The blink reflex is often diminished or absent in the comatose patient. The eyelids may be flaccid and may depend on body positioning to remain in a closed position, and edema may prevent complete closure. Loss of these protective mechanisms results in drying and ulceration of the cornea, which can lead to permanent scarring and blindness.1

Two interventions that are commonly used to protect the eyes are instilling saline or methylcellulose lubricating drops and taping the eyelids in the shut position. Evidence suggests that an alternative technique may be more effective in preventing corneal epithelial breakdown. In addition to instillation of saline drops every 2 hours, a polyethylene film is taped over the eyes, extending beyond the orbits and eyebrows. The film creates a moisture chamber around the cornea and assists in keeping the eyes moist and in the closed position. This technique also prevents damage to the eyes that results from placement of tape or gauze directly on the delicate skin of the eyelids.¹⁰

Collaborative management of the patient in a coma is outlined in the Collaborative Management box on Coma.

An embolic stroke occurs when an embolus from the heart or lower circulation travels distally and lodges in a small vessel, obstructing the blood supply. At least 20% of ischemic strokes are attributed to a cardioembolic phenomenon.12 The most common cause of cardiac emboli is atrial fibrillation. It is responsible for about 50% of all cardiac emboli.¹⁶ Other sources of cardiac emboli are mitral stenosis, mechanical valves, atrial myxoma, endocarditis, and recent myocardial infarction.¹³ Researchers hypothesize that a patent foramen ovale or atrial septal aneurysms may be the cause of cryptogenic stroke.¹⁷

Ischemic stroke is a cerebral hemodynamic insult. When cerebral blood flow is reduced to a level insufficient to maintain neuronal viability, ischemic injury occurs. In focal stroke, an area of hypoperfused tissue, the ischemic penumbra, surrounds a core of ischemic cells. The ischemic penumbra can be salvaged with return of blood flow. However, sustained anoxic insult initiates a chain of biochemical events leading to apoptosis, or cellular death.18

The phenomenon of a focal ischemic stroke is identical to that associated with myocardial infarction, which is why brain attack is used in public education strategies. Often, a history of transient ischemic attacks (TIAs), brief episodes of neurological symptoms that last less than 24 hours, offers a warning that stroke is likely to occur. Sudden onset indicates embolism as the final insult to flow.^12,13 The size of the stroke depends on the size and location of the occluded vessel and the availability of collateral blood flow.¹² Global ischemia results when severe hypotension or cardiopulmonary arrest provokes a transient drop in blood flow to all areas of the brain.¹⁸

Cerebral edema sufficient to produce clinical deterioration develops in 10% to 20% of patients with ischemic stroke and can result in intracranial hypertension. The edema results from a loss of normal metabolic function of the cells and peaks at 4 days.¹² This process is commonly the cause of death during the first week after a stroke.¹⁹ Secondary hemorrhage at the site of the stroke lesion, known as hemorrhagic conversion,¹⁹ and seizures²⁰ are the two other major acute neurological complications of ischemic stroke.

The characteristic sign of an ischemic stroke is the sudden onset of focal neurological signs persisting for more than 24 hours.12 These signs usually occur in combination. Box 18-2 lists common patterns of neurological symptoms associated with an ischemic stroke. Hemiparesis, aphasia, and hemianopia are common. Changes in the level of consciousness usually occur only with brainstem or cerebellar involvement, seizure, hypoxia, hemorrhage, or elevated intracranial pressure (ICP). These changes may be exhibited as stupor, coma, confusion, and agitation.¹ The reported frequency of seizures in patients with ischemic stroke ranges from 3% to 8%. If seizures occur, they are usually seen within 24 hours of an insult.²⁰

The National Institutes of Health Stroke Scale (NIHSS) is often used as the basis of the focused neurological examination. The score ranges from 0 to 42 points; the higher the score, the more neurologically impaired the patient. A change of 4 points on the scale indicates significant neurological change. The components of the NIHSS include level of consciousness (LOC); LOC questions; LOC commands; gaze; visual fields; face, arm, and leg strength; sensation; limb ataxia; and language function.¹² A copy of the NIHSS with complete instructions can be retrieved at http://www.ninds.nih.gov/disorders/stroke/strokescales.htm.

Confirmation of the diagnosis of ischemic stroke is the first step in the emergency evaluation of these patients. Differentiation from intracranial hemorrhage is vital. Noncontrast CT scanning is the method of choice for this purpose and is considered the most important initial diagnostic study. In addition to excluding intracranial hemorrhage, CT can assist in identifying early neurological complications and the cause of the insult.¹² MRI can demonstrate infarction of cerebral tissue earlier than CT but is less useful in the emergency differential diagnosis.²¹ Because of the strong correlation between acute ischemic stroke and heart disease, 12-lead electrocardiography, chest radiography, and continuous cardiac monitoring are suggested to detect a cardiac cause or coexisting condition. Echocardiography is valuable in identifying a cardioembolic phenomenon when a sufficient index of suspicion warrants its use.¹ Laboratory evaluation of hematological function, electrolyte and glucose levels, and renal and hepatic function is also recommended. Arterial blood gas analysis is performed if hypoxia is suspected, and an electroencephalogram is obtained if seizures are suspected. Lumbar puncture is performed only if SAH is suspected and the CT appearance is normal.¹

