As shown in Chapter 10, the physiology of the nervous system is extremely complex. Many neurologic care units have emerged because of the specific type of care needed in the perioperative period. Special education on the physiology, pharmacology, and nursing care is necessary to facilitate appropriate outcomes for the neurosurgical patient. Because nurses in the postanesthesia care unit (PACU) are able to render highly specialized nursing care to these patients, most facilities require that these patients first recover from anesthesia in the PACU before returning to the neurologic care unit or a routine care unit. Neurosurgical patients, or those with underlying neurologic conditions, present a challenge to the perianesthesia nurse. In addition to familiarity with routine perianesthesia care, the nurse must have a basic understanding of the nervous system and pathologic conditions or injuries that may affect this system and must be able to translate this knowledge into the skills necessary to assess, provide care for, and evaluate the neurosurgical patient. This chapter is divided into two sections: cranial surgery and spinal surgery. The division is made solely for this discussion because some aspects of care related to each topic are common to both areas. In addition, disease or injury in any portion of the nervous system may also affect other organs and systems of the body. In caring for the neurosurgical patient, the nurse must consider each structure of the nervous system (see Chapter 10) as it relates to the individual as a whole.

Cranial surgery

Diagnostic tools

Techniques used to ascertain the presence and extent of cranial injury or disease include invasive and noninvasive techniques. A brief discussion of invasive and noninvasive diagnostic procedures is included to familiarize the PACU nurse with the techniques and special considerations necessary in the care of these patients. Many interventional neuroradiology procedures with general anesthesia are now done; these patients go to the PACU after the procedure is completed. The specific PACU care is presented; if information on types of sedation (usually dexmedetomidine) for these patients is needed, please see Chapter 21.

Cerebral angiography

Arteriography, or angiography, is the diagnostic tool for aneurysms, arteriovenous malformations, and other cerebrovascular abnormalities. A cannulated needle ² is introduced into the femoral or axillary artery and threaded to the level of the common carotid artery. Radiopaque dye is then injected, and radiographs record its path through the cerebral vasculature (Fig. 38-1). Irritation brought on by use of the dye may manifest itself in altered states of consciousness, hemiparesis, or speech difficulties that are usually transient. During and after arteriography, the patient may have an allergic reaction to the dye that can range from mild urticaria to anaphylaxis. Resuscitative equipment must be immediately available until the danger of allergic reaction has passed.

FIG. 38-1 Cerebral angiography allows x-ray visualization of the brain’s vascular system when a contrast dye is injected arterially. A, Insertion of dye through a catheter in the common carotid artery, subsequently outlining vessels of the brain. B, An angiogram using the subtraction technique. 1, Internal carotid artery. 2. Middle cerebral artery. 3, Anterior cerebral artery A1 segment.

(From Black JM, Hokanson Hawks JH: Medical-surgical nursing: clinical management for positive outcomes, ed 7, St. Louis, 2005, Saunders.)

Postprocedure care includes proper hydration to prevent renal complications from the dye.³ In addition, the patient will require close neurologic and cardiovascular monitoring. The proceduralist may have used a closure device at the arterial site. Manufacturer recommendations, institutional policies and proceduralist orders should all be maintained. These orders will consist of bedrest, puncture site checks for bleeding or hematoma and vascular check of the affected limb.⁴ Intravenous fluids are maintained until the danger of untoward reaction has passed and the patient no longer has the transient nausea that occasionally occurs.

Injuries and pathologic conditions of the brain

Types of injuries

When a head injury occurs, the most crucial concern is the extent of injury to the brain itself. The injury becomes more severe when the fracture involves depression of fragments into the brain, penetration of a foreign object, leakage of CSF, expanding hematomas, or signs and symptoms of herniation. The primary goal is to protect the brain and facilitate the patient’s return to an optimal level of functioning.

Skull fractures are categorized as linear, comminuted, depressed, or basilar. The linear skull fracture associated with mild brain injury ⁴ and do not require treatment. A comminuted fracture, also known as the eggshell fracture, is a culmination of multiple linear fractures.⁵ A depressed skull fracture is an inward depression of the skull and is classified as open (compound) or simple (closed).⁵ Infection is a primary concern, and surgery may be necessary to remove bony fragments, clean the wound, and elevate the depressed bone. Basilar skull fractures occur in the base of the skull and are difficult to diagnose with radiographs. Diagnosis is confirmed with clinical data. Patients often have “raccoon’s eyes” (periorbital ecchymosis), Battle sign (ecchymosis around the mastoid process), or CSF otorrhea.

Concussion is caused by a violent jar or shock to the skull, such as rapid acceleration-deceleration. The patient may be dazed, “see stars,” or have a period of impaired consciousness. When consciousness is regained, these patients may have posttraumatic amnesia and remember nothing of the injury itself or the events immediately preceding the injury.

Contusion is a bruising of the brain or hemorrhage on its surface. The extent of severity depends on the site and degree of brain injury. Consciousness may or may not be lost, but coma indicates diffuse injury. Laceration is the tearing of the brain. Laceration and contusions of the brain are usually found in the frontal and parietal lobes.

Consequences of injury

Traumatic head injury can cause hemorrhage beneath a skull fracture or from a shearing of the veins or cortical arteries and results in epidural, subdural, subarachnoid, or intraventricular hemorrhage (Fig. 38-2). The signs and symptoms of brain ischemia and increased intracranial pressure (ICP) vary with the speed at which the functions of vital centers are altered. A small clot that accumulates rapidly may be fatal; however, the patient may survive a slowly developing, much larger hematoma through effective compensatory mechanisms.

FIG. 38-2 Types of hematomas. A, Subdural hematoma. B, Epidural hematoma. C, Intracerebral hematoma.

(From Black JM, Hokanson Hawks JH: Medical-surgical nursing: clinical management for positive outcomes, ed 8, St. Louis, 2009, Saunders.)

An epidural hematoma, or extradural hematoma, accumulates in the epidural space, which is between the skull and the dura mater. The hematoma is most often arterial and caused from a rupture or laceration of the middle meningeal artery, which runs between the dura and the skull in the temporal region. Epidural hematomas may also be seen in the frontal, occipital, and posterior fossa regions. The patient usually loses consciousness and then has a lucid period after which a rapid deterioration occurs. The hemorrhage may be massive, and treatment consists of evacuation of the clot through burr holes made in the skull.

Subdural hematoma may result from trauma and the shearing of the bridging veins. Venous blood usually accumulates beneath the dura and spreads over the surface of the brain. A subdural hematoma may be acute, subacute, or chronic, depending on the size of the vessel involved and the amount of blood present. Patients with acute subdural hematomas have a rapid deterioration in condition and are critically ill.

Subacute subdural hematomas fail to show acute signs and symptoms at onset. Brain swelling is not great, but the hematoma may become large enough to produce symptoms. Progressive hemiparesis, obtundation, and aphasia often appear 2 to 14 days after injury. The degree of ultimate recovery depends on the extent of damage produced at the time of injury.

Chronic subdural hematomas are seen most often in older adults. A history of head injury may be lacking because the causative injury is often minimal and long forgotten or deemed insignificant by the patient. The history is usually one of progressive mental or personality changes with or without focal symptoms as blood slowly accumulates and compresses the brain. The blood itself becomes thicker and darker within 2 to 4 days and within a few weeks resembles motor oil in character and color. Papilledema may be present. Chronic subdural hematomas can mimic any disease that affects the brain or its coverings. Treatment consists of evacuation of the defibrinated blood through multiple burr holes or a craniotomy incision.

Intracerebral hematomas are more commonly found in the elderly, often after a fall, but are also seen as a result of spontaneous rupture of a weakened blood vessel or aneurysm. Hemorrhage may be scattered or isolated and occurs in the brain parenchyma. Surgical evacuation of an isolated or well-defined clot may be attempted, but the mortality rate remains high.

Subarachnoid hemorrhage may occur as the result of traumatic brain injury. Bleeding into the subarachnoid space may result in a vasospasm. A vasospasm is the narrowing of the blood vessel lumen and places the patient at risk for a delayed ischemic event. The risk of development of vasospasms is greatest 3 to 7 days after the bleed.

