Increased Intracranial Pressure
The rigid cranial vault contains brain tissue (1,400 g), blood (75 mL), and CSF (75 mL) (Hickey, 2003). The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP. ICP is usually measured in the lat-eral ventricles; normal ICP is 10 to 20 mm Hg (Hickey, 2003).
The Monro-Kellie hypothesis states that because of the lim-ited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others. Because brain tissue has limited space to change, compensation typically is accomplished by displacing or shifting CSF, increas-ing the absorption of CSF, or decreasing cerebral blood volume. Without such changes, ICP will begin to rise. Under normal cir-cumstances, minor changes in blood volume and CSF volume occur constantly due to alterations in intrathoracic pressure (coughing, sneezing, straining), posture, blood pressure, and sys-temic oxygen and carbon dioxide levels.
Increased ICP is a syndrome that affects many patients with acute neurologic conditions. This is because pathologic conditions alter the relationship between intracranial volume and pressure. Although an elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other condi-tions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies. Increased ICP from any cause de-creases cerebral perfusion, stimulates further swelling (edema), and shifts brain tissue through openings in the rigid dura, result-ing in herniation, a dire, frequently fatal event.
Increased ICP may significantly reduce cerebral blood flow, re-sulting in ischemia and cell death. In the early stages of cerebral ischemia, the vasomotor centers are stimulated and the systemic pressure rises to maintain cerebral blood flow. Usually a slow bounding pulse and respiratory irregularities accompany this. These changes in blood pressure, pulse, and respiration are im-portant clinically because they suggest increased ICP.
The concentration of carbon dioxide in the blood and in the brain tissue also has a role in the regulation of cerebral blood flow. A rise in carbon dioxide partial pressure (PaCO2) causes cerebral vasodilatation, leading to increased cerebral blood flow and in-creased ICP; a fall in PaCO2 has a vasoconstrictive effect (Young, Ropper & Bolton, 1998). Decreased venous outflow may also in-crease cerebral blood volume, thus raising ICP.
Cerebral edema or swelling is defined as an abnormal accumula-tion of water or fluid in the intracellular space, extracellular space,or both, associated with an increase in brain tissue volume. Edema can occur in the gray, white, or interstitial matter. As brain tissue swells within the rigid skull, several mechanisms at-tempt to compensate for the increasing ICP. These mechanisms include autoregulation and decreasing the production and flow of CSF. Autoregulation refers to the brain’s ability to change the diameter of its blood vessels automatically to maintain a constant cerebral blood flow during alterations in systemic blood pressure.
As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage. The brain can maintain a steady perfusion pressure when the arterial systolic blood pressure is 50 to 150 mm Hg and ICP is less than 40 mm Hg. The cerebral perfusion pressure is calculated by subtracting the ICP from the mean arterial pressure. For example, if the mean arterial pressure is 100 and the ICP is 15, then the cerebral per-fusion pressure is 85 mm Hg. The normal cerebral perfusion pressure is 70 to 100 mm Hg (Hickey, 2003; Young et al., 1998). As ICP rises, however, and the autoregulatory mechanism of the brain is overwhelmed, cerebral perfusion pressure can rise to greater than 100 mm Hg or fall to less than 50 mm Hg. Patients with a cerebral perfusion pressure less than 50 mm Hg experience irreversible neurologic damage. If ICP equals mean arterial pres-sure, cerebral circulation ceases (Porth, 2002).
A clinical phenomenon known as the Cushing’s response (or Cushing’s reflex) is seen when cerebral blood flow decreases significantly. When ischemic, the vasomotor center triggers a rise in arterial pressure in an effort to overcome the increased ICP. A sympathetically mediated response causes a rise in the systolic blood pressure with a widening of the pulse pressure and cardiac slowing. This response, which is mediated by the sympathetic nervous system, is seen clinically as a rise in systolic blood pres-sure, widening of the pulse pressure, and reflex slowing of the heart rate. This is a sign requiring immediate intervention; how-ever, perfusion may be recoverable if treated rapidly.
At a certain volume or pressure, the brain’s ability to auto-regulate becomes ineffective and decompensation (ischemia and infarction) begins (Young et al., 1998). When this occurs, the pa-tient exhibits significant changes in mental status and vital signs. The bradycardia, hypertension, and bradypnea associated with this deterioration are known as Cushing’s triad, a grave sign. At this point, herniation of the brain stem and occlusion of the cerebral blood flow occur if therapeutic intervention is not initiated. Her-niation refers to the shifting of brain tissue from an area of high pressure to an area of lower pressure (Fig. 61-2).