Major changes have taken place in the medical management of ischemic stroke since 1996. On the basis of results of the National Institute of Neurologic Disorders and Stroke (NINDS) rtPA Stroke Study, thrombolytic therapy with intravenous recombinant tissue-type plasminogen activator (rtPA) was initially recommended within 3 hours of onset of ischemic stroke. This time frame has now been expanded from 3 hours to 4.5 hours.22 Patients who should be considered for thrombolysis are listed in Box 18-3. Confirmation of diagnosis with CT must be accomplished before rtPA administration. The recommended dose of rtPA is 0.9 mg/kg up to a maximum dose of 90 mg. Ten percent of the total dose is administered as an initial intravenous bolus, and the remaining 90% is administered by intravenous infusion over 60 minutes.^17,21

The desired result of thrombolytic therapy is to dissolve the clot and reperfuse the ischemic brain. The goal is to reverse or minimize the effects of stroke. The major risk and complication of rtPA therapy is bleeding, especially intracranial hemorrhage. Unlike thrombolytic protocols for acute myocardial infarction, subsequent therapy with anticoagulant or antiplatelet agents is not recommended after rtPA administration in ischemic stroke. Patients receiving thrombolytic therapy for stroke should not receive aspirin, heparin, or warfarin for at least 24 hours after treatment.^12,17

The major barriers to effective application of thrombolytic therapy for ischemic stroke are prehospital and in-hospital delays. To help decrease delays, the public needs to be educated about stroke symptoms and activation of the emergency medical system (EMS). EMS responders need adequate education and training on managing a patient with an acute ischemic stroke, focusing on stabilization and quick transport of the patient to the emergency department. The receiving hospital should ideally be primary stroke certified and have expert staff and the infrastructure to care for the complex stroke patient.²¹

Other emergency care of the patient with ischemic stroke must include airway protection and ventilatory assistance to maintain adequate tissue oxygenation.¹⁹ Hypertension is often present in the early period as a compensatory response, and in most cases, blood pressure (BP) must not be lowered (Table 18-2). For the patient who has not received thrombolytic therapy, antihypertensive therapy is considered only if the diastolic blood pressure is greater than 120 mm Hg or the systolic blood pressure is greater than 220 mm Hg.¹² Criteria are different for patients who have received rtPA. Their blood pressure is kept below 180/105 mm Hg to prevent intracranial hemorrhage. Intravenous labetalol or nicardipine is used to achieve blood pressure control. If these agents are not effective, nitroprusside, hydralazine, or enalaprilat should be considered.¹² Body temperature and glucose levels also must be normalized.^12,19

Medical management also includes the identification and treatment of acute complications such as cerebral edema and seizure activity. Prophylaxis for these complications is not recommended. Deep vein thrombosis (DVT) prophylaxis, however, should be initiated to decrease the risk of pulmonary embolism.¹² One study demonstrated that improved outcomes for ischemic stroke patients can be achieved by managing swallowing issues, initiating DVT prophylaxis, and treating hypoxemia.²³ Surgical decompression is recommended if a large cerebellar infarction compresses the brainstem.¹⁹

Cerebral aneurysm rupture accounts for approximately 85% of all cases of spontaneous SAH.24 An aneurysm is an outpouching of the wall of a blood vessel that results from weakening of the wall of the vessel (Table 18-3).²⁴ Ninety percent of aneurysms are congenital—the cause of which is unknown. The other 10% can be the result of traumatic injury (that stretches and tears the muscular middle layer of the arterial vessel) or infectious material (most often from infectious vegetation on valves of the left side of the heart after bacterial endocarditis) that lodges against a vessel wall and erodes the muscular layer, or they are of undetermined cause.²⁶ Multiple aneurysms occur in approximately 30% of the cases and often are bilateral, occurring in the same location on both sides of the cerebral vascular system.²⁷

TABLE 18-3

ANEURYSM CLASSIFICATION ACCORDING TO TYPE, SHAPE, LOCATION, AND COMMON CHARACTERISTICS

TYPES OF ANEURYSMS	CHARACTERISTICS
Berry or saccular	Most common type, usually congenital; appears at a bifurcation in the anterior circulation, primarily at the base of the brain or the circle of Willis and its branches; grows from the base of the arterial wall with a neck or stem; contains blood; thinned dome is usually the site of rupture
Giant or fusiform	Can have an irregular shape and can be larger than 2.5 cm and atherosclerotic; involves mainly the internal carotid or vertebrobasilar artery; rarely ruptures; has no stem; can act like a space-occupying lesion in the brain; difficult to manage
Mycotic	Rare form; usually occurs from septic emboli, usually results from bacterial infection, which weaken the vessel wall, causing dilation involving the distal branches of the middle cerebral arteries
Dissecting	May occur during angiography; caused by trauma, syphilis, or arteriosclerosis, or when blood is forced between layers of the arterial wall; intima is pulled away from the medial layer, allowing blood to enter
Traumatic	Sometimes called a pseudoaneurysm, which may resolve after trauma
Charcot-Bouchard	Small aneurysm that can be seen in the area of the basal ganglia or the brainstem in individuals with a history of hypertension; chronic hypertension causes fibrinoid necrosis in the penetrating and subcortical arteries, weakening the arterial walls and causing formation of small aneurysmal outpouching

AVM rupture is responsible for roughly 6% of all SAHs.²⁷An arteriovenous malformation is a tangled mass of arterial and venous blood vessels that shunt blood directly from the arterial side into the venous side, bypassing the capillary system. They may be small, focal lesions or large, diffuse lesions that occupy almost an entire hemisphere.²⁶ AVMs are always congenital, although the exact embryonic cause for these malformations is unknown. They also occur in the spinal cord and the renal, gastrointestinal, and integumentary systems.²⁷ In contrast to SAH from aneurysm, which occurs in the middle-aged population, SAH from an AVM usually occurs in the second to fourth decades of life.²⁷

The patient with an SAH characteristically has an abrupt onset of pain, described as the “worst headache of my life.” A brief loss of consciousness, nausea, vomiting, focal neurological deficits, and a stiff neck may accompany the headache.24,26–28 The SAH may result in coma or death.