Intraventricular hematoma, which is usually caused by a subarachnoid or intracerebral hemorrhage, is bleeding into the ventricles.⁶ This can be caused by brain trauma such as penetrating wounds or from an anterior communicating and basilar tip aneurysm.⁵ An intraventricular hematoma is associated with high mortality, and treatment includes a ventriculostomy with CSF drainage and ICP management.⁶

Herniation of the brain occurs from untreated, increased ICP. Supratentorial herniation is regarded as an emergency more severe than an epidural hematoma. The tentorium is an extension of the dura mater, which forms a transverse partition or shelf that divides the cerebral hemispheres from the cerebellum and brain stem. The superior portion of the brain stem passes upward through an aperture in the tentorium known as the tentorial hiatus. No space-occupying mass or lesion that expands within the cerebral hemispheres can escape upward or outward because of the confinement of the skull. Consequently, expansion within and compression of the hemispheres cause herniation of its contents (usually a portion of the temporal lobe known as the uncus) through the tentorial hiatus.

Uncal herniation is accompanied by compression of the lateral brain stem on the same side, which thus shuts off its blood supply and suppresses certain basic functions. The third cranial nerve (oculomotor) is in close proximity to the herniated uncus, and the pupil on the injured side becomes fixed and dilated. The reticular-activating system located in the brain stem that is responsible for waking and alertness becomes affected, and the patient rapidly becomes less and less responsive. Displacement of the midbrain causes compression of the pyramidal tract and results in contralateral hemiparesis or hemiplegia and plantar extensor responses (Babinski reflex). The respiratory center in the medulla may be affected, which results in changes in the respiratory pattern or cessation of respiration altogether.

In addition to these changes, the cerebellum itself may be so compressed that the cerebellar tonsil herniates inferiorly through the foramen magnum. This condition usually results in immediate death because the centers vital to life are compressed or sheared. The best treatment for supratentorial herniation is prevention through early detection and treatment of increased ICP and its causes. If efforts to minimize edema and increased ICP fail, surgical intervention, if possible, is necessary as a life-saving measure.

Types of pathologic conditions

Cerebral aneurysms are round dilations of the arterial wall that develop as a result of weakness of the wall from defects in the media layer of the artery. Most cerebral aneurysms occur at bifurcations close to the circle of Willis and usually involve the anterior portion. Common bifurcations include those with the internal carotid, the middle cerebral, and the basilar arteries and in relation to the anterior and posterior communicating arteries. The exact cause or precipitating factor is not well defined but may be related to congenital abnormality, arteriosclerosis, embolus, or trauma. Aneurysms are usually asymptomatic and present no clinical problem to the patient unless rupture occurs, which results in neurologic deficits. Ruptured cerebral aneurysm is the major cause of subarachnoid hemorrhage or hemorrhagic stroke. Depending on the severity of the cerebral bleed, the rupture of a cerebral aneurysm can often be fatal.⁶ If treatable, surgical intervention usually involves clipping or coiling of the aneurysm after identification through angiography. Careful consideration is given to the complications that can occur after aneurismal rupture or bleeding, which are rebleeding, vasospasm, and hydrocephalus.⁶

An intracranial arteriovenous malformation (AVM) is a vascular network that appears as a tangled mass of dilated vessels that create an abnormal communication between the arterial and venous systems. The communication may be singular or multiple and resembles an arteriovenous fistula in that no connecting capillary system between the arteries and the veins exists. AVMs most commonly occur in the supratentorial structures and usually involve the vessels of the middle cerebral arteries. AVMs are usually present at birth as the result of congenital abnormalities, but may have a delayed age of onset. Patients may never experience symptoms until the AVM ruptures, causing an intracranial hemorrhage and increased ICP. If symptoms do occur, they most commonly appear between the ages of 10 and 20 years. These symptoms may include headache, seizures, and altered level of consciousness (LOC). The treatment of choice is complete surgical excision via dissection or obliteration with ligation of feeder vessels. Radiation is used to treat AVMs that are not surgically accessible. Although AVMs are rare, their impact can be enormous and cause serious neurologic problems or even death.

Intracranial tumors are space-occupying lesions. Through invasion, infiltration, and compression, they destroy brain tissue and nerve structures and produce an increased ICP.

Intracranial tumors can be primary or metastatic. Primary tumors are classified as primary intracerebral (intraaxial) tumors, which originate from glia cells, or primary extracerebral (extraaxial) tumors, which originate from supporting structures of the nervous system. Metastatic tumors most commonly arise from breast malignant disease in women and lung malignant disease in men. Clinical manifestations can be both localized and generalized in nature. Local pathophysiologic changes, such as focal neurologic deficits, seizures, visual disturbances, cranial nerve dysfunction, and hormonal changes, result from the tumor itself destroying tissue at a particular site in the brain. Generalized pathophysiologic changes result from the effects of increased ICP. The treatment for cerebral tumors is surgical excision or surgical decompression if total excision is not possible. Surgery is often performed before, during, or after radiation treatment and chemotherapy.

Hydrocephalus is not a disease entity, but is a clinical syndrome characterized by excess fluid within the cerebral ventricular system, the subarachnoid space, or both. Hydrocephalus occurs because of abnormalities in overproduction, circulation, or reabsorption of CSF. Hydrocephalus can be classified into two categories: noncommunicating (obstructive) or communicating (nonobstructive). Noncommunicating hydrocephalus is the result of an obstruction in the ventricular system or the subarachnoid space that prevents the flow of CSF to the location of the arachnoid villi, where reabsorption occurs. The obstruction can be caused by congenital abnormalities or space-occupying lesions. Communicating hydrocephalus occurs when the flow of CSF is normal, but absorption of the fluid at the arachnoid villi is impaired. Common causes of communicating hydrocephalus include inflammation of the meninges, subarachnoid hemorrhage, congenital malformation, and space-occupying lesions.

Intracranial pressure dynamics

ICP is pressure that is exerted against the skull by its contents: brain tissue, CSF, and blood. These contents are essentially not compressible, and a volume change in any compartment requires a reciprocal change to occur in one or both of the other compartments if the ICP is to remain constant (Monro-Kellie hypothesis). The contents of the skull allow for partial compensation when increased ICP occurs. These compensation capabilities are limited because of the small amount of CSF that the spinal subarachnoid space can hold, and total displacement of cerebral blood results in cerebral ischemia. Normal ICP is 0 to 15 mm Hg. Intracranial hypertension occurs when a sustained increased ICP at the level of the head occurs and exceeds 15 mm Hg.

Volume may be added to any of the cerebral compartments and results in increased ICP when the compensatory capacity is exceeded. Brain volume can be increased by a tumor, a hematoma, or edema. Blood volume can be increased through dilation of the vascular bed. CSF volume can be increased through obstruction in the ventricles, resistance to reabsorption, or, in rare instances, increased production of the CSF. Large brain tumors increase pressure by their mass, by blocking the rate of CSF reabsorption, or both. If the tumor is near the surface of the brain, it can cause inflamed meninges that may exude large quantities of fluid and protein into the CSF, thus increasing ICP. Hemorrhage or infection also causes increases in ICP. Large numbers of cells suddenly appear in the CSF and can almost totally block CSF absorption through the arachnoid villi. Regardless of the mechanism, when the volume added exceeds the volume that can be displaced, intracranial compliance is greatly reduced and ICP begins to increase.

Fig. 38-3 illustrates the relationship between intracranial volume and pressure. Phase I shows the success of compensatory mechanisms in maintenance of a constant ICP despite early increases in volume. In phase II, the limited capability of compensatory mechanisms has been exceeded and ICP begins to rise. In phase III, even a slight increase in volume causes a dramatic rise in ICP and thus results in complete decompensation and death. The shape of the curve may be altered by the rate at which the volume increases. Slowly developing increases in volume broaden the curve, whereas rapid increases narrow it.

FIG. 38-3 Pressure-volume curve.

Perianesthesia care for the patients with the potential for increased ICP requires an understanding of cerebral blood flow (CBF) and the factors that affect it; these factors become defective during increased ICP and are manipulated to reduce ICP. CBF is directly proportional to cerebral perfusion pressure (CPP) and inversely proportional to cerebrovascular resistance. CPP described as the pressure required to perfuse the brain.⁷ CPP is typically expressed as the difference between the mean arterial pressure (MAP) and the ICP:

Consequently, any increase in ICP or reduction in MAP reduces CPP and resultant CBF. Average CBF is 50 mL per 100 g/min.⁴ The CBF below which cerebral ischemia occurs has been termed the critical CBF, which is a flow rate of 16 or 17 mL per 100 g/min. Average CPP is 80 mm Hg.⁴ CBF begins to fail at a CPP of 30 to 40 mm Hg.⁶ Irreversible hypoxia occurs at a CPP less than 30 mm Hg. When ICP equals MAP, CPP equals zero and CBF ceases.

