Increased Intracranial Pressure Management

Management of Increased Intracranial Pressure

A Primer for the Non-neuro Critical Care Nurse
Linda Josephson, RN, BSN, CCRN

Brain edema and the resulting increase in intracranial pressure may be the result of several conditions: head trauma, intracranial hemorrhage, embolic stroke, infections, tumors, and alterations in cerebral spinal fluid production or absorption. At times, these patients may be treated outside of the neuroiogical intensive care unit (ICU) fora variety of reasons. Therefore, generai criticai care nurses may find themselves in the position of caring for these patients. Maintaining expertise outside of one s area of focus is increasingly difficult to do, and the non-neuro critical care nurse may be unfamiliar with some of the newer research findings and trends in treating these patients. The purpose of this article is to review several of the concepts of neurological care and to update critical care nurses in various newer approaches to caring for patients with increased intracranial pressure. Keywords: Cerebral spinal fluid, intracranial pressure, Intensive care unit.
CRIT CARE NURS, 2 O O 4 ; 2 3 ( 5 ) : 1 94-207]

Brain edema and the resulting increase in intracranial pressure (ICP) may result from many conditions including head trauma, intracranial hemorrhage, embolic stroke, infections, tumors, and alterations in cerebral spinal fluid (CSF) production/absorption.'- Once the initial insult to the brain occurs, the damage it causes cannot be prevented; however, that is not necessarily the end of the damage done. Because of the initial insult, a cascade of cellular changes occurs. These changes, known as secondary brain injury, can lead to further damage. The initial insult causes changes in the regulation of blood flow to the brain, producing an insufficient blood supply to the brain. The lack of blood supply causes hypoxia to the brain tissue, disruption of the blood brain barrier (BBB), edema formation, and intracranial hypertensioti. Secondary injuries can be far
194 Dimensions of Critical Care Nursing Vol. 23 / No. 5

more devastating then the original injury.' Controlling the damage done by tbese secondary mechanisms is the primary focus of much of the medical and nursing care of patients with brain injuries.'* Increased ICP can occur with a number of conditions, and at times, such patients may be treated outside of the neurologic intensive care unit (ICU). The purpose of this article is to review several of the concepts of neurologic care and to update critical care nurses in a variety of the newer approaches to caring for patients with increased ICP. NORMAL CEREBRAL DYNAMICS A review of normal cerebral dynamics is helpful in understanding of the pathophysiology of secondary brain injury. The skull presents a rigid container that houses 3 noncompressible volumes:

Increased Intracranial Pressure Management brain tissue-accounts for approximately 80% of the skull's total volume CSF accounts for approximately 10% of the volume blood volume accounts for approximately 10% of the volume in the skull."'" The state of continually changing pressures from these 3 volumes makes up the iCP. The 3 volumes stay nearly constant, keeping the ICP between 5 and 15 mmHg." If the volume of one of the skulls components increases, then there must be a corresponding decrease in one of the other components, of equal degree, in order to avoid an increase in the ICP.^ The ability of the ICP to remain constant through this mechanism is called compliance. This is also known as the modified iMonroe-Kellie hypothesis.^'' When compliance is adequate, the body is able to compensate for increases in the volume of blood, CSF, or brain tissue without a significant rise in ICP. However, compliance has its limits, and when the upper limits of this mechanism are reached, a small increase in the skull's contents can be enough to significantly raise the ICP to dangerous levels.* The body has several mechanisms for handling an increase in the skull's contents and trying to maintam a normal ICP: Displacement of CSF from the skull into the lumbar cistern. Increasing the rate of CSF reabsorption. Compression of low-pressure venous blood vessels and shunting the blood out into the venous sinuses.' See Figure 1 for a diagram for circulatory pathway of CSF. To match the brain's metabolic needs with an adequate blood supply, the cerebral vascular system is able to autoregulate, allowing for a close matching of metabolic requirements with blood supply. This close matching of demand and supply is referred to as coupling. Autoregulation is accomplished by altering the diameter of the cerebral vasculature."' Under normal conditions, autoregulation allows the brain to maintain a constant rate of CBF over a range of systemic mean arterial pressures (MAP) from 50 to 150 mmHg.''"* If the coupling of the brain's metabolic needs and blood supply were not maintained in close relationship, then excessive blood supply (hyperemia) could result in cerebral edema and increased ICP; or, if there was insuffi-

CEREBRAL BLOOD FLOW AND AUTOREGULATION Cerebral blood flow (CBF) provides the brain with a constant supply of oxygen and glucose. The brain has such a limited supply of these 2 factors that they are depleted within seconds to minutes." To prevent this from occurring, the brain receives a rich supply of blood, approximately 15% of the total cardiac output. The brain represents approximately 2% of the body's total weight, but is responsible for 20% of the body's oxygen consumption.'' The demand for oxygen and glucose varies with the brain's metabolic rate. For example, during seizure activity, metabolic demands increase dramatically, requiring a matching increase in the CBF to meet the increased demand. Other conditions that can increase metabolic requirements for the brain are an increase in physical activity, increased temperature, and posturing.'

Figure 1. Path of cerebral spinal fluid. Cerebral spinal fluid is produced by a complex of capillary tufts, the choroid plexus, located in the first and second lateral ventricles. The fluid circulates out of the lateral ventricles into the centrally placed 3rd ventricle through the foramen of Monroe. From the third ventricle it passes into the fourth ventricle via the cerebral aqueduct, or the foramen of Sylvius, From the fourth ventricle the fluid passes into the pontin cisterns via the foramen of Magendie, and then the CSF enters the subarachnoid spaces around the brain and spinal column. The final destination for the CSF is to be reabsorbed via tbe subarachnoid villa into the venous system.'

September/October 2004

195

Increased Intracranial Pressure Management cient blood flow to meet metabolic demands of the brain, then ischemia and infarction could be the result. Autoregulation helps to avoid both of these harmful situations from occurring. Autoregulation is also affected by certain chemicals that are the byproducts of cellular metabolism: lactic acid, pyruvic acid, and carbon dioxide. All these byproducts release hydrogen ions. Hydrogen is a potent vasodilator for the cerebral arterioles. Carbon dioxide seems to be the most potent vasodilator for the cerebral arterial system.' Whether the source for the increased carbon dioxide is from increased cerebral metabolism or hypercapnea related to respiratory insufficiency, the result is the same: vasodilatation of the cerebral arteries. The vasodiiatation causes an increase in CBF; this is a protective mechanism that allows for the removal of the increased carbon dioxide and other byproducts, and provides a fresh supply of oxygen to the brain.'"' The brain's ability to autoregulate is disrupted when certain parameters are exceeded or injuries occur. The loss of autoregulation may be regional or global. When the systemic MAP is <50 mmHg or >150 mmHg, then autoregulation is lost. It is also lost when the brain has sustained traumatic injury, intracranial bleeds, or iscbemic strokes, and when ICP is >35 mmHg for more than 20 to 30 minutes." CEREBRAL BLOOD SUPPLY The main blood supple to the brain is derived from the vertebral arteries and the internal carotid arteries. Together, these arteries form the Circle of Willis, which is found at the base of the skull. As the name implies, the Circle of Willis is a circle of arteries that presents a unique solution to providing collateral blood flow. The vertebral arteries arise from the left and right subclavian arteries and after entering the base of the skull, join to form the basilar artery. The basilar artery becomes the posterior cerebral arteries that make up the posterior portion of the circle. The internal carotid arteries originate from the common carotid artery and form the anterior portion of the Circle of Willis. They provide a proportionally greater amount of blood compared to the basilar arterial system. It is from the internal carotid portion of the circle that the middle and anterior cerebral arteries are derived.'" As with other arterial beds, the main arteries of the brain subdivide into arterioles and then capillaries. At this level of the brain's circulatory system, the arterioles and capillaries are delicate and susceptible to being compressed by tissue edema, if it is present. When this occurs, the delicate vessels are unable to provide a normal blood flow, and the oxygen and glucose supply to
196 Dimensions of Critical Care Nursing W Vol. 23 / No. 5