The patient’s history may reveal one or more incidences of sudden onset of headache with vomiting in the weeks preceding a major SAH. These are small “warning leaks” of an aneurysm in which small amounts of blood ooze from the aneurysm into the subarachnoid space. The presence of blood is an irritant to the meninges, particularly the arachnoid membrane, and the irritation causes headache, stiff neck, and photophobia. These warning leaks seldom are detected because the condition is not severe enough for the patient to seek medical attention.²⁸ If a neurological deficit, such as third cranial nerve palsy, develops before aneurysm rupture, medical intervention is sought, and the aneurysm may be surgically secured before the devastation of a rupture can occur. Symptoms of unruptured AVM—headaches with dizziness or syncope or fleeting neurological deficits—also may be found in the history.²⁷

Diagnosis of SAH is based on clinical presentation, CT findings, and lumbar puncture results. Noncontrast CT is the cornerstone of definitive SAH diagnosis. In 95% of the cases, CT can demonstrate blood in the subarachnoid space if performed within 48 hours of the hemorrhage.^24,28 On the basis of the appearance and the location of the SAH, diagnosis of the cause—aneurysm or AVM—may be made from the CT scan.²⁶ MRI is not routinely used, but it may provide greater sensitivity for detecting areas of SAH clot and potential location of bleed.²⁸

If the initial CT finding is negative, a lumbar puncture is performed to obtain cerebrospinal fluid (CSF) for analysis. CSF after SAH appears bloody and has a red blood cell count greater than 1000 cells/mm³. If the lumbar puncture is performed more than 5 days after the SAH, the CSF fluid is xanthochromic (dark amber) because the blood products have broken down.²⁹ Cloudy CSF usually indicates some type of infectious process, such as bacterial meningitis, not SAH.²⁸

After the SAH has been documented, cerebral angiography is necessary to identify the exact cause of the hemorrhage. If a cerebral aneurysm rupture is the cause, angiography is essential for identifying the exact location of the aneurysm in preparation for surgery.^27,29,30 After the aneurysm has been located, it is graded using the Hunt and Hess classification scale. This scale categorizes the patient on the basis of the severity of the neurological deficits associated with the hemorrhage (Box 18-4).³¹ If AVM rupture is the cause, angiography is necessary to identify the feeding arteries and draining veins of the malformation.²⁶

SAH is a medical emergency, and time is of the essence. Preservation of neurological function is the goal, and early diagnosis is crucial. Initial treatment must always support vital functions. Airway management and ventilatory assistance may be necessary.19 A ventriculostomy is performed to control ICP if the patient’s level of consciousness is depressed.³⁰

Evidence suggests that only 19% of the deaths attributable to aneurysmal SAH are related to the direct effects of the initial hemorrhage.³² Rebleeding accounts for 22% of deaths from aneurysmal SAH, cerebral vasospasm for 23%, and nonneurological medical complications for 23%.³² Principal nonneurological causes of death are systemic inflammatory response syndrome (SIRS) and secondary organ dysfunction.³³ After initial intervention has provided necessary support for vital physiologic functions, medical management of acute SAH is aimed primarily toward prevention and treatment of the complications of SAH that can produce further neurological damage and death.²⁸

Rebleeding.

Rebleeding is the occurrence of a second SAH in an unsecured aneurysm or, less commonly, an AVM.6 The incidence of rebleeding during the first 24 hours after the first bleed is 4%, with a 1% to 2% chance per day for the following month. The mortality rate associated with aneurysmal rebleeding is approximately 70%.^26,27

Historically, conservative measures to prevent rebleeding have included blood pressure control and SAH precautions (see “Nursing Management”). An elevation in blood pressure is a normal compensatory response to maintain adequate cerebral perfusion after a neurological insult. In the belief that hypertension contributes to rebleeding, intravenous antihypertensive agents are used to maintain a systolic blood pressure no greater than 140 mm Hg.²⁸ Individualized guidelines must be determined on the basis of the clinical condition and preexisting values of the patient. Evidence suggests that rebleeding has more to do with variations in blood pressure than it does with absolute values and that blood pressure control does not lower the incidence of rebleeding.³⁰

Surgical Clipping of Aneurysms.

Definitive treatment for the prevention of rebleeding is surgical clipping or endovascular coiling with complete obliteration of the aneurysm.27,28 Timing of the operation is a key medical management issue. Since the introduction of microsurgery and improved surgical techniques, patients are commonly taken to the operating room within the first 48 hours after rupture.²⁸ This early surgical intervention to secure the aneurysm eliminates the risk of rebleeding and allows more aggressive therapy to be used in the postoperative period for the treatment of vasospasm.²⁶ Early surgery also allows the neurosurgeon to flush out the excess blood and clots from the basal cisterns (reservoir of CSF around the base of the brain and circle of Willis) to reduce the risk of vasospasm.³³ Careful consideration of the patient’s clinical situation is necessary in determining the optimal time for surgery.