Factors that influence CBF regulation are partial pressure of oxygen in arterial blood (PaO₂) and partial pressure of carbon dioxide in arterial blood (PaCO₂; metabolic regulation), arterial blood pressure and autoregulation, and venous blood pressure. Metabolic regulation works in two ways. The first is regulation of blood flow based on the tissue needs for metabolic substrates: oxygen and glucose. As the activity of neuronal and glial cells in the brain increases, the demand for oxygen and glucose increases. The increased demand causes vasodilatation of arterioles, which increases CBF. Likewise, if the metabolic demand decreases, vasoconstriction occurs and CBF decreases.

The second, and most significant, way metabolic regulation affects CBF is the presence of metabolic byproducts, specifically carbon dioxide. Carbon dioxide is the most potent vasodilator of cerebral blood vessels. Normal cerebral vessels respond to changes in carbon dioxide by dilating when carbon dioxide increases and constricting when carbon dioxide decreases. The relationship between CBF and carbon dioxide is linear, and changes in CBF are in direct proportion to changes in carbon dioxide. A decrease of 1 mL per 100 g/min in CBF occurs for every 1 mm Hg decrease in carbon dioxide. In treatment of elevated ICP, carbon dioxide levels of 30 to 35 mm Hg are used to lower CBF.

Autoregulation is the ability of the cerebral vasculature in normal brain tissue to alter its resistance so that CBF remains relatively constant over a wide range of CPP. This mechanism causes vasoconstriction when perfusion pressure increases and vasodilation when perfusion pressure decreases. The limits of autoregulation are at a CPP of approximately 60 mm Hg at the lower end and 160 mm Hg at the upper end. Beyond the limits of autoregulation, CBF becomes passively dependent on CPP. When CPP increases to more than the upper limit of autoregulation, it exceeds the ability of the vasculature to constrict; CBF becomes directly related to and possibly dependent on CPP.

The lower limit of CBF autoregulation is the blood pressure below which vasodilatation becomes inadequate and CBF decreases. When CPP decreases to less than 60 mm Hg because of increases in ICP, autoregulation ceases to be beneficial or effective in regulation of CBF. Defective autoregulation aggravates pressure increases and creates critical or irreversible levels of ICP by increasing the blood volume within the cranium in an effort to maintain CBF. Defective autoregulation generally occurs when ICP exceeds 30 to 35 mm Hg. Eventually, autoregulation ceases altogether, and blood flow fluctuates passively with changes in arterial pressure, regardless of metabolic activity or regulation.

When ICP is increased, CPP and CBF are reduced, which renders the tissues ischemic. Ischemic cerebral tissue releases acid metabolites that cause a relatively fixed reduction in cerebrovascular tone. Autoregulation ceases and any increase in MAP causes further increase in cerebral blood volume and elicits further increase in ICP. CPP is reduced and thus causes ischemic areas to enlarge, such as those that surround an expanding intracranial mass. As can be seen in Fig. 38-4, a pathologic cycle ensues in which ICP and MAP eventually equilibrate, the CPP drops to zero, CBF stops, and death occurs.

FIG. 38-4 Intracranial pressure dynamics with failed compensatory mechanisms.

Neurosurgical procedures

With further developments in technology, neurosurgeons have more options in the treatment of patients. Surgical procedures that use instrumentation, lasers, and radiation therapy have increased the surgeon’s ability to treat neurologic disorders.

Stereotaxis

Stereotaxis enables precise localization of a specified point. A stereotactic frame is applied to the patient’s head, and the target tissue is located with the stereotactic frame’s coordinates and CT scanning. Hemorrhage evacuation, catheter, shunt, or electrode placement and implantation of radioactive seeds are all procedures that may benefit from the use of stereotaxis. Additional uses include destruction of intracranial sensory pathways and the treatment of intractable chronic pain.⁸

Stereotactic radiosurgery

The most common approaches to stereotactic radiosurgery (SR) are gamma knife and medical linear accelerator units. Stereotactic radiosurgery can destroy deep and surgically inaccessible areas. The goal of SR treatment is the delivery of high-dose radiation to a specific target area without delivery of the radiation to surrounding tissue. Regardless of the type of SR, a stereotactic frame is secured to the patient’s head for accurate determination of target location. The placement of the stereotactic frame necessitates local anesthesia. Complications after SR may not appear for months to years later. Potential complications include permanent neurologic deficit, rebleeding, and worsening clinical symptoms.

Laser surgery

The benefit of laser surgery is that it enables the neurosurgeon to access areas that were surgically inaccessible with conventional surgery. With laser surgery, the surgeon can dissect a structure without trauma to the surrounding tissue, shrink tumors, and coagulate blood vessels. See Chapter 47 for a complete discussion on laser surgery.

Anesthetic agents and intracranial pressure

Although the brain represents only 2% of the body’s total weight, it receives 12% to 15% of the total cardiac output because of the brain’s high metabolic rate.⁹ Anesthetic agents alter ICP by increasing or decreasing CBF and cerebral metabolic rate (CMR). In addition to the effects on ICP, some of these agents may also reduce systemic blood pressure and cause cerebral ischemia as a result of inadequate CPP.

Inhalation anesthetics

The inhalation anesthetic agents generally decrease blood pressure and may increase ICP in the patient for cranial surgery. They produce a clinically significant degree of cerebrovascular vasodilation and metabolic depression and can modify autoregulation. In fact, high doses of volatile anesthetic agents can cause a total loss of autoregulation. The resulting increase in CBF ultimately leads to increased ICP. In patients with decreased intracranial compliance from neurologic disease, anesthetic agents that increase CBF may produce marked changes in ICP.

Isoflurane (Forane) at normocarbia has been shown to increase ICP. The initiation of hyperventilation simultaneously with the introduction of isoflurane prevents the increase in ICP that occurs at normocarbia. Isoflurane does not alter production of CSF and actually decreases resistance to absorption. It does not cause excitation of the central nervous system. Isoflurane produces reductions in CMR, and autoregulation is not impaired to any degree. The greater decrease in CMR may explain why CBF increases are minimal at low concentrations.

Desflurane and sevoflurane have essentially the same characteristics as isoflurane. During normocarbia, desflurane and sevoflurane cause cerebral vasodilation with resultant increases in CBF and ICP. The cerebrovascular response to carbon dioxide is maintained; therefore the increase in CBF can be attenuated with hyperventilation. The CMR is reduced in a dose-dependent manner similar to that of isoflurane, and no neuronal excitation is seen. Both agents cause cardiovascular depression and can be used with caution for controlled hypotension to reduce CBF. Desflurane, unlike sevoflurane, can result in an increase in MAP and heart rate when used for induction or at initially high concentrations. This effect may be reduced with the use of opioids or beta blockers. Both desflurane and sevoflurane have relatively low blood–gas partition coefficients that allow for rapid elimination of the agent, which makes them desirable for use because of the more rapid recovery.

Nitrous oxide has become controversial for use during intracranial surgical procedures. When used alone, nitrous oxide can cause an increase in CBF, ICP, and CMR at normocarbia. These effects, however, are attenuated with the use of barbiturates, benzodiazepines, opioids, and hyperventilation. To a small extent, nitrous oxide is a cerebral vasodilator and does not interfere with autoregulation of the CBF. Nitrous oxide may be an acceptable choice when combined with other agents to benefit from its rapid onset and elimination for neurosurgical patients in whom increased ICP is not a problem; however, it should be used cautiously in patients with increased ICP.

Intravenous anesthetics

A combination of inhalation and intravenous anesthetic agents are frequently used, but intravenous anesthetic agents (with the exception of ketamine) are usually the anesthetics of choice in cranial surgery.

Barbiturates, such as thiopental (Pentothal), are potent cerebral vasoconstrictors that can reduce CBF with subsequent reduction in elevated ICP. Cerebral vasoconstriction that is produced by barbiturates and the effect on CBF and ICP are dose related. The reduction in CBF produced by barbiturates is even greater if hypocarbia is also present and is maintained at a constant level. Deep thiopental anesthesia during normocarbia results in an approximately 50% reduction in both CMR and CBF.

Benzodiazepines, such as diazepam (Valium) and midazolam (Versed), produce sedation and amnesia by stimulating specific receptors in the brain. The benzodiazepines produce dose-related reductions in CMR and CBF. When central benzodiazepine receptors are pharmacologically saturated, these drugs can decrease CMR by as much as 40%.

Opioids, such as fentanyl, morphine, and meperidine, are typically classified as cerebral vasoconstrictors, with resultant reductions in CBF. This effect is readily abolished by vasodilation that can accompany opioid-induced ventilatory depression and the resultant increase in PaCO₂. Inconsistencies do exist throughout the literature related to the actual effect CBF and CMR has on the unstimulated nervous system.⁹ During normocarbia, the combination of nitrous oxide and morphine does not significantly alter CBF or autoregulation. Fentanyl causes a reduction in CBF and ICP in patients with normal CSF pathways. Alfentanil and sufentanil may in fact cause increased ICP in patients with compromised cerebral compliance.

