent with noncompliant lungs such that hypotensive-mediated increases in CBV do not occur.

Historically, use of high PEEP has been associated with potential for ICP elevation; however, the intuitive notion that PEEP increases cerebral venous pressure to increase ICP is not as straightforward as some may indicate. For PEEP to increase cerebral venous pressure to levels that will increase ICP, the cerebral venous pressure must at least equal the ICP. Thus, the higher the ICP, the higher PEEP must be in order to have such a direct hydraulic effect on ICP. This concept was proven by Huseby et al. in dog studies in which PEEP was increased progressively with different starting levels of ICP ( Fig. 24.19 ). It is important to note that they prevented PEEP-induced decrements in blood pressure, thus avoiding any reflex increases in cerebral blood volume. They suggested a hydraulic model to conceptualize this better ( Fig. 24.20 ). Thus, for example, if all of a 10 cm H ₂ O PEEP application was transmitted to the cerebral vasculature, which is unlikely given the decreased pulmonary compliance associated with the need for such PEEP, then ICP will only be affected if it is < 10 cm H ₂ O (7.7 mmHg) with it increasing to a level no higher than the applied PEEP. Such observations are consistent with the notion that there is a Starling resister regulating cerebral venous outflow.

Increases in intracranial pressure (ICP) with positive end-expiratory pressure (PEEP) in dogs. Values are mean ± standard error of the mean. Group 1 included 12 animals with initial ICP less than 20 cmH ₂ O; group 2 included 7 animals with initial ICP of 21 to 39 cmH ₂ O; group 3 included 9 animals with initial ICP greater than 40 cmH ₂ O. Blood pressure was maintained constant in all animals. Note that with blood pressure maintained constant that the most significant increases in PEP occur in the animals with the lowest starting PEEP level.

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