chapter 66 patients with neurologic function

nursing process for altered level of consciousness

NURSING PROCESS The Patient With an Altered Level of Consciousness Assessment Assessment of the patient with an altered LOC often starts with assessing the verbal response through determining the patient's orientation to time, person, and place. Patients are asked to identify the day, date, or season of the year, as well as where they are or the clinicians, family members, or visitors present. Other questions such as "Who is the president?" or "What is the next holiday?" may be helpful in determining the patient's processing of information. Verbal response cannot be evaluated if the patient is intubated or has a tracheostomy, and this should be clearly documented. Alertness is measured by the patient's ability to open the eyes spontaneously or in response to a vocal or noxious stimulus (pressure or pain). Patients with severe neurologic dysfunction cannot do this. The nurse assesses for periorbital edema (swelling around the eyes) or trauma, which may prevent the patient from opening the eyes, and documents any such condition that interferes with eye opening. Motor response includes spontaneous, purposeful movement (e.g., the awake patient can move all four extremities with equal strength on command), movement only in response to painful stimuli, or abnormal posturing. If the patient is not responding to commands, the motor response is tested by applying a painful stimulus (firm but gentle pressure) to the nail bed or by squeezing a muscle. If the patient attempts to push away or withdraw, the response is recorded as purposeful or appropriate ("Patient withdraws to painful stimulus"). This response is considered purposeful if the patient can cross the midline from one side of the body to the other in response to a painful stimulus. An inappropriate or nonpurposeful response is random and aimless. Posturing may be decorticate or decerebrate (see Fig. 66-1; see also Chapter 65). The most severe neurologic impairment results in flaccidity. The motor response cannot be elicited or assessed when the patient has been given pharmacologic paralyzing agents (i.e., neuromuscular blocking agents). Figure 66-1 • Abnormal posture response to stimuli. A. Decorticate posturing and flexion of the upper extremities, internal rotation of the lower extremities, and plantar flexion of the feet. B. Decerebrate posturing, involving extension and outward rotation of upper extremities and plantar flexion of the feet. Adapted from Posner, J. B., Saper, C. B., Schiff, N. D., et al. (2007). Plum and Posner's diagnosis of stupor and coma (4th ed.). Oxford, UK: Oxford University Press. In addition to LOC, the nurse monitors parameters such as respiratory status, eye signs, and reflexes on an ongoing basis. Table 66-1 summarizes the assessment and the clinical significance of the findings. Body functions (circulation, respiration, elimination, fluid and electrolyte balance) are examined in a systematic and ongoing manner. Diagnosis NURSING DIAGNOSES Based on the assessment data, major nursing diagnoses may include the following: Ineffective airway clearance related to inability to maintain an airway due to altered LOC Risk for injury related to lack of adaptive and defensive resources due to decreased LOC Deficient fluid volume related to inability to take fluids by mouth Risk for imbalanced nutrition: less than body requirements related to inability to ingest nutrients to meet metabolic needs Impaired oral mucous membrane related to mouth breathing, absence of pharyngeal reflex, and altered fluid intake Risk for impaired skin integrity related to prolonged immobility Risk for impaired tissue integrity of cornea related to diminished or absent corneal reflex Ineffective thermoregulation related to damage to hypothalamic center Impaired urinary elimination (incontinence or retention) related to impairment in neurologic sensing and control Bowel incontinence related to impairment in neurologic sensing and control and also related to changes in nutritional delivery methods Ineffective health maintenance related to neurologic impairment Interrupted family processes related to health crisis COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS Potential complications may include the following: Respiratory distress or failure Pneumonia Aspiration Pressure ulcer Venous thromboembolism (VTE) Contractures Planning and Goals The patient with altered LOC is subject to all of the complications associated with immobility. Therefore, the goals of care for the patient with altered LOC include maintenance of a clear airway, protection from injury, attainment of fluid volume balance, maintenance of nutritional needs, achievement of intact oral mucous membranes, maintenance of normal skin integrity, absence of corneal irritation, attainment of effective thermoregulation, and effective urinary elimination. Additional goals include bowel continence, restoration of health maintenance, maintenance of intact family or support system, and absence of complications. Because the protective reflexes of the patient who is unconscious are impaired, the quality of nursing care provided may mean the difference between life and death. The nurse must assume responsibility for the patient until the basic reflexes (coughing, blinking, and swallowing) return and the patient becomes conscious and oriented. Therefore, the major nursing goal is to compensate for the absence of these protective reflexes. Nursing Interventions MAINTAINING THE AIRWAY The most important consideration in managing the patient with altered LOC is to establish an adequate airway and ensure ventilation. Obstruction of the airway is a risk because the epiglottis and tongue may relax, occluding the oropharynx, or the patient may