Etomidate (Amidate) produces a maximum 45% decrease in cerebral metabolic rate and CBF; like the barbiturates, it can produce complete electroencephalographic suppression and appears to be comparable with lowering of ICP. Unlike the barbiturates, etomidate has less effect on MAP and offers greater stability in patients with hemodynamic compromise.

Propofol (Diprivan) reduces CMR, CBF, and ICP and increases cerebrovascular resistance in a dose-dependent manner. The use of propofol in patients with elevated ICP might not be appropriate because of the substantial decrease in MAP and resultant decrease in CPP. Although often used in rapid sequence intubation and continuous infusion during surgery, propofol has a short half-life and is therefore also used for sedation purposes in the neurosurgical patient; this facilitates the neurologic evaluation when needed.¹⁰

Dexmedetomidine (Precedex) is a sedative that allows for the patient to be easily aroused and often calm and cooperative while sedated; this enables the completion of the neurologic assessment. Although some precautions remain with this somewhat new drug, respiratory and hemodynamic stability are typically maintained with dexmedetomidine.⁶^,¹¹

Ketamine (Ketalar, Ketaject) can rapidly increase ICP and often reduce CPP, despite mild increases in blood pressure. Ketamine is generally contraindicated for use in neurosurgical patients unless the fontanels are open, CSF aspiration is instituted, or ventilatory control is maintained.

The use of controlled ventilation to produce PCO₂ levels in the range of 30 to 38 mm Hg and administration of nitrous oxide and oxygen and possibly low concentrations of isoflurane, together with opioids and muscle relaxants, is a generally accepted anesthetic technique for the neurosurgical patient.¹²

Adjunctive drugs and interventions used to reduce intracranial pressure

Diuretics

Mannitol and furosemide (Lasix) are diuretics often used to control increased ICP. Mannitol, an osmotic diuretic, is the agent of choice for intracranial hypertension because it decreases intracellular edema.⁶ Appropriate infusion of crystalloid and colloid solutions is often necessary to prevent adverse changes in plasma concentrations of electrolytes and intravascular fluid volume because of the rapidity of diuresis. Potential complications of the use of mannitol include hyperosmolarity, electrolyte loss, changes in blood viscosity and coagulation, transient intravascular hypervolemia, and rebound or secondary elevation of ICP.

Whereas mannitol reverses edema, furosemide is a loop diuretic and is more effective in decreasing circulating blood volume, thus reducing edema.⁵ Furosemide is more effective than mannitol in reducing ICP and is the drug of choice in patients with congestive heart failure.

Furosemide, when combined with mannitol, has been shown to potentiate the ICP-reducing effects of mannitol at the cost of rapid loss of intravascular volume and electrolytes. The ICP effects of these drugs are lost after 1 or 2 hours.

Corticosteroids

The drugs most commonly used are dexamethasone and methylprednisolone. Steroids are effective in lowering increased ICP because of localized vasogenic cerebral edema associated with mass-type lesions, such as neoplasm, abscess, and intracerebral hematoma. Use is controversial with head trauma and cerebral infarctions with edema. The mechanism for the beneficial effect of corticosteroids is not known but may involve stabilization of capillary membranes, reduction in CSF production, blood-brain barrier repair, prevention of lysosomal activity, enhanced cerebral electrolyte transport, improved brain metabolism, and promotion of water and electrolyte excretion.

Evidence-Based Practice

A literature search by the Brain Trauma Foundation produced a Level I recommendation for the use of steroids. This was the only Level 1 recommendation contained in the Guidelines for the Management of Severe Traumatic Brain Injury. “Level I recommendations are based on the strongest evidence for effectiveness, and represent principles of patient management that reflect a high degree of clinical certainty.” Guideline XV, Steroids states, “The use of steroids is not recommended for improving outcome or reducing intracranial pressure (ICP). In patients with moderate or severe traumatic brain injury (TBI), high-dose methylprednisolone is associated with increased mortality and is contraindicated.” There are numerous patient trials related to this, mostly prospective and double-blind, as noted in the guideline. “The majority of available evidence indicates that steroids do not improve outcome or lower ICP in severe TBI. There is strong evidence that steroids are deleterious; thus their use is not recommended for TBI.”

Implications for practice

Knowledge of perianesthesia nurses related to appropriate treatment options in traumatic brain injury is beneficial to the patient. Awareness of the difference between steroid use in patients with localized vasogenic cerebral edema and traumatic brain injury patients is imperative.

Source: Brain Trauma Foundation, et al: Guidelines for the management of severe traumatic brain injury, ed 3, New York, 2007, Brain Trauma Foundation.

Barbiturate therapy

Initiation of barbiturate therapy is the last medication adjunct used in treatment of intracranial hypertension. The patient must have an intracranial pressure–monitoring device, usually started when ICP is more than 30 mm Hg for 30 minutes and CPP is less than 70 mm Hg. The most common barbiturate is pentobarbital, which lowers the ICP by inhibiting free radical–mediated lipid peroxidation, altering vascular tone, suppressing metabolism, and hopefully maintaining an ICP of 15 to 20 mm Hg.⁵

Temperature management

Hyperthermia is a common crisis in neurocritical care, occurring in an estimated 70% of head-injured patients.⁴^,¹³ As the patient’s temperature increases, so does CBF and CMR, which could therefore also increase ICP.⁶ Temperature should be monitored closely, and the patient’s body temperature should be maintained at normothermia or even permissive hypothermia, which is becoming the current trend.¹² Other advanced cooling methods include cool saline intravenous infusion and surface-cooling pads or wraps.⁴ Cooling measures such as antipyretics, hypothermia blankets, and other traditional cooling methods are used as needed.⁴^,⁵ Methods such as intravascular temperature management may be effective as well.¹³

Positioning

Body positioning, among many other factors described previously is yet another aspect in proper care of the neurology patient. Positioning can affect ICP, CPP, and MAP.¹⁴ Although elevating the head of the bed to 30 degrees is preferred by most physicians, this is a topic of recent discussion.⁶

Intracranial pressure monitoring

The most precise indicator of the pressure state within the cranium is the CSF pressure, which is obtained through an ICP monitoring device. Trends in ICP, CPP measurement, and intracranial compliance are all functions of ICP monitoring.⁸ Monitoring of ICP is the standard of care for patients at risk for intracranial hypertension.

A measurement of this pressure can be obtained from the lateral ventricles, subarachnoid space, epidural or subdural spaces, or the intraparenchymal. Values from these areas are meaningful indicators of ICP only if pressure is freely transmitted between these compartments. Because injury and disease of the brain often create obstruction in CSF flow, the most accurate values are those obtained from the ventricle.

Lumbar puncture values reflect only a relative index of the actual ICP. These values depend on the state of the spinal canal and all the factors that affect it. However, measuring the ventricular fluid pressure gives a direct and absolute value of the ICP, regardless of the influence or condition of the spinal canal. Lumbar puncture has other limitations; its use is limited to patients without suspected intracranial mass or to those whose ICP is not elevated or is elevated only slightly. In patients with these conditions, herniation of the brain tissue with the removal of CSF is a risk. ICP monitoring does not present this risk and can be used in a variety of conditions.

The ICP monitoring devices are categorized into two primary categories. The first category includes devices that use fluid or hydrostatic coupling to transmit to an external transducer. Ventricular catheters, subarachnoid bolts or screws, and subdural catheters fall into this group. The second group uses a transducer to directly monitor ICP. These intracranial devices use fiberoptics to transmit ICP pressures and can be placed in the intraventricular, subarachnoid, intraparenchymal, epidural, or subdural spaces (Fig. 38-5).⁶

FIG. 38-5 Intracranial pressure monitoring devices. A, Intraventricular catheter monitoring system with a closed cerebrospinal fluid (CSF) drainage system. B, Subarachnoid bolt monitoring system. C, Epidural monitoring system.

(From Barker E: Neuroscience nursing, ed 3, St. Louis, 2008, Mosby.)

The subarachnoid bolt or screw was developed in 1973 and requires only a twist-drill hole in the skull and a nick in the dura for insertion. As the name implies, the sensor lies in the subarachnoid space. The advantages of this type of monitoring device are less risk of infection and use in patients with small ventricles. However, in the presence of moderately severe cerebral edema, a small piece of brain tissue may be driven into and occlude the proximal end of the screw, thus rendering it useless.

