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.