The surgical procedure involves a craniotomy to expose and isolate the area of aneurysm. A clip is placed over the neck of the aneurysm to eliminate the area of weakness (Figure 18-2). This is a technically difficult procedure that requires the skill of an experienced neurosurgeon. It is not uncommon, particularly in early surgery, for the clot to break away from the aneurysm as it is surgically exposed. Extensive hemorrhage into the craniotomy site results, and cessation of the hemorrhage often causes increased neurological deficits. Deficits also may occur as a result of surgical manipulation to gain access to the site of the aneurysm.²⁸

Surgical Excision of Arteriovenous Malformations.

Management of AVMs has traditionally involved surgical excision or conservative management of such symptoms as seizures and headache. The decision for surgical excision depends on the location and size of the AVM. Some malformations are located so deep in the cerebral structures (thalamus or midbrain) that attempts to remove the AVM would cause severe neurological deficits. History of a previous hemorrhage and the patient’s age and overall condition are also taken into account in the decision regarding surgical intervention.28

Surgical excision of large AVMs includes the risk of reperfusion bleeding. As feeding arteries of the AVM are clamped off, the arterial blood that usually flowed into the AVM is diverted into the surrounding circulation. In many cases, the surrounding tissue has been in a state of chronic ischemia, and the arterial vessels feeding these areas are maximally dilated. As arterial blood begins to flow at a higher volume and pressure into these dilated arteries, blood may seep from the vessels. Evidence of reperfusion bleeding in the operating room is an indication that no more arterial blood can be diverted from the AVM without risk of serious ICH. In the postoperative phase, a low blood pressure is maintained to prevent further reperfusion bleeding. For large AVMs, two to four stages of surgery may be required over 6 to 12 months.²⁸

Embolization.

Embolization is used to secure a cerebral aneurysm or AVM that is surgically inaccessible because of size or location or because of the medical instability of the patient. Embolization involves several new interventional neuroradiology techniques. All of the techniques use a percutaneous transfemoral approach in a manner similar to an angiogram. Under fluoroscopic guidance, the catheter is threaded up to the internal carotid artery. Specially developed microcatheters are then manipulated into the area of the vascular anomaly, and embolic materials are placed endovascularly. Three embolization techniques are used, depending on the underlying pathologic derangement.26

The first type of embolization is used to embolize an AVM. Small polymeric silicone (Silastic) beads or glue is slowly introduced into the vessels feeding the AVM. Blood flow carries the material to the site, and embolization is achieved. This procedure may be used in combination with surgery. One to three sessions of embolization of the feeding vessels are performed to reduce the size of the lesion before a craniotomy is performed for total excision. The primary risk of this procedure is lodging of the embolic substance in a vessel that feeds normal tissue, which creates an embolic stroke with the immediate onset of neurological symptoms.²⁶

The second type of embolization involves placement of one or more detachable coils into an aneurysm to produce an endovascular thrombus (Figure 18-3). The advantage of this technique is that an electrical current creates a positive charge on the coil, which induces electrothrombosis. Complications include embolic stroke, coil migration, overproduction of the clot, subtotal occlusion and intraprocedural rupture of the vasculature, and death.²⁶

ICH is most often caused by hypertensive rupture of a cerebral vessel, resulting from a long-standing history of hypertension.35 Other possible causes of spontaneous ICH are anticoagulation or thrombolytic therapy, coagulation disorders, drug abuse, and hemorrhage into cerebral infarct or brain tumors.^27,38 Often on questioning, the patient with a hypertensive hemorrhage admits to having discontinued antihypertensive medication 2 to 3 weeks before the hemorrhage.

The pathophysiology of ICH is caused by continued elevated blood pressure exerting force against smaller arterial vessels that have become damaged from arteriosclerotic changes. Eventually, these arteries break, and blood bursts from the vessels into the surrounding cerebral tissue, creating a hematoma. ICP rises precipitously in response to the increase in overall intracranial volume.38

Initial assessment usually reveals a critically ill patient who often is unconscious and requires ventilatory support. History from a relative or significant other describes a sudden onset of focal deficit often accompanied by severe headache, nausea, vomiting, and rapid neurological deterioration.39 Signs and symptoms vary depending on the location of the ICH.³⁸ One third of the patients have maximal symptoms at onset. Assessment of vital signs usually reveals a severely elevated blood pressure (200/100 to 250/150 mm Hg). Signs of increased ICP are often present by the time the patient arrives in the emergency department. Diagnosis is established with CT. Angiography is recommended for patients considered surgical candidates without a clear cause of hemorrhage.^35–39

ICH is a medical emergency. Initial management requires attention to airway, breathing, and circulation. Intubation is usually necessary. Blood pressure management must be based on individual factors. Reduction in blood pressure is usually necessary to decrease ongoing bleeding, but lowering blood pressure too much or too rapidly may compromise cerebral perfusion pressure (CPP), especially in the patient with elevated ICP. National guidelines recommend keeping the mean arterial blood pressure below 130 mm Hg in patients with a history of hypertension by means of moderate blood pressure reduction to a mean arterial pressure below 110 mm Hg.39 Vasopressor therapy after fluid replenishment is recommended if systolic blood pressure falls below 90 mm Hg.³⁶