The intraventricular catheter (IVC) is the most common and least expensive ICP monitoring device, and it allows for drainage of CSF.⁶ The tip is introduced into a CSF-containing ventricle via a twist-drill burr hole and is connected to an external transducer that converts the hydrostatic pressure force into a graph and numeric readout. The advantages of the IVC are that it provides a direct ICP reading and is easily kept patent. Another advantage is that CSF can be drained through the catheter for treatment of ICP elevations. In this way, the IVC may serve as a temporary artificial extension of the CSF-shunting compensatory mechanism. Intracranial compliance can also be tested with injecting fluid into the cranium and reading the responding pressure. If an abrupt and steep rise in ICP occurs, one can assume that compliance no longer exists and that the volume-pressure curve is a steep one. When the patient’s arterial pressure is monitored simultaneously, exact CPP can be calculated at any time. The ventricular catheter also has the advantage of allowing instillation of contrast media or air for study of the size and patency of the ventricle. The principal disadvantage of the IVC is the risk of infection and hemorrhage.

The fiberoptic catheter uses the fiberoptic transducer-tipped probe and can be placed in the ventricles and in subarachnoid, subdural, and intraparenchymal sites. The advantages are its easy placement and lack of relation to ventricular size. The major disadvantages are its expense, its inability to allow for CSF sampling or drainage, its possible need for probe replacement, and the fragility of the fiberoptic cable, which breaks easily.

Intracranial pressure monitoring is a valuable tool in assessing the efficacy of nursing interventions that are intended to decrease ICP. Continuous monitoring of the pressure state within the cranium accelerates the treatment of elevations in ICP before the patient’s condition deteriorates.

Pressure waves in increased intracranial pressure

Pressures waves are discussed in two separate categories: the ICP waveform and the ICP waveform trends (Fig. 38-6).

FIG. 38-6 A, ICP waveform. B, ICP waveform trends

(From Barker E: Neuroscience nursing, ed 3, St. Louis, 2008, Mosby.)

The ICP waveform is valuable at the bedside as a means for the nurse to determine the adaptability of the patient.⁵ The waves correlate with the patient’s heart rate. Ideally there are three or more peaks in the wave, with the P1 (percussion) wave as the first and most prominent. P1 is thought to be arterial in origin and consistent in its amplitude. P2, the tidal wave, is also arterial in origin and is related to the state of compliance. The last wave is the dicrotic wave or dicrotic notch and is venous in origin.³^–⁵ Decreased intracranial adaptive capability and impaired autoregulation are thought to be associated with an elevation in the P2 wave.⁴

Three patterns have been identified with the ICP waveform trends. The first and most significant type is the A wave, which is more commonly called a plateau wave. These waves are associated with increases in ICP between 50 and 100 mm Hg that last for 5 to 20 minutes. They are seen only in advanced stages of increased ICP (the last phase of the volume-pressure curve) and superimpose themselves when the baseline ICP is elevated and exceeds 20 mm Hg. Early increases in mean systolic arterial pressure do not accompany plateau waves, and autoregulation is impaired. Thus, plateau waves signal hypoxia of brain cells and a decrease in CPP. They may cause both transient and irreversible damage to the brain and may be premonitory signs of acute incidents.

The second type of pressure wave pattern is called the B wave. These waves are sharp rhythmic oscillations with a sawtooth pattern that occurs every 30 seconds to 2 minutes. These waves can indicate increases in ICP as much as 50 mm Hg and are more commonly seen in patients with unstable increases in ICP usually from accelerations producing apneic episodes.⁵

The third type of pattern is the C wave. These waves are smaller rhythmic oscillations in ICP that occur 4 to 8 times per minute ⁴^,⁶ and indicate increases in ICP by as much as 20 mm Hg. These waves are associated with respiratory influence on blood pressure, but their significance is questionable.

Intracranial pressure assessment

With the availability of high-resolution noninvasive imaging techniques such as CT scanning and MRI, these studies themselves may be the chief determining factor in the decision to initiate ICP monitoring. Some of the indications for ICP monitoring are expanding intracranial tumors, hydrocephalus, benign intracranial hypertension, trauma, vascular anomalies, certain cases of metabolic coma with cerebral edema, certain cases of viral hepatitis or fulminant hepatic encephalopathy, and patients in a controlled barbiturate coma for status epilepticus.

Continuous ICP monitoring is the only accurate method of assessing ICP at any given time. This method has two advantages: (1) it provides an ongoing record of the ICP and (2) it provides a means of assessment of intracranial dynamics. These advantages allow guided therapy and management of ICP through CSF drainage. The clinical signs of increased ICP are numerous. The early signs are often vague and overlooked, and research has shown the unreliability of these signs in determination or recognition of increased ICP. Regardless, frequent clinical assessment is necessary and often is the first sign of deterioration.

Early signs of increased ICP are change in LOC (restlessness, confusion, agitation, irritability, lethargy), abnormal pupillary function, deterioration of motor function, and severe headache.⁴^,⁸ Nausea, vomiting, paralysis, visual field deficits, conjugate deviation of the eyes, sensory loss, and nuchal rigidity are also early signs. The presence of these signs may or may not confirm a diagnosis of increased ICP, but they can still inform treatment while treatment is effective.

The late signs of increased ICP are decreasing responsiveness and LOC; additional pupillary changes; increased systolic blood pressure; bradycardia; widening pulse pressure; alteration in respiratory pattern; decorticate or decerebrate posturing; and absence of or decrease in cough, gag, corneal, and deep tendon reflexes. A positive Babinski reflex is normal in infants younger than 18 months of age, but indicates increased ICP in those older than 18 months.

Most of these signs are manifestations of brain shift, with resultant dysfunction of the reticular-activating system, brain stem, and medulla. Pressure either has to elevate rapidly or be sustained at high levels to affect these structures so dramatically. Primary injury to these structures may elicit the same signs without appreciable increases in ICP. In this situation, they could indicate the level of brain function and the gravity of the situation, but not reflect the pressure dynamics that exist at that moment.

Just as these signs may be present without increase in ICP, ICP may be dangerously high with few signs, if any. Classic brainstem signs (reflecting changes in cardiac, respiratory, or vasomotor function) usually occur late, after the onset of intracranial hypertension, if at all. The most important factor in determining the degree of secondary brain damage incurred by elevated ICP is the effect of altered CPP on the brain. Clinical research has shown that the level of CPP is the best indicator of outcome from severe head injuries. CPP less than 40 mm Hg has been associated with poor outcomes. CPP needs to be maintained at no less than 50 to 60 mm Hg to provide a minimally adequate blood supply to the brain.

Most hospitals with the capacity for cranial surgery also have the capacity for continuous ICP monitoring. It is still important to be able to recognize signs and symptoms of intracranial hypertension without the assistance of an ICP monitor. Thus, the traditional signs and symptoms of increased ICP are discussed here, although they are not precise or infallible as indicators of increased ICP. At the least, they indicate that “something is not right” and that constant vigilance and further investigation are necessary. Even the transient appearances of these pressure signs are important; they indicate the development of a highly delicate and unstable intracranial situation, a sign that the patient may be having plateau waves.

Perianesthesia nursing management

The following four major areas of assessment are necessary in PACU care of the cranial surgical patient: (1) vital signs, (2) LOC, (3) motor and sensory functioning, and (4) pupillary signs. These areas should be assessed routinely at least every 15 minutes for the first 2 hours after surgery. Then, if results are within normal limits or unchanged since surgery, the areas should be assessed every 30 minutes. If the patient’s condition is unstable or deteriorating or if the surgeon specifies, assessments should be made more frequently. If the patient’s ICP is monitored, correct calibration of the monitor must be ensured, ICP value recorded, and waveform described. The same approach is used for arterial pressure recording.

Reports should be taken from both the anesthesia provider and the surgeon. Of particular importance are surgical procedure, pathologic findings, bone flap presence, allergies, preexisting medical problems, anesthetics, and any problems that occurred during surgery. Special positioning orders or restrictions, the presence of drains, and known CSF leaks must be noted. The Glasgow Coma Scale (GCS; Table 38-1) is a widely used neurologic assessment tool because of its simplicity, consistency, and reliability between raters who use it. However, the GCS cannot be used to assess subtle changes in the patient’s neurologic status. When the GCS is used, the patient’s responses are scored on a scale of 3 to 15. A score of 3 indicates coma, and a score of 15 indicates a fully alert oriented person with all neurologic functions intact.