TTie brain represents approximately 2% of the body's total weigbt.

the brain are compromised. This can further contribute to iscbemic injury.

CEREBRAL PERFUSION PRESSURE

Cerebral perfusion pressure (CPP) is the pressure difference across the brain. It is the difference between the incoming MAP (which is the propelling force) and the ICP (which is the force opposing the flow of blood). The CPP is calculated by finding the difference between the MAP and the ICP. It is an estimate of the adequacy of cerebral perfusion.'*'' CPP = MAP - ICP The normal range for CPP is between 50 and 150 mmHg, with an average of 80 to 100 mmHg. A CPP of <50 mmHg can lead to hypo-perfusion of the brain, causing hypoxia and ischemic damage, while a CPP of >150 mmHg can lead to a hyperemic state and can cause cerebral edema and hypertensive encepalopathy.'" In order to calculate the CPP, it is necessary to be able to measure the ICP. Inserting a probe into the lateral ventricle and measuring the pressure exerted on the CSF within the ventricle is the most common and accurate method of doing this.' BLOOD BRAIN BARRIER The BBB is comprised of the cells from the capillary wall and the astrocytes, a type of supporting cell in the central nervous system (CNS). The astrocytes fill the spaces between the neurons and the blood vessels. Together these cells form a very tight junction, which becomes a protective enclosure that selectively controls what substances can cross the capillary membranes and gain entrance to the neurons." The BBB controls the transport of substances between the cerebral blood supply, CSF, and brain tissue. The barrier is most soluble to water, gases (oxygen and carbon dioxide) and glucose.'^ The purpose of the BBB is to inhibit the ability of toxic substance from gaining access to the CNS.' However, this protective mechanism also inhibits the effective use of certain drug therapies in the treatment of neurologic system diseases. In general, the brain is slower to take up drugs, dyes, anion, and cation sucb as sodium and potassium from the circulating blood than are other organs. Trauma, brain tumors, radiation, and certain toxins damage the BBB.'^

Increased Intracranial Pressure Management increased production of leukotrienes, thromboxanes, and prostaglandins (also called arachidonic acid derivatives). There is also increased production of toxic-free radicals as well. Together, these substances cause several damaging effects, among them, vascular occlusion and vasospasm, which leads to further worsening of ischemia, and vascular paralysis."'^"" Along with the increased production of arachadonic acid derivatives, the ischemia results in an accumulation of neurotransmitters in the synaptic space, glutamate in particular. Normally when the neuron is stimulated, glutamate is released into the presynaptic space. It travels across the synapse and stimulates the next neuron. The glutamate is then taken up from the synaptic space so that it does not accumulate. Glutamate is an excitatory neurotransmitter and it facilitates the fast signaling pathways in the CNS."'* With a decrease in the production of ATP caused by the ischemia, the reuptake of glutamate is significantly diminished and glutamate accumulates to the point that it becomes toxic to the surrounding neural tissues."'" The accumulation of the glutamate causes increased amounts of the neurt)transmitter to bind to its receptors. When this occurs, the channels that are normally open only for depolarization stay open and there is an increased influx of sodium and calcium into the neurons, and efflux of potassium out of the cell. This causes a prolonged depolarization state for the neuron, with increased metabolic activity and energy demands, further depleting more ATP.'"* " The influx of calcium into the cell has multiple toxic effects; cerebral vasospasm mitochondria! dysfunction activation of proteases and lipases leading to cell death platelet activation increased capillary permeability production of oxygen-free radicals.^-'" The consequence of these changes on a cellular level causes the movement of fluid from the plasma to the intracellular and extracellular space, resulting in both vasogenic and cytotoxic edema. Another result of the movement of fluid, is that as fluid moves out of the vascular space, the plasma becomes more viscous which causes increased resistance to blood flow. As the edema accumulates, it causes increased pressure on the blood vessels and reduces blood even more. The cells experience increased ischemia, further anaerobic metabolism, and breakdown of the Na-K pump, with more formation of cytotoxic edema.''' As the swelling increases in the brain tissue, the compliance within the skull is less able to compensate for rhe
September/October 2004 197

CEREBRAL EDEMA The most common cause of increased ICP is cerebral edema.'" When the cells of the brain are svi'ollen by extra water, then the volume of brain tissue is increased. This increases the pressure within the noncompliant skull and causes compression of the surrounding tissues and small blood vessels. There are two types of cerebral edema, vasogenic and cytotoxic, and they may occur either separately or simultaneously.'Vasogenic edema is an increase in the fluid in the extracellular space. This occurs when there is a breakdown in the BBB. When the barrier is disrupted, capillary permeability is increased and there is leakage of plasma proteins into the extra-cellular space. As the proteins accumulate outside of the capillaries, they pull fluid from the surrounding tissues into the extra-cellular space. This type of edema is associated with cerebral trauma, neurosurgery, brain tumors, and brain abscesses." Cytotoxic edema is the accumulation of fluid within the cellular space. It is usually due to an acute hypoxic episode, which causes anaerobic metabolism to occur. With the anaerobic metabolism, there is a marked decreased in ATP production and a breakdown in cellular functions, including the sodium-potassium pump. When this occurs, potassium rushes out of the cell, and sodium (along with water) rushes into the cell. This causes the cell to swell, and may progress to disruption of the cellular membrane, resulting in cell death."' Cytotoxic edema can also be caused by hypo-osmolality. In this situation, there is higher water content within the blood stream, relative to the contents of the cell. This creates an osmotic gradient, pulling water out of the blood stream and into the cell.'*

PATHOPHYSIOLOGY OF SECONDARY BRAIN INJURY After the brain sustains the initial insult, the damage done can he exacerbated by the development of secondary injury.'^Typically, the secondary injuries are a result of the neurons' biochemical response to the ischemia and uncoupling of blood supply caused b\' the primary injury. After cerebral injury has occurred, CBF is markedly decreased, causing ischemia for brain tissue.^"'" The cerebral cells, deprived of an adequate oxygen supply, are forced to utilize anaerobic metabolic pathways. This results in a deficiency of ATP and energy, so that normal cellular processes fail. Among them is the failure of the sodium-potassium (Na-K) pump. When this occurs, sodium, water, and calcium can enter the cell, and potassium leaves. The lack of sufficient energy also leads to a breakdown of the cell membrane. This causes a release of phospholipids and

Increased Intracranial Pressure Management

increased volume and the ICP rises. As the ICP rises, the CPP decreases and results in less CBF with worsenitig ischemia resulting. The increased ICP causes the loss of autoregulation and CBF becomes dependent on systemic MAP. Thus, increases in ICP and decreased in CBF cause a self-perpetuatitig downward spiral and explains why iticreased ICP is serious cause of death and permanent disability.^ ""' (See Figure 2 for the interrelatedness of pathophysiology of secondary brain injury.)