The herniated tissue exerts pressure on the brain area to which it has herniated or shifted, interfering with the blood supply in that area. Cessa-tion of cerebral blood flow results in cerebral ischemia and in-farction and brain death.
When ICP increases to the point at which the brain’s ability to adjust has reached its limits, neural function is impaired; this may be manifested by clinical changes first in LOC and later by abnormal respiratory and vasomotor responses.
Any sudden change in the patient’s condition, such as rest-lessness (without apparent cause), confusion, or increasing drowsi-ness, has neurologic significance. These signs may result from compression of the brain due to swelling from hemorrhage or edema, an expanding intracranial lesion (hematoma or tumor), or a combination of both.
As ICP increases, the patient becomes stuporous, reacting only to loud auditory or painful stimuli. At this stage, serious impair-ment of brain circulation is probably taking place, and immedi-ate intervention is required. As neurologic function deteriorates further, the patient becomes comatose and exhibits abnormal motor responses in the form of decortication, decerebration, or flaccidity (see Fig. 61-1). When the coma is profound, with the pupils dilated and fixed and respirations impaired, death is usu-ally inevitable.
The diagnostic studies used to determine the underlying cause of increased ICP. The patient may undergo cerebral angiography, computed tomography (CT) scanning, magnetic resonance imaging (MRI), or positron emis-sion tomography (PET). Transcranial Doppler studies provide information about cerebral blood flow. The patient with increased ICP may also undergo electrophysiologic monitoring to monitor cerebral blood flow indirectly. Evoked potential monitoring mea-sures the electrical potentials produced by nerve tissue in response to external stimulation (auditory, visual, or sensory). Lumbar puncture is avoided in patients with increased ICP because the sudden release of pressure can cause the brain to herniate.
Complications of increased ICP include brain stem herniation, diabetes insipidus, and syndrome of inappropriate antidiuretic hormone (SIADH).
Brain stem herniation results from an excessive increase in ICP, when the pressure builds in the cranial vault and the brain tissue presses down on the brain stem. This increasing pressure on the brain stem results in the cessation of blood flow to the brain, causing irreversible brain anoxia and brain death.
Diabetes insipidus is the result of decreased secretion of anti-diuretic hormone. The patient has excessive urine output, and hyperosmolarity results (Young et al., 1998). Therapy consists of administration of fluid volume, electrolyte replacement, and va-sopressin (desmopressin, DDAVP) therapy.
SIADH is the result of increased secretion of antidiuretic hor-mone. The patient becomes volume-overloaded, urine output di-minishes, and serum sodium concentration becomes dilute. Treatment of SIADH includes fluid restriction, which is usually sufficient to correct the hyponatremia; severe cases call for judi-cious administration of a 3% hypertonic saline solution (Hickey, 2003). Patients with chronic SIADH may respond to lithium car-bonate or demeclocycline, which reduces renal tubule respon-siveness to antidiuretic hormone.
Increased ICP is a true emergency and must be treated promptly. Invasive monitoring of ICP is an important component of man-agement, but immediate management to relieve increased ICP involves decreasing cerebral edema, lowering the volume of CSF, or decreasing cerebral blood volume while maintaining cerebral perfusion (Cunning & Houdek, 1999). These goals are accom-plished by administering osmotic diuretics and corticosteroids, restricting fluids, draining CSF, controlling fever, maintaining systemic blood pressure and oxygenation, and reducing cellular metabolic demands. Judicious use of hyperventilation is recom-mended only if the ICP is refractory to other measures.
The purposes of ICP monitoring are to identify increased pressure early in its course (before cerebral damage occurs), to quantify the degree of elevation, to initiate appropriate treatment, to provide access to CSF for sampling and drainage, and to evaluate the ef-fectiveness of treatment. An intraventricular catheter (ventricu-lostomy), a subarachnoid bolt, an epidural or subdural catheter, or a fiberoptic transducer-tipped catheter placed in the subdural space or the ventricle can be used to monitor ICP (Fig. 61-3).