Table 38-1 Glasgow Coma Scale

CATEGORY	RESPONSE	SCORE
Eye opening	Spontaneous	4
	To speech	3
	To pain	2
	None	1
Best verbal response	Oriented to person, place, and time	5
	Confused	4
	Inappropriate words	3
	Incomprehensible sounds	2
	No response	1
Best motor response	Obeys commands	6
	Localizes to pain	5
	Withdrawal from pain	4
	Abnormal flexion	3
	Abnormal extension	2
	Flaccid	1

Vital signs

Assessment of vital signs includes blood pressure, pulse, respirations, and ICP (if monitored). Changes in vital signs may indicate increasing ICP, shock, hemorrhage, electrolyte imbalance, or other disturbances. The perianesthesia nurse should keep in mind that the injured patient may have other pathophysiologic processes unrelated to the head injury. Temperature is always monitored, and an elevation usually represents an infectious process, most often in the respiratory or urinary tract. Infrequently, elevations are attributable to direct damage to the temperature-regulating center in the hypothalamus. Temperature elevation also increases the metabolic rate of the brain, which may further increase ICP.

Airway patency is ensured, and the rate, depth, and rhythm are noted. If the rhythm is irregular, its pattern should be determined. Changes in the respiratory pattern may indicate injury to the respiratory center of the brain and the severity of the neurologic injury (Fig. 38-7). If the patient requires a ventilator, the machine should be checked for proper functioning and settings; however, mechanical ventilation can mask changes in the respiratory pattern.

FIG. 38-7 Abnormal respiratory patterns with corresponding levels of central nervous system activity.

(From Urden LD et al: Critical care nursing, ed 6, St. Louis, 2010, Mosby.)

For many years, the nursing literature has documented a relation between changes in blood pressure and pulse and increases in ICP. These changes are often referred to as Cushing reflex, Cushing triad, or Cushing response. Cushing reflex is described as elevated systolic blood pressure, bradycardia, and widening pulse pressure. Additional increases in ICP can lead to Cushing triad, which is described as bradycardia, hypertension, and bradypnea. Cushing reflex and triad are late clinical signs of increased ICP and may indicate brain stem herniation. Patients with head injury often have a higher than normal blood pressure and heart rate that may be the result of pain, hypoxia, and agitation or the release of endogenous catecholamines.

Level of consciousness

The most important indicator of brain function is the LOC, but it is not necessarily indicative of altered ICP. A decreased LOC in the PACU can be caused by the lingering effects of the anesthesia or by neuromuscular-blocking agents sometimes used with patients on positive-pressure ventilation. A change in LOC may also be the result of hypoxia, hypoglycemia, vitamin deficiency, or fluid and electrolyte imbalances. Other underlying pathologic changes can cause alterations in LOC. For assessment of LOC, a description of the patient’s response is best instead of vague terms such as stuporous, semiconscious, or unconscious. A standard assessment form such as the GCS (see Table 38-1) should be available for assessment of the LOC. A change in LOC may also be indicative of deterioration or improvement in the patient’s condition.

Motor and sensory functioning

Assessment of motor and sensory function is part of an ongoing neurologic assessment and is performed to note changes from the baseline assessment. It can also provide clues to extending hemorrhage or expanding edema. Focal changes, such as decreased hand strength unilaterally or an inability to move one side of the body, often accompany these events. Sensations may be decreased because of brain involvement, not just spinal cord injury (SCI). Observe whether the patient can move all four extremities. Check both hand grasps simultaneously. Are they weak or strong; equal or unequal? Foot strength can be tested by having the patient push or pull against the nurse’s hands. (Be sure the patient uses only the foot and ankle, not the entire leg.) If the patient does not respond to simple commands, test to see whether a painful stimulus such as a pin prick or pinch induces movement. (Test both sides to determine sensory impairment.) If the patient does not respond to pain, test for motor function by raising both arms or both legs and letting them fall together. A paralyzed limb falls to the bed more quickly than an unaffected one. To further check leg motor ability, flex both of the patient’s knees with the feet flat on the bed; release them at the same time. The healthy leg maintains its position momentarily and then resumes the original position. The affected limb abducts while falling and maintains knee flexion.

Facial muscle movement should also be tested. If possible, ask patients to wrinkle the forehead, shut the eyes tightly, smile, and show the teeth. Any asymmetry should be noted. If the patient is not responsive to verbal commands, noxious stimulation may elicit a grimace or other facial movement. The presence of a Babinski reflex is pathologic and indicates pyramidal tract dysfunction in any person older than 18 months. Starting at the heel and using a moderately sharp object, such as the rounded tip of a bandage scissors or the tip of a retracted pen, stroke the lateral sole and proceed to the ball of the foot. Firm pressure is necessary to elicit an accurate response. The Babinski reflex is present when the great toe dorsiflexes (bends toward the head) and the remaining toes “fan out.” The Babinski reflex is not present when the stimulus elicits a plantar or downward flexion of the great toe.

Motor response to a painful stimulus may be one of decerebrate or decorticate rigidity, or these postures may exist in the absence of any stimulation. Decerebrate posturing is characterized by rigidity and contraction of all the extensor muscles. The legs are stiffly extended with the feet plantar flexed. The arms are extended and hyperpronated. Decerebrate rigidity is usually the result of upper brain stem damage, which means that the cerebral hemispheres are functionally cut off. Decorticate posturing indicates that function has been cut off at a lower level and that the entire cortex is physiologically cut off. In this instance, the legs are extended and internally rotated, and the feet are plantar flexed. The arms are flexed at all joints, and the hands are often held beneath the chin.

Pupillary activity

Pupillary reactions are controlled by the third cranial nerve. In assessment of the pupils, the perianesthesia nurse should examine both simultaneously for shape, size, and equality. Normal pupils are round and, at a midpoint diameter, within the range of 1 to 9 mm. Instead of using terms such as constricted or dilated, measurement of the diameter directly with a pocket millimeter ruler is more precise. Test the direct light reflex of each pupil with a small bright flashlight. Normally the pupil constricts briskly. If it reacts sluggishly or not at all, the reaction is abnormal. To test the consensual light reflex, hold both eyelids open, shine the light in one eye, and observe the other pupil. The opposite pupil should constrict simultaneously with the lighted one, although perhaps not to the same degree.

Normal pupillary size and reactivity can be altered by some medical situations and by certain drugs. Previous surgery or direct injury to the eye may alter or abolish reactivity. Blindness abolishes reactivity to light because the sensory part of the reflex pathway is absent.

Unusual eye movements should be noted. Normal gaze in a person who is awake and alert is straight ahead, with no involuntary movements. This condition is generally true of unresponsive patients, although the eyes may rove slowly and in random fashion. (In detection of this movement, do not be misled into thinking that the patient is actually following you or your movements.) The eyes should move together in the same direction (conjugate gaze). If the eyes are disconjugate, they move in a jerky oscillatory fashion (nystagmus) or the gaze deviates from the midline. These ocular movements are abnormal and should be detailed in the nursing notes.

Nursing care in the postanesthesia care unit

The PACU nurse has three primary responsibilities in the care of the neurosurgical patient: (1) to institute measures of care to sustain optimal physiologic function in the perianesthesia patient, (2) to recognize and prevent conditions that increase ICP beyond normal limits, and (3) to detect and communicate signs and symptoms of the patient’s condition to the physician (Box 38-1).

BOX 38-1 General Postoperative Considerations

Airway, oxygenation status

• Determine length of time to remain intubated, if applicable.

• Obtain respiratory vitals and arterial blood gases as needed before extubation.

• Ensure that the patient is able to ventilate to maintain a PaCO₂ of 35 to 45 mm Hg.

• Before extubation, assess difficulty of maintaining airway and reintubation.

Cardiovascular and hemodynamic status

• Cardiac rhythm

• Fluid loss, replacement

• Electrolyte values

• Monitoring lines

Pain assessment and treatment

• Measure intake and output

• By shift and cumulative from first encounter

• Drains, drainage

Documentation

• Document critical information and the manufacturer lot number of any implantable device placed in the patient during surgery.

PaCO₂, Partial pressure of carbon dioxide in arterial blood; ICP, intracranial pressure; CPP, cerebral perfusion pressure.

Adapted from Bitters L: Perioperative surgical considerations. In Bader MK, Littlejohns LR, editors: AANN core curriculum for neuroscience nursing, Glenview, Ill, 2010, American Association of Neuroscience Nursing.

Spinal surgery

In the United States there are approximately 200,000 people living with SCI, and 12,000-20,000 new cases are estimated to occur annually.¹⁵ The goal of surgical intervention is minimization of complications related to SCIs, spinal cord tumors, or developmental abnormalities. Complete or incomplete SCI, bony fragments in the canal, unstable dislocation, and evidence of cord compression are some indications for immediate surgical intervention.

Diagnostic tools

Several methods are used in the diagnosis of injury or disease involving the spine or spinal canal.