MANAGEMENT OF THE BRAIN-INJURED PATIENT For interventions to be effective in preventing or minimizing secondary brain injury, they should be instituted immediately upon treatment of the patient." Perhaps the most important preventative measure for minimizing secondary brain injury is to prevent ischemia from occurring. Standard treatment for brain-injured patients to avoid ischemia is to establish therapies that will

Initial insult to brain tissue

Decreased btood flow to the brain, causes ischemia to cells and issues Anaerobic metabolisni occurs, with increased production of lactic acid and other by-products

Influx of Na, Ca ft water into the celt, with K leaving the cell.

Failure of Na-K pump, and other essential cell

functions

Insuffident ATP prod uctem occurs, and there is a depletion of energy supplies

Celts swell, may burst and cytotoxic edema is created

Ca in the cell causes mitochondria I dysfunction Diminishes energy decreased ATP suppiies, cause even more interfering with normal cell processes

Ca activates lipases and proteases in cell, causes rupture of cell membranes and cell death.

Excessive Ca leads to disruption of capillary function, vasospasm, vasoparalysis, and increased permeability

Worsening unawpling of the blood supply and brain metabolk needs leads to further ischemia and cytotoxic edema. Capillary permeability and dysfunction leads to vasogenic edema

A
Figure 2. A, Pathophysiology of secondary brain injury.

198

Dimensions of Critical Care Nursing

Vol. 23 / No. 5

Increased Intracranial Pressure Management

Worsentflo wwoupltng of the blood supply atid brain metabolic needs leads to further Ischemia and cytotoxic edema. Capillary penneability and dysfunction leads to va5ogenic edema

Neurons are unable to take-up gf utamate from the synaptic space as usual

Inadequate su|^ty of eneryy and ATP for cell use Glutamate accumulates in synapse to exciotoxic ievets

Intracranial pressure increases because of the cytotoxic and vasogenic edema

Increased ICP causes the loss of autoregulation ft CBF becomes dependent on Systemic mean arterial pressure

Excessive amounts of gtutamate result in a prolonged depolarization State, with increased energy demand

More Ha, H20 ft Ca enter cdl, with K ieaving ceil, increased cytotoxic edema

Neurons continue to nre, untji Uiey are exhausted and can no longer repolaHze

Dependence on sy^emic mean arterial pressure results in htaflequate cerebral perfusion pressure, wrth decreased cerebral blood now

Worsening ischemia and overall worsening of clinical picture

B
Figure 2. B, Pathophysiology of secondary brain injury.

maintain a sufficient CBF Un the brain's metabolic needs.-""It is the adequacy of CBF, which is the ultimate predictor of whether the brain tissue will experience ischemia.'-'** (See Table I for factors that affect CBF.)

Hemodynamic Management Hemodynamic management can be the most difficult aspect of caring for patients with brain injuries. There is evidence that following brain injury, vasospasm and changes in perfusion pressure and autoregulation
September/October 2004 199

Increased Intracranial Pressure Management

Factors Affecting Cerebral Blood Flow

Systemic hypotension Anemia Derangement in gas exchange: Retention of carbon dioxide Cerebral vasospasm Increased intracraniai pressure

Summation of Study by Robertson et al for prevention of Secondary Ischemic Insults After Severe Head Injury
Variable iCP MAP CP P ICP-Targeted Protocol <20 >70 >59
SBP>150labetol Map<70 volume, dop3mine, phenylephrine

CBF-Targeted Protocol -20 >90 >70 None MAP < 7 0 volume, dopamine, phenylephrine

occur." These changes and the decrease in CBF that rends to occur after brain injury leads to areas of the brain being ischemic, or bordering on ischemia. If there is any drop in systemic blood pressure (SBP) then a drop in CPP is also likely. This can cause ischemia to develop for those areas of the brain that are already borderline." Patients who exhibit early hypotension, generally defined as a SPB <90 mmHg, have a rate of mortality that is twice as high as patients with a normal blood pressure.'"*'" Most researchers agree that the CPP should be kept at a level of 60 to 70 mmHg or higher in order to maintain a sufficient CBF. Recently there has been an emphasis on maintaining the CPP at levels of 80 mmHg or higher. There is increasing evidence that indicates a significant improvement in outcome when this is done.''^'"*"*'"" However, in order to maintain the CPP at this level, it may be necessary to use increased volume or vasopressors and/or intropic drugs.'-'"'"'*''" The goal is to maintain the hemodynamic status of these patients so that they have a MAP of >90 mmHg and a CPP of >70 mmHg. If a pulmonary artery catheter is used to help manage the volume status, then the pulmonary capillary occlusive pressure is usually kept between 10 and 15 mmHg.'"'** If the VIAPs remain below 90 mmHg and CPP below 70 mmHg, then most protocols call for the use of vasopressor drugs such as dopamine or phenylephrine to increase the MAP and CPP/'' Maintaining the CPP at levels greater than 70 mmHg, sometimes even at the expense of the ICP, has gained popularity in the neurological community.-'*''''---' However, none of the studies reporting improvement in outcomes with this level of CPP were randomized, prospective clinical trials done for this treatment alone. As a result, the improvement in outcome cannot be attributed direaly to the CPP management only.'" In the only class I study designed to test the hypothesis of improved outcome with higher CPP levels,' an ICP-targeted protocol was compared to a CBF-targeted protocol. The primary end-point for the project was the frequency of venous desaturation. Desaturation was measured at the jugular venous bulb, and defined as an oxygen saturation level of less than 50% for more than 10 minutes. The main differences between the 2 protocols are summarized in Table 2.

Hypertension Hypotension

ICP, intracranial pressure; CBF, cerebrai blood flow; MAP, mean arterial pressure; CPP, cerebral perfusion pressure; SBP, systolic blood pressure.

Interestingly, there was no significant difference in outcome between the 2 groups when assessed using the Glascow Outcome Scale at 3 and 6 months. In this study, although the incidence of jugular venous desaturation was significantly decreased in the CBF-targeted protocol, it did not translate into an improved outcome for the patients. As well, it was noted that the incidence of adult respiratory distress syndrome (ARDS) was 5 times greater in the CBF targeted group. Of the patients who did develop ARDS, the greatest risk factor seems to have been related to the greater fluid intake that these patients had in association with the protocol. (They had no comorbidities either preexisting or due to trauma that would predispose them to ARDS.) The development of the ARDS may be one reason why a better outcome was not seen in this group of patients. The development of acute lung injury (ALI) has been associated with a three-fold increase in mortality for patients with head injury.'