Increased ICP is common with ICH and is a major contributor to mortality. Recommended management includes mannitol when indicated, hyperventilation, and neuromuscular blockade with sedation. Steroids are avoided. The CPP must be kept higher than 70 mm Hg.^36,37

The goal for fluid management is euvolemia, with a recommended pulmonary artery occlusion pressure (PAOP) of 10 to 14 mm Hg. Body temperature is maintained at less than 38.5° C through the use of acetaminophen or cooling blankets. Euglycemia, a blood glucose level less than 140 mg/dL, is maintained with insulin therapy, but hypoglycemia should be avoided. Use of short-acting benzodiazepines or propofol is recommended to treat agitation or hyperactivity. Pneumatic compression devices are used to decrease risk of pulmonary embolism. Anticonvulsant therapy is initiated if the patient experiences seizures. Coagulation disorders should be treated, and any anticoagulation medications should be withheld.^36,39

The benefit of surgical treatment of spontaneous ICH is unclear. Recommendations for surgical removal of the clot depend on the size and location of the hematoma, the patient’s ICP, and other neurological symptoms.³⁹ Surgical evacuation of the clot is recommended for patients with cerebellar hemorrhage greater than 3 cm with neurological deterioration or hydrocephalus with brainstem compression, as well as for young patients with moderate or large lobar hemorrhage with clinical deterioration. Numerous techniques are being investigated to lessen the risk of brain damage associated with craniotomy for ICH.³⁹

Evidence-based guidelines for the management of the patient with ICH are listed in the Evidence-Based Practice box on Spontaneous Intracerebral Hemorrhage Management Guidelines.

The patient with stroke should be monitored closely for signs of bleeding, vasospasm, and increased ICP. Other complications of stroke include aspiration, malnutrition, pneumonia, DVT, pulmonary embolism, pressure ulcers, contractures, and joint abnormalities.29 Nursing measures to prevent these complications are well known.

Additional complications that may be seen in the patient with stroke are related to the area of the brain that has been damaged. Damage to the temporoparietal area can create a variety of disturbances that affect the patient’s ability to interpret sensory information. Damage to the dominant hemisphere (usually left) produces problems with speech and language and abstract and analytic skills. Damage to the nondominant hemisphere (usually right) produces problems with spatial relationships. The resulting deficits include agnosia, apraxia, and visual field defects. Perceptual deficits are not as readily noticeable as motor deficits but may be more debilitating and can lead to the inability to perform skilled or purposeful tasks. The patient also may have impaired swallowing.^26,29

Collaborative management of the patient with a stroke is outlined in the Collaborative Management box on Stroke.

Continuous assessment of the progressive paralysis associated with GBS is essential to timely intervention and the prevention of respiratory arrest and further neurological insult. After the patient is intubated and started on mechanical ventilation, close observation for pulmonary complications, such as atelectasis, pneumonia, and pneumothorax, is necessary. Autonomic dysfunction (dysautonomia) in the GBS patient can produce variations in heart rate and blood pressure that can reach extreme values.40,41,46 Hypertension and tachycardia may require beta-blocker therapy. All patients with GBS must be observed for this phenomenon.

In patients with GBS, immobility may last for months. The usual course of the disease involves an average of 10 days of symptom progression and 10 days of maximal level of dysfunction, followed by 2 to 48 weeks of recovery. Although GBS usually is completely reversible, the patient requires physical and occupational rehabilitation because of the problems of long-term immobility. Rehabilitation starts in the critical care area, with a multidisciplinary team designing and implementing an individualized plan to maximize the patient’s potential for rehabilitation.46

Pain control is another important component in the care of the patient with GBS. Although patients may have minimal to no motor function, most sensory functions remain, causing patients considerable muscle aching and pain. Because of the duration of this illness, a safe, effective, long-term solution to pain management must be identified.46 These patients also require extensive psychological support. Although the illness is almost 100% reversible, lack of control over the situation, constant pain or discomfort, and the long-term nature of the disorder create coping difficulties for the patient. GBS does not affect the level of consciousness or cerebral function. Patient interaction and communication are essential elements of the nursing management plan.

Early in the patient’s hospital stay, the patient and family must be taught about GBS and its different treatments. As the patient moves toward discharge, teaching focuses on the interventions to maximize the patient’s rehabilitation potential. The patient’s family must be encouraged to participate in the patient’s care and to learn some basic rehabilitation techniques. The importance of participating in a neurological rehabilitation program (if necessary) must be stressed (Patient Education box on Guillain-Barré Syndrome).46

Collaborative management of the patient with Guillain-Barré syndrome is outlined in the Collaborative Management box on Guillain-Barré syndrome.