Conventional radiography and fluoroscopy are used to identify fractures and fracture-dislocations. Narrowing of an intervertebral space is sometimes evident as a result of a herniated nucleus pulposus (slipped disk). Fluoroscopy is used to show instability of the injured part on manipulation. Splintered or displaced bone fragments and radiopaque foreign bodies, such as bullets or other metal fragments, are also seen on radiographs. Radiographs also show abnormalities such as scoliosis and osteoporotic and arthritic changes. Tumors may be evidenced by erosion, calcium deposits within the mass, increased interpediculate distance, enlargement of an intervertebral foramen, or collapse of a vertebra.

CT scanning is used to delineate mass lesions that exist in the same plane as the spine and spinal cord and when conventional radiography is not adequate. Large blood clots may also be localized with this method.

MRI is being used increasingly for accurate detection and assessment of space-occupying lesions of the spine, such as herniated nucleus pulposus and tumors. In addition, MRI is appropriate to detect the degree of an SCI.

Myelography is one of the most valuable tools available in the diagnosis of compression of the spinal cord caused by tumor, fracture-dislocation, or herniated nucleus pulposus. A lumbar puncture is performed, at which time a Queckenstedt test may also be done. The myelogram consists of the injection of a radiopaque dye into the CSF canal and the fluoroscopic observation of its flow in the suspected area. Cord compression is evidenced by an interruption in the contour of the spinal cord. Disruption of the contours of the spinal nerve roots may also be found.

Injuries of the spine

The spine protects the spinal cord and the terminal nerve roots. Injuries to the spine and spinal cord occur as a result of flexion, hyperextension, rotation with both flexion and extension, compression, and penetrating wounds (Fig. 38-8). Head injuries often accompany injuries to the spine and vice versa. The cervical spine is extremely mobile and therefore particularly susceptible to injuries that hyperflex or hyperextend the neck. Propulsion can occur anteroposteriorly or laterally. The spinal cord is relatively large in the cervical area and sustains damage fairly easily after injury. This area is unique in that the superior portion of C2 lacks a vertebral body. Instead, the neck has a dens, or projection, called the odontoid. Many injuries to the odontoid extend into C1, or atlas, which has no vertebral body at all.

FIG. 38-8 Patterns of cervical spine injury. A, Hyperflexion injury of the cervical spine ruptures the posterior ligaments. B, Hyperextension injury of the cervical spine ruptures the anterior ligaments. C, Compression fractures crush the vertebrae and force bony fragments into the spinal canal.

(From Black JM, Hokanson Hawks JH: Medical-surgical nursing: clinical management for positive outcomes, ed 8, St. Louis, 2009, Saunders.)

The thoracic spine is fixed by the ribs, but the lumbar spine is not; therefore an increased incidence rate is seen of injury to the thoracic, lumbar, or sacral regions of the spine. Motor vehicle crashes are the leading cause of spinal cord injuries.¹⁵

Consequences of injury to the spine are the result of the mechanical insult or biochemical and hemodynamic changes. Mechanical insult includes the direct injury and changes to the cord structure, motion stress on the cord, and continuous compression to the cord. This physical injury to the cord results in the primary or initial spinal cord dysfunction. Edema of the cord, which causes cellular changes and ischemia, may occur in the hours after the initial injury. This process is called secondary injury and can last up to 5 days.

The primary goal in the early treatment of spinal cord injuries is prevention of further compromise of spinal cord tissue from secondary injury. If the damage to tissue as the result of the direct injury cannot be altered, an attempt is made to protect the remaining tissue by alleviating compression and movement of the spinal cord. Spinal cord immobilization, surgical intervention to alleviate cord compression, and pharmacologic therapies to reduce edema are used as immediate therapies.

Complete spinal cord lesion

The extent of injury to the spinal cord is described as a complete or incomplete lesion. In a complete SCI, no motor or sensory function is seen more than three levels below the level of injury. When this type of injury lasts more than 24 hours, no recovery of distal function is indicated. Clinical findings during the acute phase after total cord transection include the following:

1. There is immediate loss of all sensory, motor, autonomic, and reflex functions below the level of the injury from spinal shock. Spinal shock can persist for days or weeks, depending on the injury and the patient’s general state of health. It usually lasts 4 to 8 weeks.

2. Urinary retention as a result of bladder sphincter paralysis is present.

3. Paralytic ileus with progressive abdominal distention is present.

4. There is respiratory insult or cessation. Injury to the lower cervical or upper thoracic spine results in cessation of intercostal function. In this event, respiration is under the sole stimulus of the phrenic nerve, and breathing is diaphragmatic. Injury to the cord at the levels of C3 to C5 affects the phrenic nucleus and thus paralyzes the diaphragm and causes respiratory failure.

5. There is a loss of sweating below the level of the lesion.

6. Point tenderness over the injured part is present. Crepitus may or may not be present.

Initial therapeutic efforts are directed at the preservation of life. Mechanical stability, protection of nervous tissue, and freedom from pain are long-term therapeutic goals.

Incomplete spinal cord lesion

Incomplete spinal cord lesion indicates residual motor or sensory function more than three segments below the level of injury. Indications of incomplete lesion are sensation, sense of position, or voluntary movement of the legs; sensation around the anus; voluntary rectal sphincter contraction; and voluntary toe flexion.

Various syndromes or types of incomplete lesions may result from the injury. Incomplete lesions include central cord syndrome, Brown-Séquard syndrome, anterior cord syndrome, and posterior cord syndrome.

Central cord syndrome (CCS) is the most common type of incomplete lesion. CCS occurs more commonly in older adults as a result of a hyperextension injury, such as a blow to the face or forehead. CCS from sports injuries is also seen in younger patients.

The center of the cord is contused and may hemorrhage, thus resulting in bilateral upper extremity weakness and a burning sensation. If CCS is caused by a contusion, lower extremity function usually returns first, then bladder function, upper extremities, and lastly finger movement.

Brown-Séquard syndrome may occur after injuries that transect the cord, such as knife or gunshot wounds, epidural hematoma, herniated cervical disc, spinal cord tumor, spinal AV malformation, and cervical spondylosis. Clinical signs are ipsilateral loss of motor, touch, pressure, and vibration below the lesion and contralateral loss of pain and temperature below the lesion. This type of lesion has the best functional recovery rate; many patients regain independent ambulation.

Anterior cord syndrome usually occurs as the result of compression of the anterior portion of the cord and loss of blood supply from the anterior spinal artery. Clinical signs are loss of motor function, pain, temperature, and sensation below the level of injury. Touch, position, and vibration sensation are still intact. Anterior cord syndrome is usually caused by flexion injuries in the cervical area.

Posterior cord syndrome is a rare disorder. Clinical signs are pain and paresthesias in the neck, upper arms, and torso. Mild paresis of the upper arms may occur.

Surgical intervention for spinal cord injuries

Surgeons differ in opinions about the optimal timing for surgical decompression and fusion. Early surgical intervention is indicated to decompress the spinal canal from bone or disk fragments, provide stabilization, and repair damage caused by penetrating objects.

Patients who need surgery may have exploration, insertion of Harrington rods or stabilization instruments, or decompression laminectomy procedures. Procedures can be performed through an anterior or posterior approach, depending on the cord lesion. Fusion is accomplished with the placement of a bone graft taken from tibial or iliac bone into the involved interspace or of a fixation device. External immobilization is often used after surgery until osseous union is complete.

General contraindications to surgery are the existence of associated life-threatening injuries, depressed respiratory function caused by high cervical injuries, lack of skilled personnel and necessary equipment, improved neurologic status, and need for stabilization.⁶

Perianesthesia nursing care for the patient with spinal cord injury

Permanent injuries of this nature are devastating to the patient and the patient’s family. The nursing responsibilities are great during the acute, rehabilitative, and chronic phases. Patients with SCI may be sent to the PACU in any of these phases, and care requires special consideration and knowledge of SCI pathophysiology.

The initial assessment of the patient with SCI in the PACU needs to focus on airway patency, adequate respiration, and maintenance of systemic and spinal cord perfusion. Vital signs should be assessed every 15 minutes until the condition is stable. Baseline neurologic assessment including motor and sensory evaluation should be completed with the initial and ongoing assessments.

Immobilization is a primary intervention to help prevent the process of secondary injury. The standard of care for immobilization is placement of the neck in a neutral position and in a rigid cervical collar. Stabilization of fractures may be accomplished with several devices that promote alignment.