Ischemia results in an accumulation of neurotransmitters in the synaptic space.:

Nursing Considerations: Although most nurses working outside of a neuro-ICU will not be caring for patients with CPP monitoring equipment, maintaining an adequate blood pressure remains an important aspect of care to prevent possible ischemia for these patients. These patients may receive volume or inorropic/vasopressor support to maintain blood pressure.^*" However, this remains an area that needs to be further delineated and an area where there is most likely to be change in the treatment patterns of patients with increased ICP.

200

Dimensions of Critical Care Nursing fli Vol. 2 3 / N o . 5

Increased Intracranial Pressure Management Hyperventilation and Normocapnia Hyperventilation to decrease ICP has been a standard treatment modality in brain-injured patients for 20 years or more.''""' Hyperventilarion has been used as an effective and quick way to decrease ICP. This treatment is based on the effect that changes in pH have on cerebral vascultature. A decrease in pH causes vasodilatation of the cerebral vessels. A rise in pH or alkalosis causes vasoconstriction of the cerebral blood vessels. Carbon dioxide is one of the substances that diffuse freely across the BBB. Once across this barrier, it combines with water to form carbonic acid. Carbonic acid freely dissociates to form a bicarbonate ion and hydrogen ion. = H,CO, = + HCO3 As more carbon dioxide diffuses across the BBB, the more hydrt)gen ions there are. As the pH of the cerebral environment becomes more acidotic, vasodilatation occurs. By eliminating the carbon dioxide, the cerebral environment becomes more alkalotic and vasoconstriction occurs. For mechanically ventilated patients this is done by increasing the respiratory rate or increasing the amount of tidal volume to allow the patient to "blown off" CO,.' " " It has been assumed that the vasoconstriction results in a decrease in the ICP. For every decrease in paCO^ by I mmHg, it is estimated that there is a 3% decrease in CBF.""' Increased CO^ = Vasoconstriction and Decreased ICP Decreased CO^ = Vasodilatation and Increased ICP Within the past decade or so, several medical centers have been deviating from the standard use of prophylactic hyperventilation for the control of increased ICP. This is due to numerous studies that have shown that after head injury, CBF is already compromised.'"* Hyperventilation causes a greater reduction in CBF than for increased ICP. Hyperventiiation can reduce the amount of CBF to the point of causing ischemia.*"'"'- " Another effect of hyperventilation is to decrease the amount of oxygen available for the tissues. As the cere-

Euglycemia

Hyperglycemia in patients with increased ICP and other brain injuries has been associated with a worse outcome.''' After brain tissue has been injured, glutamate is released. When glutamate accumulates., it becomes toxic to the ceils." Because glutamate increases the metabolism of the neurons, it causes an increase in the rate of glucose usage by the cells as well. This increase in metabolism when there is insufficient oxygen and glucose, forces the cells to switch to anaerobic metabolism.'"The lactic acid and hydrogen ions, byproducts of anaerobic metabolism, cause cerebral acidosis to develop. The acidosis acts as a key mediator in secondary brain damage via several mechanisms. The acidosis breaks down the ionic channels within the cell walls, allowing sodium, chloride, water, and calcium to enter the cell; this is also a cause of cytotoxic edema. The acidosis causes vasoparalysis and vasodilatation, increasing CBF, and increasing ICP. Acidosis also damages cellular mitochondria and destroys the lipid membrane of the cell, which releases phospholipids and arachiodonic derivatives.' '^ The impaired functioning of the mitochondria worsens the depletion of ATP and interrupts normal cell functions in general. The continued delivery of glucose to the ATPdepleted cerebral tissue has been show to exacerbate ischemic acidosis and to be associated with a higher mortality and morbidity profile for brain-injured patients.'"-'' (See Table 3 for a summation of the effects of acidosis.) Nursing Considerations: Patients with brain damage should be closely monitored to maintain a normal glucose blood serum level between 80 and 120mg/dL. Insulin doses should be titrated to maintain glucose within this range. Intravenous fluids (IVF) and medications should not be mixed in 5% dextrose and water.'" Nutritional replacement, whether by gut or parental means, should be given along with sufficient insulin to maintain a normal blood sugar level.'*"'""

Cerebral Acidosis Factors

Causes:
Disruption of ionic channels in cell walis Vasoparalysis and vasodilatation Damages cellular mitochondria

Results In:
Ailows Ma, Ci, H,0, and Ca 10 flood into the cell; the cell swells and causes cyioioxic edema Increased cerebral blood flow and increased intracranial pressure Less supply of ATP; cell lacks energy and is unable to carr^ out normal cell functions, including maintaining the Na-Kpump

Na, sodium; CI, chloride; H.O, water; Ca, calcium; ATP, adenosine triphosphale; Na-K, sodium potassium.

September/October 2004

201

Increased Intracranial Pressure Management

bral environment becomes more alkalotic, there is a greater affinity of oxygen for the hemoglobin molecule. Oxygen is less readily given up to the brain's tissue as the oxy-hemoglobin curve is shifted to the left. This shift in the oxy-hemogiobin curve can decrease the available oxygen supply by as much as 25%.'" Current Brain Trauma Foundation Guidelines recommend avoiding chronic or prolonged hyperventilation (defined as hyperventilation causing a PaCO, of <15 torr.). The use of hyperventilation is most appropriate to use for the patient vi'ith deteriorating neurologic status that is refractory to other treatment options. Tbe treatments to be used first, listed in order of preference, are:"* Drainage of CSF via the ICP monitoring system. Maintain a CPP of >70 mmHg by maintaining a MAP of >90 mmHg. Administer a bolus of 5% Albumin or Normal Saline bolus of 500 cc to achieve a CVP or 5 to 10 mmHg/ or a PCWP of 10 to 15 mmHg. Use of neosynephrine or dopamine to maintain a MAP of >90 mmHg once the patient is volume loaded. Ativan or morphine for sedation and analgesia.-'"-' Nursing Considerations: Although the option of draining CSF will most likely be unavailable outside the neuro ICU, other options will exist. It is important to maintain an adequate MAP to help support sufficient CPP and to be aware of the changes that can occur in cerebral vasodynamics as a result of changes in blood pH. Optimal Oxygenation After injury to brain tissue occurs, chemical mediators are released, and these cause an increase in cerebral metabolism.^ '* '" In order to meet the increased need for oxygen, especially in the face of decreased amounts of CBF, the brain tissue increases the amount of oxygen it extracts from the blood.'" If tbe oxygen supply in the blood decreases, as with hypoxemia, then the brain tissues are at greater risk for experiencing ischemia. If this occurs, then the ischemia promotes anaerobic metabolism, with an accompanying increase in lactic acid production, acidosis, and development of cytotoxic edema. Another deleterious effect of cerebral hypoxia, particularly if paO, is less than 50 mmHg, is that vasodilatation can occur, which leads to increase CBF and increased ICP.'-^" Nursing Considerations: Patients with increased ICP can be at risk for impaired alveolar-ventilation and derangements of gas exchange. Lung function can be impaired in this population of patients by several mechanisms.
202 Dimensions of Critical Care Nursing Voi. 2 3 / N o . 5