When a ventriculostomy or ventricular catheter monitoring device is used for monitoring ICP, a fine-bore catheter is inserted into a lateral ventricle, usually in the nondominant hemisphere of the brain (Hickey, 2003). The catheter is connected by a fluid-filled system to a transducer, which records the pressure in the form of an electrical impulse. In addition to obtaining continu-ous ICP recordings, the ventricular catheter allows CSF to drain, particularly during acute rises in pressure. The ventriculostomy also can be used to drain the ventricle of blood. Also, continuous drainage of ventricular fluid under pressure control is an effective method of treating intracranial hypertension. Another advantage of an indwelling ventricular catheter is the access it provides for the intraventricular administration of medications and the instil-lation of air or a contrast agent for ventriculography. Complica-tions include ventricular infection, meningitis, ventricular collapse, occlusion of the catheter by brain tissue or blood, and problems with the monitoring system.
The subarachnoid bolt (or screw) is a hollow device inserted through the skull and dura mater into the cranial subarachnoid space (Hickey, 2003). It has the advantage of not requiring a ven-tricular puncture. The subarachnoid screw is attached to a pres-sure transducer, and the output is recorded on an oscilloscope. The hollow screw technique has the advantage of avoiding com-plications from brain shift and small ventricle size. Complications include blockage of the screw by clot or brain tissue, which leads to a loss of pressure tracing and a decrease in accuracy at high ICP readings.
An epidural monitor uses a pneumatic flow sensor that func-tions on a nonelectrical basis. This pneumatic epidural ICP monitoring system has a low incidence of infection and complications and appears to read pressures accurately. Calibration of the system is maintained automatically, and abnormal pressure waves trig-ger an alarm system. One disadvantage of the epidural catheter is the inability to withdraw CSF for analysis.
A fiberoptic monitor, or transducer-tipped catheter, is be-coming a widely used alternative to standard intraventricular, subarachnoid, and subdural systems (Hickey, 2003). The minia-ture transducer reflects pressure changes, which are converted to electrical signals in an amplifier and displayed on a digital moni-tor. The catheter can be inserted into the ventricle, subarachnoid space, subdural space, or brain parenchyma or under a bone flap. If inserted into the ventricle, it can also be used in conjunction with a CSF drainage device.
Waves of high pressure and troughs of relatively normal pressure indicate changes in ICP. Waveforms are captured and recorded on an oscilloscope. These waves have been classified as A waves (plateau waves), B waves, and C waves (Fig. 61-4). The plateau waves (A waves) are transient, paroxysmal, recurring ele-vations of ICP that may last 5 to 20 minutes and range in ampli-tude from 50 to 100 mm Hg (Hickey, 2003). Plateau waves have clinical significance and indicate changes in vascular volume within the intracranial compartment that are beginning to com-promise cerebral perfusion. A waves may increase in amplitude and frequency, reflecting cerebral ischemia and brain damage that can occur before overt signs and symptoms of raised ICP are seen clinically. B waves are shorter (30 seconds to 2 minutes), with smaller amplitude (up to 50 mm Hg). They have less clinical significance, but if seen in runs in a patient with depressed con-sciousness, they may precede the appearance of A waves. B waves may be seen in patients with intracranial hypertension and de-creased intracranial compliance. C waves are small, rhythmic os-cillations with frequencies of approximately six per minute. They appear to be related to rhythmic variations of the systemic arte-rial blood pressure and respirations.
Osmotic diuretics (mannitol) may be given to dehydrate the brain tissue and reduce cerebral edema. They act by drawing water across intact membranes, thereby reducing the volume of brain and extracellular fluid. An indwelling urinary catheter is usually inserted to monitor urinary output and to manage the re-sulting diuresis. When a patient is receiving osmotic diuretics, serum osmolality should be determined to assess hydration sta-tus. Corticosteroids (eg, dexamethasone) help reduce the edema surrounding brain tumors when a brain tumor is the cause of increased ICP.
Another method for decreasing cerebral edema is fluid restric-tion (Hickey, 2003). Limiting overall fluid intake leads to dehy-dration and hemoconcentration, drawing fluid across the osmotic gradient and decreasing cerebral edema. Conversely, overhydra-tion of the patient with increased ICP is avoided, as this will in-crease cerebral edema.
It has been hypothesized that lowering body temperature will decrease cerebral edema, reduce the oxygen and metabolic re-quirements of the brain, and protect the brain from continued is-chemia. If body metabolism can be reduced by lowering body temperature, the collateral circulation in the brain may be able to provide an adequate blood supply to the brain. The effect of hypothermia on ICP requires more study (Slade, Kerr & Marion, 1999), but as yet induced hypothermia has not been proven to be beneficial in the brain-injured patient (Clifton, Miller, Choi et al., 2001). Inducing and maintaining hypothermia is a major clini-cal procedure and requires knowledge and skilled nursing obser-vation and management.