Complications associated with spinal cord injury

Spinal shock

Spinal shock is a form of neurogenic shock characterized by a loss of motor, sensory, autonomic, and reflex activity below the level of the lesion and resulting in flaccid paralysis and paralytic ileus. The classic signs and symptoms of spinal shock include systemic hypotension, bradycardia, and hypothermia. Spinal shock is a condition that occurs immediately after injury or up to hours after an SCI that progressively worsens and may last hours to months, depending on severity of the injury.⁶

Hypotension

Hypotension is not uncommon because of vasodilation of the vessels below the level of the injury. The goal of treatment is maintenance of systemic and renal perfusion. Bradycardia may accompany the hypotension. Dopamine is indicated for the treatment of hypotension and bradycardia. Other causes of hypotension, such as a gastrointestinal hemorrhage, must be considered and ruled out. Hypotension is usually not caused by hemorrhagic shock; therefore the patient volume status should be monitored closely and not overloaded with intravenous fluids.

Bradycardia

Bradycardia is associated with spinal shock and nursing interventions such as manipulation of an endotracheal tube, suctioning, turning, and insertion of a nasogastric tube, which may elicit a vasovagal response that leads to bradycardia. Nursing interventions should closely monitor for and provide prevention from a vasovagal response.

Thrombosis

Conditions are optimal for the development of deep vein thrombosis and pulmonary embolus because of venous pooling and loss of movement below the level of injury. Calf measurements, antiembolism stockings, compression devices, low-dose heparin, and low–molecular weight heparin are used to prevent these complications.

Autonomic dysreflexia

Autonomic dysreflexia is a syndrome of massive imbalanced reflex sympathetic discharge.¹⁶ It occurs in patients with SCI greater than the splanchnic sympathetic outflow (T5-T6)¹⁶ and after the resolution of spinal shock and the return of reflex activity. Autonomic dysreflexia results from excessive reflex stimulation of the sympathetic nerves below the level of injury. Causes of the reflex stimulation include bladder distension, fecal impaction, and noxious stimuli. Symptoms of autonomic dysreflexia are pounding headache, excessively high hypertension, decreased heart rate, profuse sweating, and flushed skin above the level of injury, pallor and goose bumps below the level of the injury, anxiety, and visual disturbances. Treatment is aimed at removing the noxious stimulus and preventing complications from hypertension.

The PACU nursing care focuses on the routine prevention of known precipitants of autonomic dysreflexia. For example, the bladder must not become distended, and skin breakdown must be prevented. If signs and symptoms appear, the stimulus must be sought and removed as rapidly as possible. If the symptoms cannot be alleviated, the nurse should notify the physician, elevate the head of the bed (if not contraindicated), and monitor the blood pressure every 5 minutes. Severe cases can require treatment with spinal anesthesia and the administration of ganglionic-blocking agents. For chronic problems, subarachnoid blocks or rhizotomy may be necessary.

Pain management

Patients may have pain in areas about the level of injury. The pain may be described as sharp, dull, or burning and often is associated with muscle spasms. Morphine for pain or diazepam, cyclobenzaprine, or other antispasmodic agents may be ordered. Intramuscular medications should never be administered below the level of the lesion, because they cause local inflammation and tissue breakdown and absorption is negligible.

Concomitant head injury

Every patient with acute injury to the spine must be observed for signs and symptoms that indicate head injury. Evaluation of cranial status should be done at the same intervals as the vital sign measurements. Abnormawl neurological signs should be reported to the physician immediately, because they may indicate injury to the brain or increased ICP that results from the upward expansion of cord edema.

Respiratory complications

Respiratory insufficiency or failure is the most serious complication of SCI. Respiratory complications can be independent of the level of injury. C4 and higher injuries require mechanical ventilation because of the direct involvement of the phrenic nerves. Assessment of a patient’s ventilation should include the following parameters: status, rate, depth, pattern, and oxygen saturation. Evaluation of pulmonary function should include tidal volume, inspiratory force, and vital capacity. Changes in pulmonary function are early indicators of deterioration in respiratory status and may necessitate ventilator support. Intubation of the patients may depend on the ability to clear secretions and to maintain adequate gas exchange. A program of chest physiotherapy and the use of pressure support ventilation and positive end-expiratory pressure assists with the prevention of atelectasis. Auscultation of lung sounds should also be performed routinely to assess the presence of abnormal lung sounds. Chest radiographic examinations and arterial blood gas determinations should be monitored routinely and ordered immediately if signs of deterioration occur. Potential respiratory complications that result from SCI include pneumonia, aspiration, pulmonary edema, and pulmonary embolism. Rotational beds before surgical stabilization facilitate the mobilization of secretions and help prevent respiratory complications. A team approach by nursing staff members, physicians, respiratory therapists, and physical therapists is necessary for the treatment of SCI. Because of the rapid onset of pulmonary complications, the PACU nurse must be aggressive in caring for the patient with SCI.

Skin breakdown

As with the patient for cranial surgery, skin care for the patient with SCI is an important aspect of PACU nursing care. Skin breakdown is one of the most obvious, costly, and detrimental complications that a patient with SCI can have. The patient must be turned and repositioned at least every 2 hours to prevent skin breakdown and damage to underlying body tissues. A specialty surface such as an air mattress or alternating pressure mattress may be necessary to prevent skin breakdown.

Gastrointestinal complications

Generalized atony and loss of motility render the stomach and intestine distended and highly susceptible to fecal impactions and obstructions. Distention is relieved with intermittent nasogastric suction. Programs of bowel training are initiated within 24 hours of admission.

A high incidence rate of stress ulcers is seen among these patients, especially in those with quadriplegia. Here, parasympathetic vagal action is unopposed because of sympathetic block from the ascending and descending visceral nerve paths, and gastric acid secretion by the parietal cells of the stomach is increased. This stressful situation can be further compounded by the administration of corticosteroids used to reduce cord edema. Corticosteroids alone are capable of inducing hyperacidity of gastric juices. Antacids or a histamine-2 antagonists, or both, are given prophylactically to prevent stress ulcers. If gastric juices are accessible through a nasogastric tube, gastric pH can be monitored as a guide to treatment. Serial hematocrit determinations establish a baseline and may be the first indication of “silent” gastrointestinal hemorrhage.

Urologic complications

After transection of the spinal cord, the bladder sphincter becomes paralyzed and urinary stasis develops. Indwelling urinary catheterization is necessary to prevent bladder distention during the acute phase.

Long-term catheterization, osteoporosis, decreased muscle tone, fluid and electrolyte abnormalities, alterations in cardiovascular dynamics, anemia, and catabolism contribute to urologic complications. Stasis, calculi and fistula formation, and chronic urinary tract complications can lead to septicemia. Pneumonia and septicemia have the greatest effect on reduced life expectancy in patients with SCI.¹⁷

Anesthetic considerations

The most influential factors in the anesthetic management of the patient with SCI are the duration of the injury (acute or chronic), fluid and electrolyte status, airway management, and autonomic hyperreflexia.

The use of a depolarizing muscle relaxant (succinylcholine) for intubation purposes in the patient with SCI is conservatively contraindicated because of the release of potassium. The succinylcholine-induced release of potassium is the result of proliferation of cholinergic receptors in muscle tissue below the level of transection. The resultant hyperkalemia, often as high as 14 mEq/L, can lead to ventricular fibrillation and cardiac arrest. The release of potassium caused by succinylcholine administration can be seen as early as 1 day after injury and as long as 9 months later. The degree of muscle involvement, not the dose of succinylcholine, is the determining factor in the amount of potassium released.

Patients with SCI may have some degree of hypotension because of a relative hypovolemia that results from sympathetic nervous system depression. The degree of the hypotension depends on the level of transection and the duration of the injury in regard to whether the patient still has spinal shock. The patient must be adequately resuscitated with fluids, and measures must be taken to monitor fluid status and ensure adequate organ perfusion.

Airway management is a significant problem in patients with SCI whose injuries involve the cervical spine. Endotracheal intubation must be performed without manipulation of the cervical spine to avoid further irreversible damage. Intubation may be accomplished with awake blind oral or nasal approach, fiberoptics, or retrograde intubation. When the airway obstruction is severe, tracheostomy or cricothyrotomy may be necessary. Patients may arrive in the PACU with the endotracheal tube in place and not undergo extubation until adequate management of the airway and ventilation are ensured.

Herniated intervertebral disk

Herniated intervertebral disk is also known as herniated nucleus pulposus (Fig. 38-9).⁸ This condition can occur in any of the intervertebral disks, but is most commonly found in one of the last two lumbar interspaces. Pain and some degree of compromise in sensory or motor function along the distribution of the involved nerve are common preoperative findings. Before surgical intervention is undertaken, diagnostic confirmation is sought and the suspected herniated nucleus pulposus is differentiated from tumor, subluxation of the facets, or rheumatoid spondylitis.