Injury or damage to the respiratory centers may cause alterations in the depth, rate, or pattern of breathing, causing ineffective alveolar ventilation. Changes in mental status can lead to aspiration of gastric contents, a diminished cough reflex, and/or ineffective airway clearance resulting in a ventilation-perfusion mismatch.' Another problem that can develop for these patients is neurogenic pulmonary edema and ALL'-" The mechanisms for the development of neurogenic pulmonary edema and ALI have not been clearly elaborated. However, neurogenic pulmonary edema is associated with a variety of neurologic conditions, including subarachnoid hemorrhage, intracranial hemorrhage, stroke, head trauma, and seizures.''ALI is a known complication of brain injury. It is suspected of being caused, in part, by the inflammatory process that is associated with brain injury and as a complication of the induced arterial hypertension that is frequently used as a treatment in these patients to maintain the CPP."' Because of these factors, it is important to establish and maintain effective airway management early on. This is most effectively accomplished by endotracheal intubation and mechanical ventilation.'Many centers use a rapid intubation sequence when it becomes necessary to mechanically ventilate patients with potentially increased ICP. The rapid intubation sequence is aimed at minimizing tbe noxious stimuli that can be produced by intubation and increase in ICP that can accompany it. The following is an example of rapid sequence intubationr^ Patient is supported with 100% oxygen using a bag/valve/mask device. Lidocaine given as a 1.5 mg/kg bolus; the lidocaine blocks activation of local receptors in airways and inhibits central responses that can elevate ICP in reaction to noxious stimuli. Sedative/hypnotic agent, such as thiopental or etomidate, is administered. A rapid-acting neuroblocking agent is given; succinylcholine or rocuronium are preferred. Thirty seconds after the neuroblocking agent is given; check for jaw relaxation and intubate if present. Confirm tube placement. Within 5 to 8 minutes after intubation, sedate patient as needed with versed 0.1 mg/kg or Ativan 0.05 mg/kg and consider giving analgesia such as morphine sulfate at 0.1 mg/kg. The goal of pulmonary management is to maintain PaO, of 100 mmHg or more at the lowest FiO, possible. The common intervention of suctioning, while necessary to maintain adequate oxygenation, can also

Increased Intracranial Pressure Management increase ICP. To help minimize this effect, different strategies during suctioning have been used, including medicating the patient with IV lidocaine, opiates, or even neuromuscular blocking agents prior to suctioning. Patients should also be hyper-oxygenated before suctioning is begun. Suctioning should be limited to 2 passes of the suction catheter, not exceeding 10- to 15seconds' duration.^' Osmotherapy Increased ICP has been treated with hyperosmolar fluids for several years. The premise is that the increased intra-vascular osmotic gradient helps to move fluid out of the tissues and into the bloodstream, causing tissue dehydration and shrinkage of cells.'' Mannitol is the most commonly used hyper-osmolar fluid in North America.'" It has been shown to reduce ICP within several minutes after its administration.'"This effect is presumably due to its ability to create an osmotic gradient across the cerebral cell membrane and to draw fluid into the blood stream. However, the almost immediate decrease in ICP that results cannot be totally due to the osmotic effect, it is more likely due to the ability of mannitol to expand the plasma almost directly after administration. This expansion of the plasma causes a reduction in the hematocrit and blood viscosity. Mannitol has also been shown to make the RBC membrane more pliable and able to flow through the small cerebral vessels more easily. Together these effects increase CBF and oxygen delivery. This effect may be of greater importance than that of causmg cerebral tissue dehydration."'" Another effect of mannitol is related to its osmotic diuretic effect. As free water is cleared by the kidney, the serum osmolality becomes transiently increased, causing continued dehydration of cerebral tissue.'The Brain Trauma Foundation Guidelines (BTFG) suggest that mannitol be administered as a bolus of 0.25 to 1.0 g/kg every 4 hours, rather than as a continuous infusion. Although there are no randomized, controlled studies concerning the effects of how mannitol is administered, the BTFG advocates administering mannitol as a bolus rather than as a continuous drip." " * This is based on " evidence that indicates when mannitol is given as a continuous drip, it is apt to accumulate in brain tissue when there is a breakdown in the BBB."""^ If mannitol does accumulate in brain tissue, it can cause a reverse osmotic gradient that attracts fluid into the cerebral tissue, creating or worsening vasogenic edema."' If this occurs, tbere will most likely be deterioration in neurologic functioning. Other potentially harmful effects of mannitol are acute congestive heart failure, pulmonary edema, hyperosmolar dehydration, hypotension, and electrolyte imbalances (hyponatremia, hypokalemia, and potentially acute renal failure if serum osmolality exceeds 320 mm osm.*" Nursing Considerations: Patients with intracranial injuries should be kept in a euvolemic (normal volume) state during treatment with mannitol. The patient's fluid status can be determined by measuring central venous pressure and/or pulmonary artery occlusive pressure {which should be kept near 10-15 mmHg)."-'Serum osmolality and electrolyte values should be done every 4 to 6 hours and monitored closely. The serum osmolality should be kept below 320 mm osm, along with maintaining an accurate intake and output (I&O).--'These patients need to be closely monitored for adverse side effects that can be caused by mannitol (eg, pulmonary edema, congestive heart failure, hypotension, fluid and electrolyte imbalances). Although mannitol is a standard treatment for increased ICP, there are no studies that show either that it provides a benefit to this population or patients, or that it is detrimental; this is still to be proven.''*'' Controlling Cerebral Metabolism By controlling the brain's metabolism, or at least slowing it down, it is possible to reduce the brain's need for oxygen and glucose, and thereby to decrease the blood supply to the brain. This helps to reduce ICP. Sedation is a means of helping to decrease the brain's metabolism and it is sometimes a neglected aspect of controlling increased ICP.-A patient with decreased intracranial compliance, who is not synchronized with the ventilator, will experience increased intra thoracic pressure, which is transmitted to the cerebral circulation via increased jugular venous pressure. In addition, agitation contributes to arterial hypertension and causes increased ICP.-'Sedatives can also help to blunt the patients response to noxious stimuli.'A combination of morphine and a short-acting benzodiazapine (eg, Ativan or Versed), is commonly used for patients with intracrania! injuries. The advantage of these drugs is that they can usually be titrated to allow for a continuous neurologic examination and their effects can be reversed.'-' Additionally, the benzodiazapines tend to be well tolerated by blood pressure and are effective agents for reducing cerebral metabolism and increased ICP.'"They are usually reserved for patients who are mechanically ventilated. When used for prolonged periods, narcotics and benzodiazapines (or their metabolites) can accumulate and cause extended sedation, interfering with neurologic assessments. This prolonged sedative effect can continue for several days, even after drips have been discontinued. An option to avoid this problem is to use the agent propofol (Diprivan). This