In the transcranial approach, a scalp incision is made, and a series of burr holes is drilled into the skull to form an outline of the area to be opened (Figure 18-4). A special saw is then used to cut between the holes. In most cases, the bone flap is left attached to the muscle to create a hinge effect. In some cases, the bone flap is removed completely and stored for later retrieval and implantation or discarded and replaced with synthetic material. Next, the dura is opened and retracted. After the intracranial procedure, the dura and the bone flap are closed, the muscles and scalp are sutured, and a turban-like dressing is applied.^44,47

The transsphenoidal approach is the technique of choice for removal of a pituitary tumor without extension into the intracranial vault (Figure 18-5).^44,45 This approach involves making a microsurgical entrance into the cranial vault through the nasal cavity. The sphenoid sinus is entered to reach the anterior wall of the sella turcica. The sphenoid bone and the dura are then opened to gain intracranial access. After removal of the tumor, the surgical bed is packed with a small section of adipose tissue grafted from the patient’s abdomen or thigh. After closure of the intranasal structures, nasal splints and soft packing or nasal tampons impregnated with antibiotic ointment are placed in the nasal cavities. Occasionally, epistaxis balloons are used instead. A nasal drip pad or mustache-type dressing is placed at the base of the nose to catch surgical drainage.⁴⁷

The patient may be placed in a supine, prone, or sitting position for a craniotomy procedure. A skull clamp connected to skull pins is used to position and secure the patient’s head throughout the operation. During a transsphenoidal approach or a transcranial approach into the infratentorial area, the patient’s head is elevated during surgery. This position puts the patient at risk for an air embolism. Air can enter the vascular system through the edges of the dura or a venous opening. Continuous monitoring of the patient’s heart sounds by Doppler ultrasonography signal allows immediate recognition of this complication. If it occurs, an attempt may be made to withdraw the embolus from the right atrium through a central line. Flooding the surgical field with irrigation fluid and placing a moistened sterile surgical sponge over the surgical site creates an immediate barrier to any further air entrance.^44,47

Postoperative cerebral edema is expected to peak 48 to 72 hours after surgery. If the bone flap is not replaced at the time of surgery, intracranial hypertension produces bulging at the surgical site. Close monitoring of the surgical site is important so that integrity of the incision can be maintained. Postcraniotomy management of intracranial hypertension is usually accomplished through CSF drainage, patient positioning, and steroid administration.44

Surgical hemorrhage after a transcranial procedure can occur in the intracranial vault and is manifested by signs and symptoms of increasing ICP. Hemorrhage after a transsphenoidal craniotomy may be evident from external drainage, the patient’s complaint of persistent postnasal drip, or excessive swallowing. Loss of vision after pituitary surgery indicates an evolving hemorrhage. Postoperative hemorrhage requires surgical reexploration.45

Fluid imbalance in the postcraniotomy patient usually results from a disturbance in production or secretion of antidiuretic hormone (ADH). ADH is secreted by the posterior pituitary (neurohypophysis) gland. It stimulates the renal tubules and collecting ducts to retain water in response to low circulating blood volume or increased serum osmolality. Inoperative trauma or postoperative edema of the pituitary gland or hypothalamus can result in insufficient ADH secretion. The outcome is unabated renal water loss even when blood volume is low and serum osmolality is high. This condition is known as diabetes insipidus (DI). The polyuria associated with DI is often more than 200 mL/hour. Urine specific gravity of 1.005 or less and elevated serum osmolality provide evidence of insufficient ADH. The loss of volume may provoke hypotension and inadequate cerebral perfusion. DI is usually self-limiting, and fluid replacement is the only required therapy. In some cases, however, it may be necessary to administer vasopressin intravenously to control the loss of fluid.44

The syndrome of inappropriate antidiuretic hormone [secretion] (SIADH) commonly occurs with neurological insult and results from excessive ADH secretion. SIADH is manifested by inappropriate water retention with hyponatremia in the presence of normal renal function. Urine specific gravity is elevated, and urine osmolality is greater than serum osmolality. The dangers associated with SIADH include circulating volume overload and electrolyte imbalance, both of which may impair neurological functioning. SIADH is usually self-limiting, with the mainstay of treatment being fluid restriction.⁴⁴

Leakage of cerebrospinal fluid (CSF) results from an opening in the subarachnoid space, as evidenced by clear fluid draining from the surgical site. When this complication occurs after transsphenoidal surgery, it is signified by excessive, clear drainage from the nose or persistent postnasal drip. To differentiate CSF drainage from postoperative serous drainage, a specimen is tested for glucose content. A CSF leak is confirmed by glucose values of 30 mg/dL or greater. Management of the patient with a CSF leak includes bed rest and head elevation. Lumbar puncture or placement of a lumbar subarachnoid catheter may be used to reduce CSF pressure until the dura heals. The risk of meningitis associated with CSF leak often necessitates surgical repair to reseal the opening.44,45

Research has demonstrated that neurosurgical patients have a higher risk for development of a DVT than non-neurosurgical patients. This difference is due to numerous additional risk factors significantly associated with neurosurgery, including preoperative leg weakness, longer preoperative critical care unit stay, longer recovery room time, longer postoperative critical care unit stay, more days of bed rest, and delay of postoperative mobility and activity.48 Clinical manifestations of DVT include leg or calf pain, edema, localized tenderness, and pain with dorsiflexion or plantar flexion (Homans’ sign). Unfortunately, the patient with a DVT is often asymptomatic and the diagnosis is not made until the patient experiences a pulmonary embolus.