The cardiac output may be manipulated to provide adequate perfusion to the brain. Improvements in cardiac output are made using fluid volume and inotropic agents such as dobutamine hydro-chloride. The effectiveness of the cardiac output is reflected in the cerebral perfusion pressure, which is maintained at greater than 70 mm Hg (Young et al., 1998). A lower cerebral perfusion pres-sure indicates that the cardiac output is insufficient to maintain adequate cerebral perfusion.
CSF drainage is frequently performed because the removal of CSF with a ventriculostomy drain may dramatically reduce ICP and restore cerebral perfusion pressure. Caution should be used in draining CSF because excessive drainage may result in collapse of the ventricles.
Hyperventilation, which results in vasoconstriction, has been used for many years in patients with increased ICP. Recent re-search has demonstrated that hyperventilation may not be as ben-eficial as once thought (Hickey, 2003). The reduction in the PaCO2 may result in hypoxia, ischemia, and an increase in cere-bral lactate levels. Maintaining the PaCO2 at 30 to 35 mm Hg may prove beneficial. Hyperventilation is indicated in patients whose ICP is unresponsive to conventional therapies, but it should be used judiciously.
Preventing a temperature elevation is critical because fever in-creases cerebral metabolism and the rate at which cerebral edema forms. Strategies to reduce temperature include administration of antipyretic medications, as prescribed, and use of a cooling blan-ket. Additional strategies for reducing fever are included in the Nursing Process: The Patient With an Altered Level of Consciousness section. The patient’s temperature is monitored closely, and the patient is observed for shivering, which should be avoided because it increases ICP (Sund-Levander & Wahren, 2000).
Arterial blood gases must be monitored to ensure that systemic oxygenation remains optimal. Hemoglobin saturation can also be optimized to provide oxygen more efficiently at the cellular level.
Cellular metabolic demands may be reduced through the ad-ministration of high doses of barbiturates when the patient is un-responsive to conventional treatment. The mechanism by which barbiturates decrease ICP and protect the brain is uncertain, but the resultant comatose state is thought to reduce the meta-bolic requirements of the brain, thus providing some protection (Greenberg, 2001).
Another method of reducing cellular metabolic demand and improving oxygenation is the administration of pharmacologic paralyzing agents. The patient who receives these agents cannot move, decreasing the metabolic demands and resulting in a de-crease in cerebral oxygen demand. Because the patient cannot re-spond or report pain, sedation and analgesia must be provided because the paralyzing agents do not provide either.
Patients receiving high doses of barbiturates or pharmacologic paralyzing agents require continuous cardiac monitoring, endo-tracheal intubation, mechanical ventilation, ICP monitoring, and arterial pressure monitoring. Pentobarbital (Nembutal), thiopen-tal (Pentothal), and propofol (Diprivan) are the most common agents used for high-dose barbiturate therapy (Greenberg, 2001). Serum barbiturate levels must be monitored (Hickey, 2003).
The ability to perform serial neurologic assessments on the pa-tient is lost with the use of barbiturates or paralyzing agents (Greenberg, 2001). Therefore, other monitoring tools are needed to assess the patient’s status and response to therapy. Important parameters that must be assessed include ICP, blood pressure, heart rate, respiratory rate, and response to ventilator therapy (eg, bucking the ventilator). The level of pharmacologic paralysis is adjusted based on serum levels and the assessed parameters. Po-tential complications include hypotension due to decreased sym-pathetic tone and myocardial depression (Greenberg, 2001).
One controversial trend in cerebral monitoring is the ongoing measurement of venous oxygen saturation in the jugular bulb (SjO2). Readings taken from a catheter residing in the jugular outflow tract theoretically allow for a comparison of arterial and venous oxygen saturation, and the balance of cerebral oxygen supply and demand is demonstrated. Venous jugular desatura-tions can reflect early cerebral ischemia, alerting the clinician prior to a rise in ICP. Minimizing elevations in ICP can poten-tially improve outcome (Clay, 2000). This type of monitoring appears beneficial in the management of patients at risk for cere-bral ischemia; however, the invasive nature of this type of moni-toring and current limitations in technology mandate caution in its use. More study is needed before SjO2 monitoring can be con-sidered a valid and reliable tool for the management of cerebral ischemia (Clay, 2000).
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