September/October 2004

203

Increased Intracranial Pressure Management is a fast-acting, nonbenzodiazapine sedative/hypnotic, that rapidly crosses the BBB. It also has a short duration of action. This profile allows propofol to be quickly weaned off, so a thorough neurologic assessment can be made, and then the drug can be rapidly titrated up to increase the level of sedation as needed.^'"''' At times, in addition to sedatives and analgesic agents, nondepolarizing neuroblocking agents are also required. These agents do not decrease ICP, but they do decrease the systemic oxygen consumption and carbon dioxide production. Paralysis also prevents coughing and gagging reflexes, which can increase ICP during suctioning. Neuromuscular paralysis should not be routinely used in this patient population. A retrospective study done by Hsiang et al. in 1994, showed that early use of neuromuscular blockade did not seem to effect the long-term outcome for brain-injured patients either positively or negatively." However, paralysis did cause detrimental side effects, such as prolonged ICU stay, increased pneumonia, and more sepsis.''^ '* Also, when these agents are used for patients with increased ICP, other factors must be considered. Once effective neuroblockade has been achieved, it is not possible to do a neurologic assessment. The possibility of missing a significant change in neurologic status that would indicate deterioration is a serious risk that must be well planned. Another difficulty is that paralysis can mask seizure activity in a patient. This can be very injurious, as seizure activity can increase brain metabolism dramatically.' Nursing Considerations; Patients who are paralyzed using neuromucscular blockers are in a very vulnerable, susceptible position and are supremely dependent on their nurse. Unable to move, these patients can be very much aware of their surroundings, susceptible to pain and emotional distress, except they cannot communicate this to others. These patients should always be treated with a generous amount of analgesic and antianxiety medications, preferably by a continuous drip to ensure constant effect. These drugs should be given simultaneously with the neuromuscular blockade. Additionally, frequent reassurance, and explanations of care and the environment should be given to these to patients.'"'"' If a patient who is neuro-blockaded becomes disconnected from the ventilator, the occurrence can be fatal. Therefore, they must be monitored especially closely. Because these patients do not become restless, and usually look quite peaceful, it can sometimes lead to less vigilante monitoring."'^" Barbituate Coma High doses of barbiturates have been known to reduce ICP since the 1930s."' Barbiturate coma as a treatment
204 Dimensions of Critical Care Nursing Vol. 23 / No, 5

for the control of ICP has long been a standard of practice in the care of patients with increased ICP. However, in the past decade the effectiveness of this treatment has been questioned, because research has shown ambiguous results.''"^'^'The Brain Trauma Foundation Guidelines suggest that barbiturate coma should not be used prophalactically. Rather, it should be reserved for the estimated 10 to 15% of patients who will develop intractable increased ICP." '" These are patients who do not respond to maximal treatment for increased ICP (ie, CSF drainage, mannitol and hyperventilation, and surgical intervention if appropriate). For these patients the mortality rate is 84 to 100% without reduction of ICP."* Research does support the use of barbiturate come for these patients if they are hemodynamically stable and considered salvageable.'" In spite of these recommendations and lack of supporting research, a recent survey of treatment regimens at various medical centers in the United States and United Kingdom, conducted in 1995 and 1996, showed that the use of barbiturates continues to be used in 33% of ICUs in the United States and in 56% of ICUs in the United Kingdom.'"-^' Barbiturates act on the CNS to inhibit neurotransmittors. They act within the reticular formation, which is responsible for relaying impulses to the cerebral cortex. The reticular formation also helps to regulate attention, awareness and sleep, and cardiac and motor functions." Barbiturates affect their hypnotic and sedative effects by decreasing the number of impulses reaching the cerebral cortex.'''' This is also the mode of action responsible for decreasing cerebral metabolism. By reducing cerebral metabolism, the demand for glucose and oxygen is decreased. This causes a corresponding decrease in CBF, which serves to help decrease cerebral volume and ICP.* Nursing Considerations: A major side effect of barbiturates is hypotension; and whenever the MAP is decreased, there is a drop in CPP. It is by this mechanism that the benefits of decreased cerebral metabolism can be offset, and why the use of barbiturate coma can cause more harm than benefit."* Patients treated with barbiturate coma will frequently need to be treated with vassopressors or inotropic agents to maintain an adequate blood pressure." Another problem with barbiturate coma is that there can be a depression of respiratory drive, so these patients need to be monitored for bypoventilation and hypoxia. Furthermore, patients treated by these means arc prone to developing hypothermia and they will need to be closely monitored for decreased body temperatures. Given that barbiturate coma makes it impossible to do a neurologic assessment, patients so treated will need to have ICP moni-

Increased Intracranial Pressure Management be avoided.^'" "' The IV solution of dilantin is extremely alkaline; it has a pH of 12. If infiltration occurs, serious tissue damage can result. The loading dose of dilantin should he followed by a dosing regimen, either orally or intravenously, that will maintain a plasma level of 40 to 80 umol/L.' " Furthermore, if dilantin is used to prevent early onset of seizures, then the nurse should be alert for any rashes that may be caused by the dilantin. Approximately 2 to 5% of patients will develop a rash; if this happens, then the drug should be stopped. Although rare, an exfoliative dermatitis (Steven-Johnson Syndrome) can develop and is potentially fatal.''^ Role of Glucocorticoids The beneficial effects of glucocorticoids on patients suffering from cerebral edema due to tumors or after surgery was first reported in 1961.'"In the years following this Initial report, clinical trials on the effectiveness of steroids have yielded ambiguous results. Clinical results have suggested that glucocorticoids might be helpful, or that they might be harmful, but no conclusive and convincing evidence has yet been produced."""*" As a result, the Brain Trauma Foundation Guidelines have suggested that steroids not be used to treat intracranial edema except for that associated with brain tumors or to reduce the amount of CSF that is produced.'" What is required is a large randomized trial to conclusively prove what effect steroids have on brain tissue that has been injured. Based on some animal models, steroids may have some beneficial effects in assisting recovery. In the animal models the window of opportunity for benefit occurred early after the initial injury. Many of the trials that have been conducted may have been outside this window of opportunity.''" Because of the large number of head traumas that occur worldwide each year and the fact that they tend to involve young people, the effect of head trauma is enormous and expensive in monetary and human terms. If steroids can be shown to improve outcomes even by only 2%, the number of people that would be salvaged would be quite significant. However, for a clinical trial to have the power to detect a 2% decrease in morbidity or mortality, the clinical trial would have to be rather large, enrolling 10,000 to 20,000 patients.*' At present, the use of steroids for increased intracranial pressure due to cerebral edema is not supported by the evidence. Furthermore, steroids have been associated with increased infection rates and episodes of hyperglycemia, which may worsen the outcome for patients.'" In spite of the lack of research to support the uses of glucocorticoids and the recommendation by the Brain Trauma Foundation Guidelines, there is anecdotal evidence that many centers continue to use steroids in this setting."""