The primary treatment for DVT is prophylaxis. In the neurosurgery patient, sequential (intermittent) pneumatic compression boots or stockings are effective in reducing the incidence of DVT. Effectiveness is enhanced when these devices are initiated in the preoperative period. Low-dose unfractionated heparin or low-molecular-weight heparin may also be used prophylactically in high-risk patients.⁴⁴

When capable of compliance, the brain can tolerate significant increases in intracranial volume without much increase in ICP. The amount of intracranial compliance, however, does have a limit. After this limit has been reached, a state of decompensation with increased ICP results. As the ICP rises, the relationship between volume and pressure changes, and small increases in volume may cause major elevations in ICP (Figure 18-6).^29,50 The exact configuration of the volume-pressure curve and the point at which the steep rise in pressure occurs vary among patients. The configuration of this curve is also influenced by the cause and the rate of volume increases within the intracranial vault; for example, neurological deterioration occurs more rapidly in a patient with an acute epidural hematoma than in a patient with a meningioma of the same size.⁴⁹ Regardless of how fast the pressure increases, intracranial hypertension occurs when ICP is greater than 20 mm Hg.⁵⁰

Cerebral blood flow (CBF) corresponds to the metabolic demands of the brain and is normally 50 mL/100 g of brain tissue/min. Although the brain makes up only 2% of body weight, it requires 15% to 20% of the resting cardiac output and 15% of the body’s oxygen demands. The normal brain has a complex capacity to maintain constant CBF, despite wide ranges in systemic arterial pressure—an effect known as autoregulation. A mean arterial pressure of 50 to 150 mm Hg does not alter CBF when autoregulation is functioning. Outside the limits of this autoregulation, CBF becomes passively dependent on the perfusion pressure.50

Factors other than arterial blood pressure that affect CBF are conditions that result in acidosis, alkalosis, and changes in metabolic rate. Conditions that cause acidosis (e.g., hypoxia, hypercapnia, ischemia) result in cerebrovascular dilation. Conditions causing alkalosis (e.g., hypocapnia) result in cerebrovascular constriction. Normally, a reduction in metabolic rate (e.g., from hypothermia or barbiturates) decreases CBF, and rises in metabolic rate (e.g., from hyperthermia) increase CBF.^49,52

Arterial blood gases exert a profound effect on CBF. Carbon dioxide, which affects the pH of the blood, is a potent vasoactive substance. Carbon dioxide retention (hypercapnia) leads to cerebral vasodilation, with increased cerebral blood volume, whereas hypocapnia leads to cerebral vasoconstriction and a reduction in cerebral blood volume. Prolonged hypocapnia, however, can lead to cerebral ischemia.⁵³ Low arterial partial pressure of oxygen (PaO₂) levels, especially below 40 mm Hg, lead to cerebral vasodilation, which increases the intracranial blood volume and can contribute to increased ICP. High PaO₂ levels have not been shown to affect CBF in either direction.^49,52

Positioning of the patient is a significant factor in the prevention and treatment of intracranial hypertension. Head elevation has long been advocated as a conventional nursing intervention to control ICP, presumably by increasing venous return. However, this may decrease CPP. Close monitoring of ICP and CPP should be done with positioning, which should be customized to maximize CPP and minimize ICP.51

Positions that impede venous return from the brain cause elevations in ICP. Obstruction of jugular veins or an increase in intrathoracic or intraabdominal pressure is communicated as increased pressure throughout the open venous system, thereby impeding drainage from the brain and increasing ICP. Positions that decrease venous return from the head (e.g., Trendelenburg position, prone position, extreme flexion of the hips, angulation of the neck) must be avoided if possible. If changes to positions such as Trendelenburg are necessary to provide adequate pulmonary care, critical care nurses must closely monitor ICP and vital signs.⁴⁹

Some routine nursing activities do affect ICP and can be harmful. Use of positive end-expiratory pressures (PEEP) greater than 20 cm H₂O, coughing, suctioning, tight tracheostomy tube ties, and the Valsalva maneuver have been associated with increases in ICP. Cumulative increases in ICP have been reported when care activities are performed one after another. Conversely, family contact and gentle touch have been associated with decreases in ICP.⁴⁹

Controlled hyperventilation has been an important adjunct of therapy for the patient with increased ICP. The rationale employed in hyperventilation is that if the PaCO₂ can be reduced from its normal level of 35 to 40 mm Hg to a range of 25 to 30 mm Hg in the patient with intracranial hypertension, vasoconstriction of cerebral arteries, reduction of CBF, and increased venous return will result. This practice is being reexamined. Additional research has indicated that severe or prolonged hyperventilation can reduce cerebral perfusion and lead to cerebral ischemia and infarction. The current trend is to maintain PaCO₂ levels on the lower side of normal (35 ± 2 mm Hg) by carefully monitoring arterial blood gas measurements and by adjusting ventilator settings.53,55

Although hypoxemia must be avoided, excessively high levels of oxygen offer no benefits, and increasing inspired oxygen concentrations above 60% may lead to toxic changes in lung tissue. The use of pulse oximetry has led to greater awareness of the circumstances, such as pain and anxiety, that can cause oxygen desaturation and therefore elevate ICP.^29,49

Directly proportional to body temperature, cerebral metabolic rate increases 10% per 1° C of increase in body temperature.51 This fact is significant because as the cerebral metabolic rate increases, blood flow to the brain must increase to meet the tissue demands. To avoid the increase in blood volume associated with a greater cerebral metabolic rate, nurses must prevent hyperthermia in the patient with a brain injury. Antipyretics and cooling devices must be used when appropriate while the source of the fever is being determined.^51,52

Maintenance of arterial blood pressure in the high-normal range is essential in the brain-injured patient. Inadequate perfusion pressure decreases the supply of nutrients and oxygen requirements for cerebral metabolic needs. However, a blood pressure that is too high increases cerebral blood volume and may raise ICP.52 Figure 18-7 shows the relationship between blood pressure and ICP.