An effect of hyperventilation is to decrease the amount of oxygen available for the tissues. I
toring instituted. In addition, because of the serious side effects that this treatment can cause, these patients should also have a pulmonary artery catheter inserted to allow for close monitoring of hemodynamics, and of course these patients are mechanically ventilated.' Anticonvutsant Prophylaxis Development of seizures with increased intracranial pressure is not easily predicted, but the consequences of seizure activity can dramatically worsen the situation of a patient with increased lCP." Seizures can lead to aspiration pneumonia, exacerbation of secondary head injuries, and an overall poorer outcome for braininjured patients.' The rate of seizures is higher for patients with a Glascow Coma Scale (GCS) of <10, depressed skull fracture, subdural hematoma, epidural hematoma, or intracranial hematoma. Seizures are generally classified as early occurring and late occurring, with the cut off being 7 days from the initial injury.'" A recent meta-analysis of the effectiveness of administering prophylactic antiepileptic drugs for the prevention of seizures after brain injury showed that there is probably no reduction in late onset seizures. However, prophylactic administration of dilantin is effective in preventing early onset seizures.*' Nonetheless, the research does not show any improvement in mortality or prevention of neurologic disability associated with the use of dilantin prophylaxis."-''' Nursing Considerations: If Dilantin is used to prevent early onset seizures, then a loading dose of 20 mg/kg (approximately 1400 mg for a 70 kg patient) is used to achieve therapeutic levels.''^ Dilantin should be administered no faster than 50 mg/min or 28 minutes for this dose; if dilantin is given too quickly, hypotension and circulatory collapse is possible.*^*'' Although it is not recommended by the manufacturer, several medical centers do drip a loading dose of dilantin, rather than having one staff member occupied for almost 30 minutes.''^" Another consideration for dripping the loading dose is that it can be placed on an intravenous (IV) pump and the dose is given more consistently than if it is given as an fV push. If the dilantin loading dose is dripped, it should only be mixed in normal saline and a 22-micron filter is used.^* It is best to use a central line if possible, and the veins in the back of the hand should

September/Ortober 2004

205

Increased Intracranial Pressure Management

Maintenance of Normothermia
The injured brain is especially vulnerable to changes in body temperature; an increased temperature causes an increase in cerebral metabolism and an increase in CBF and intracranial pressure. It is estimated that for every 1-degree increase in temperature above normal (centigrade degrees) the brains metabolism and oxygen consumption increases by 7%.' An increase in temperature can also shift the oxy-hemoglohin curve to the right, decreasing the amount of oxygen the hemoglobin molecule carries, and decreasing the oxygen available to the cerebral tissues.'" Recent research has suggested that indomethicin may be a beneficial nonsteroldal antiinflammatory drug to be used in treating fevers in patients with increased ICP. This is due to the effects that indomethicin has to help reduce CBF and IGP in animal models; the proposed mechanism of action is that indomethicin causes vasoconstriction of blood vessels and disrupts prostaglandin synthesis.^** Nursing Considerations: Fever should be treated aggressively in these patients; antipyretics should be given; sponge baths and tbe use of cooling blankets are all appropriate measures for reducing fever.'However, care should be taken to avoid allowing these patients to shiver, as shivering can increase intracranial pressure. Thus, if a cooling blanket is used, it is suggested that the blanket be turned off when the patient's temperature reaches 38C, so that the fever is not reduced too rapidly or too much.'

Research is increasingly being used to help validate or disprove standard therapies, while customary modes of treating conditions are increasingly being challenged, changed, and reassessed. It is necessary that all healthcare professionals stay current of these developments. However, this becomes increasingly difficult to do outside of one's expertise. Because of the number of conditions that may result in increased intracranial pressure, critical care nurses who do not specialize in neurologic critical care tnay find themselves caring for these patients. The critical care nurse may be unfamiliar with the recent Brain Trauma Foundation Guidelines or other trends for treating neurologic patients. It is hoped that this article will act both as a review of the pathophysiology of increased ICP, as well as a guide to several of the current treatments being used.

References
1. Arbour R. Aggressive management of intracranial dynamics. Crit Care Nurse. 1999;18(3):30-40. 2. Mayer S, Chong J. Critical care management of increased inrracranial pressure. / of Intensive Care Med. 2000;17i5567. 3. Robertson C, Valadka A, Hannay H, Contanr C, Gopinath S, Cormio M, et al. Prevention of secondary ischemic insults after severe head injtiry. Crit Care Med. 1999;10:2086-2095. 4. Fortune J, Feustel P, Graca I., Hasselbarrh J, Kuehier D. Effect of hyperventllation, mannitol, and ventriculostomy drainage on cerebral blood flow after head injury [Edirorial]./ Trauma. 199.5;6:1091-1099. 5. Slavik R, Rhoney D. Pharmacological management of severe traumatic hrain injtiry: an evidence-based review. / Inform Pharm. 2000;3:309-335. 6. Mokri B. The Monro-Kellie hypothesis; applications in CSF volume depletion. Neurology. 2001;56:l746-1748. 7. Boss B. Concepts of neurologic dysfunction. In K McCance, S Heurher, eds. Pathophysiology: The Biological Basts for Disease ifi Adults and Children, 3rd ed. St Louis, Mo: Mosby Inc; 1998:460-504. 8. Davis A, Briones T. Neurological clinical physiology. In McKinney M et al, eds. ACCN Clinical Reference for Critical Care Nursing, 4th ed. St. Louis, Mo: Mosby inc; 1998. 9. Zuccarelli LA. Altered cellular anatomy and physiology of acute brain injury and spinal cord injury. Crit Care Nurs Clin N Awer. 2000;4:403-412. 10. Nikas D. The neurologic system. In j Alspacb, ed. Core Curriculum for Critical Care Nursing. 5th ed. Philadelphia, Pa: Saunders; 1998:339-399. 11. Wong F. Prevention of secondary brain injury. Crit Care Nurse. 1000;S:\S'17. 12. Littlejohn LR, Bader MK. Guidelines for the management of severe head trauma: clinical application and changes in practice. Crit Care Nurse. 2001;6:48-65. 13. Rubin LL, Staddon JM. The cell biology of the blood brain barrier. Ann Rev Neurosci. 1999;22:l 1-28. 14. Schwarz S, Schwab S, Betram M, Aschoff A, Werner H. Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke. Stroke. 1998;29:1550-I555. 15. Nieoullon A, Had-Aissouni L, Kerkerian-le Goff L. Excitotoxicity and the putative involvement of excitatory amino acids in neurodcgencrative diseases. / AppI Biomed. 2003:1:1-5. 16. Zorumski CF. The physiology and pharmacology of atnino acid neurotransmittor systems. Neurotransmtttor Review. 1997;2:120-124.

Therapeutic Hypothermia
Therapeutic hypothermia counters several of the mechanisms of secondary brain injury. It decreases cerebral metabolism and helps to lower the demand for oxygen by the brain, thereby decreasing the need for blood flow, and decreasing intracranial pressure.'" Inducing hypothermia as a method of controlling increased intracranial pressure has shown promise in improving the outcomes of patients with brain injury in several small trials. However, patients who are hypotbermic may sustain more complications and have a longer hospital stay versus patients of normal temperature. Therefore, at present, hypothermia is not regarded as an appropriate first line treatment for patients with increased ICP. However, it seems to be most effective for patients wbo develop refractory increased ICP that is not responsive to barbiturate therapy.

CONCLUSION
Healthcare continues to become more complex, with new technologies, monitoring techniques, and medications rapidly being added to the armamentarium.
206 Dimensions of Critical Care Nursing Vol. 2 3 / N o . 5

Increased Intracraniai Pressure Management

17. Berger C. Schabitz WR, Georgiadis D, Steiner T, Aschoff A. Schwab S. Effects of hypothermia on excitatory amino acids and metabolism in stroke patients. Stroke. 2002;33:5l9-524. 18. Bullock MR, Chestnut RM. Clifton GL, Ghagar J, Marion DW, Narajan RK, er al. Management and Prognosis nf Serere Traumatic Brain Injury. New York, NY: Brain Trauma Foundation and American Association of Neurological Surgeons; 2000. 19. Robertson C. Management of cerebral perfusion pressure after traumatic brain injury. Anesthesiology. 2001;6:1513-1517. 20. Rosner JM, Rosner SD, Johnson AH. Orebral perfusion pressure: management protocol and clinical results, / Neurosurg. 1995,83:949-962. 21. Trauma.org. Controi of Intracramal Hypertension. Available at: www.trauma.org/neuro/icpcontrol.html. Accessed July 1, 2003. 22. Chestnut R.M, Guidelines for the management of severe head injury: what we know and what we think we know. / Trauma. 1997';42(5S):12S-22S. 23. Bader MK, Palmer S. Keeping the brain in the zone: applying the severe head injury guidelines to practice. Crit Care Nurs CUn N Amer. 2000:4:413-428. 24. Schneck MJ. Treating elevated intracranial pressure: Do we raise or lower the blood pressure? [Editorall Crit Care Med. ]998;tl:1787-1788. 25. Juul N, Morris CIF, Marshall SB. The Executive Committee of the Alternation Selfotel Trial and Marshall I.F. Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. yN^:/rosrg. 2000;92:l-6. 26. Drummond JC, Patel PM, Cole DJ, Paul J. The effect of the reduction of colloid reduction ot oncotic pressure, with and without reduction of osmolality, on post traumatic cerebral edema. Anesthesioi. 1998;88:993-1002. 27. Grande PO, Asbeirsson B, Nordstrom CH, Volume targeted therapy of increased intracranial pressure: the Lund concept unifies surgical and non-surgical treatments. Ada AnaesthesioiScand. 2002;46:929-941. 28. Eker C, Asgeirsson B, Grande PO, Schalen W. Nordstrom CH. Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation. Crit Care Med. 1998; 11:1881-1886. 29. Adams HP, Adams RJ, Brott T, et al. Guidelines for the early management of patients with ischemic stroke. A scientific statement from the Stroke Council of the American Stroke Association. Stroke. 2003;34:1056-1083. 30. Bruno A, Biller J, Adams HP, et al. Acute blood glucose levels and outcomes from ischemic stroke. Neurology. I999;52:280291. 31. Smith WS, Matthay MA. Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema. Chest. 1997;111:1326-1333. 32. Venkatesan AM, Karmpaliotis D, Silverman ES. Neurogenic pulmonary edema following catastrophic subarachnoid hemorrhage: a case report and patbophysiologic review. J Intens Cure Mfd.2001;16:236. 33. Schierhout GR. Mannitol for acute traumatic brain injury [abstract]. 2002. Cochrane Review. The Cochrane Library, 2. Oxford, UK: Update Software Ltd. 34. Bereczki D, Lui M, do Prado GM, Hekete I. A systematic review of mannitol therapy for acure iscbemic stroke and cerebral parencbymal hemorrhage. Stroke. 2000;31:27192722. 35. Manno E.M, Adams RF, Derdeyn CP, Powers WJ, Diringer MN. The effects of mannitoi on cerebral edema after large hemispheric cerebral infarct. Neurology. 1999:52:583-593. 36. Arbour R. Sedation and pain management in critically ill adults. Crit Care Nurse. 2000;20:39-55. 37. Hsiang jK, Chestnut RM, Crisp CB, Klauber MR, Blunt BA, Marshall L. F.arly, routine paralysis for intracranial pressure control in severe bead injury: is it necessary? Crit Care Med. 1994;9:1471-1476. 38. Cruz J. Adverse effect of pentobarbital on cerebral oxygenation of comatose patients with acute traumatic brain swelling: relationship to outcome. / Netirostirg. 1996;5:758-761. 39. Henderson CL. Using the peripheral nerve stimulator to guide neuromuscular blocking agent doses. Crit Care Nurse. November 1999 (online). 40. Loyola R, Dreber MH. Management of pharmacologically induced neuromuscular blockade using peripheral nerve stimulation. nCCN. 2003:4:157-165. 41. Roberts I. Barbiturates for acute traumatic brain injury. (Abstract) Cochrane Review. The Cochrane Library, 2003;3. Oxford, UK: Update Software Ltd. 42. Roberts 1, Schierhout G, Aldcrson P. Absence of evidence for the effectiveness of five interventions routinely used in the intensive care management pf severe head injury: a systemic review, j Neural Neurosurg Psychiatry. l998;65:729-733. 43. Jecvaratnum DR, Menon DK. Survey of intensive care of severely bead injured patients in the United Kingdom. Brit MfJ/.'l996;314:1855-1859. 44.1.ehane RA. Pharmacology for Nursmg Care, 4th ed. Philadelphia, Pa: Saunders; 2001. 45. Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury. Report of the Quality Subcommittee of the American Academy of Neurology. Neurology. 2OO3;6O:IO-16. 46. Pbenytoin Sodium Injection, USP. Parke-Davis, Division of Warner Lambert Company. Prescriptive information for pbenytoin drug manufacturer. Available at: bttp://www. oralcbelation.com/faq/ dilantml. btm#DOSAGE%20AND%20ADMINlSTRATION, Accessed July 12,200.3. 47. Alderson P, Roberts 1. Corticosteroids in acute traumatic brain injury: systematic review of randomised controlled trials. Brit Med). l'997;314:1885. 48. Yates D, Roberts L Corticosteroids in head injury [Editorials). Brit Med J. 2000;32l:128-129. 49. Gadkary CS, Alderson P, Signormi DF. Theraputic hypothermia for bead injury [Abstract). Cochrane Review. The Cocbrane Library. 2002;2. Oxford, UK: Update Software Ltd.

ABOUT THE AUTHOR L i n d a J o s e p h s o n , RN, BSN, CCRN, is currently employed at University of Massachusetts Memorial Medical Center in the cardiac and medical intensive care unit as a staff nurse. She has over 20 years of experience in critical care nursing. She is currently a matriculated student at University of Massachusetts Medical School in Worcester at the Graduate School of Nursing, and expects to graduate in June 2005 from the nurse educator tract. Address correspondence and reprint requests to Linda Josepbson, RN, BSN, CCRN. 153 Uncatena Ave, Worcester, MA 01606 (iinda@powerguide.com).

September/October 2004

207