Control of systemic hypertension may require nothing more than the administration of a sedative agent. Small, frequent doses may be sufficient to blunt noxious stimuli and prevent them from triggering increases in blood pressure. When sedation proves inadequate in controlling systemic arterial hypertension, antihypertensive agents are used. Care must be taken in choosing these agents because many of the peripheral vasodilators (e.g., nitroprusside, nitroglycerin) also are cerebral vasodilators. All antihypertensives are believed to cause some degree of cerebral vasodilation. To reduce this vasodilating effect, concurrent treatment with beta-blockers (e.g., metoprolol, labetalol) may be beneficial.^49,52

Systemic hypotension should be treated aggressively with fluids to maintain a systolic blood pressure greater than 90 mm Hg. Crystalloids, colloids, and blood products can be used, depending on the patient’s condition. Studies have demonstrated a positive effect on ICP and CPP with hypertonic saline. If fluids fail to adequately elevate the patient’s blood pressure, the use of inotropic agents may be necessary.⁴⁹

The incidence of posttraumatic seizures in the head-injured population has been estimated at 15% to 20%. Because of the risk of a secondary ischemic insult associated with seizures, many physicians prescribe anticonvulsant medications prophylactically. Seizures cause metabolic requirements to increase, resulting in elevation of CBF, cerebral blood volume, and ICP, even in paralyzed patients. If blood flow cannot match demand, ischemia develops, cerebral energy stores are depleted, and irreversible neuronal destruction occurs. The usual anticonvulsant regimen for seizure control includes phenytoin or phenobarbital, or both, in therapeutic doses.52 Fast-acting, short-duration agents such as lorazepam may be indicated for breakthrough seizures until therapeutic levels of the longer-acting drugs can be achieved.

CSF drainage for intracranial hypertension may be used with other treatment modalities (Figures 18-8 and 18-9). CSF drainage is accomplished by the insertion of a pliable catheter into the anterior horn of the lateral ventricle (ventriculostomy), preferably on the nondominant side. This drainage can help support the patient through periods of cerebral edema by controlling spikes in ICP. One of the major advantages of the ventriculostomy is its dual role as a monitoring device and a treatment modality. Care should be taken to avoid infection. However, cleansing ointment such as bacitracin or povidone is not recommended.⁵⁶

Osmotic diuretics and hypertonic saline have also been used to reduce increased ICP. In the presence of an intact blood-brain barrier, hyperosmolar therapy is used to draw water from brain tissue into the intravascular compartment. The direction of flow is from the hypoconcentrated tissue to the hyperconcentrated cerebral vasculature.52

The most widely used osmotic diuretic is mannitol, a large-molecule agent that is retained almost entirely in the extracellular compartment and has little or none of the rebound effect observed with other osmotic diuretics. Administration of mannitol increases cerebral blood flow and thus induces cerebral vasoconstriction as part of the brain’s autoregulatory response to maintain blood flow constant.⁵²

Two major complications associated with osmotic diuretics are electrolyte disturbances and dehydration. Careful attention must be paid to body weight and fluid and electrolyte stability. Serum osmolality should be kept between 300 and 320 mOsm/L. Hypernatremia and hypokalemia often are associated with repeated administration of osmotic agents. Central venous pressure readings should be monitored to assess for hypovolemia. Smaller doses of mannitol simplify fluid and electrolyte management, and their use is encouraged whenever possible.^49,52

Hypertonic saline, given in concentrations ranging from 3% to 23.4%, can also be used to treat increased ICP. Hypertonic saline can be used in hypovolemic patients when mannitol is contraindicated.⁵² Adverse effects include electrolyte abnormalities,⁵² hypotension, pulmonary edema, acute renal failure, hemolysis, central pontine myelinolyisis, coagulopathy, and dysrhythmias.⁵⁷

Any treatment modality that increases the incidence of noxious stimulation to the patient carries with it the potential for increasing ICP. Noxious stimuli include pain, the presence of an endotracheal tube, coughing, suctioning, repositioning, bathing, and many other routine nursing interventions. Agents used to reduce metabolic demands include the use of benzodiazepines such as midazolam and lorazepam, intravenous sedative-hypnotics such as propofol, opioid narcotics such as fentanyl and morphine, and neuromuscular blocking agents such as vecuronium and atracurium. These agents may be administered separately or in combination by continuous drip or as an intravenous bolus on an as-needed basis.49

The preferred treatment regimen begins with the administration of benzodiazepines for sedation and narcotics for analgesia. If these agents fail to blunt the patient’s response to noxious stimuli, propofol or a neuromuscular blocking agent is added. The use of these medications is recommended only in patients with an ICP monitor in place, because sedatives, opioids, and neuromuscular blocking agents affect the reliability of neurological assessment. The use of neuromuscular blocking agents without sedation is not recommended because these agents can cause skeletal muscle paralysis and because they have no analgesic effect and do not adequately protect the patient from pain and the physiological responses that can occur from pain-producing procedures.⁵⁸ If these agents fail to control the patient’s ICP, barbiturate therapy is considered.⁵²

The four types of supratentorial herniation syndrome are uncal; central, or transtentorial; cingulate; and transcalvarial (Figure 18-10).