aspirate vomitus or nasopharyngeal secretions. The accumulation of secretions in the pharynx presents a serious problem. Because the patient cannot swallow and lacks pharyngeal reflexes, these secretions must be removed to eliminate the danger of aspiration. Elevating the head of the bed to 30 degrees helps prevent aspiration. Positioning the patient in a lateral or semiprone position also helps because it allows the jaw and tongue to fall forward, thus promoting drainage of secretions. Positioning alone is not always adequate, however. Suctioning and oral hygiene may be required. Suctioning is performed to remove secretions from the posterior pharynx and upper trachea. Before and after suctioning, the patient is adequately ventilated to prevent hypoxia (Hickey, 2014). Chest physiotherapy and postural drainage may be initiated to promote pulmonary hygiene, unless contraindicated by the patient's underlying condition. The chest should be auscultated at least every 8 hours to detect adventitious breath sounds or absence of breath sounds. Despite these measures, or because of the severity of impairment, the patient with altered LOC often requires intubation and mechanical ventilation. Nursing actions for the patient who is mechanically ventilated include maintaining the patency of the endotracheal tube or tracheostomy, providing frequent oral care, monitoring arterial blood gas measurements, and maintaining ventilator settings (see Chapter 21). PROTECTING THE PATIENT For the protection of the patient, side rails are padded. Two rails are kept in the raised position during the day and three at night; however, raising all four side rails is considered a restraint by the Joint Commission if the intent is to limit the patient's mobility. Care should be taken to prevent injury from invasive lines and equipment, and other potential sources of injury should be identified, such as restraints, tight dressings, environmental irritants, damp bedding or dressings, and tubes and drains. Protection also includes ensuring the patient's dignity during altered LOC. Simple measures such as providing privacy and speaking to the patient during nursing care activities preserve the patient's dignity. Not speaking negatively about the patient's condition or prognosis is also important, because patients in a coma may be able to hear. The patient who is comatose has an increased need for advocacy, and the nurse is responsible for seeing that these advocacy needs are met. MAINTAINING FLUID BALANCE AND MANAGING NUTRITIONAL NEEDS Hydration status is assessed by examining tissue turgor and mucous membranes, assessing intake and output trends, and analyzing laboratory data. Fluid needs are met initially by administering the required IV fluids. However, IV solutions (and blood component therapy) for patients with intracranial conditions must be given slowly. If they are given too rapidly, they can increase ICP. The quantity of fluids given may be restricted to minimize the possibility of cerebral edema. If the patient does not recover quickly and sufficiently enough to take adequate fluids and calories by mouth, a feeding or gastrostomy tube will be inserted for the administration of fluids and enteral feedings. Research suggests that patients fed within 48 hours of injury have improved outcomes over those in whom nutrition is delayed (Wang, Dong, Han, et al., 2013). PROVIDING MOUTH CARE The mouth is inspected for dryness, inflammation, and crusting. The patient who is unconscious requires careful oral care, because there is a risk of parotitis if the mouth is not kept scrupulously clean. The mouth is cleansed and rinsed carefully to remove secretions and crusts and to keep the mucous membranes moist. A thin coating of petrolatum on the lips prevents drying, cracking, and encrustations. If the patient has an endotracheal tube, the tube should be moved to the opposite side of the mouth daily to prevent ulceration of the mouth and lips. If the patient is intubated and mechanically ventilated, good oral care is also necessary. Research suggests that comprehensive mouth care with antiseptic such as chlorhexidine and head of bed elevation decreases ventilator-associated pneumonia and improves the oral health in patients who are intubated (Munro & Ruggiero, 2014). MAINTAINING SKIN AND JOINT INTEGRITY Preventing skin breakdown requires continuing nursing assessment and intervention. Special attention is given to patients who are unconscious, because they cannot respond to external stimuli. Assessment includes a regular schedule of turning to avoid pressure, which can cause breakdown and necrosis of the skin. Turning also provides kinesthetic (sensation of movement), proprioceptive (awareness of position), and vestibular (equilibrium) stimulation. After turning, the patient is carefully repositioned to prevent ischemic necrosis over pressure areas. Dragging or pulling the patient up in bed must be avoided, because this creates a shearing force and friction on the skin surface (see Chapter 10). Maintaining correct body position is important; equally important is passive exercise of the extremities to prevent contractures. The use of splints or foam boots aids in the prevention of footdrop and eliminates the pressure of bedding on the toes. The use of trochanter rolls to support the hip joints keeps the legs in proper alignment. The arms are in abduction, the fingers lightly flexed, and the hands in slight supination. The heels of the feet are assessed for pressure areas. Specialty beds, such as fluidized or low-air-loss beds, may be used to decrease pressure on bony prominences (Hickey, 2014). PRESERVING CORNEAL INTEGRITY Some patients who are unconscious have their eyes open and have inadequate or absent corneal reflexes. The cornea may become irritated, dry, or scratched, leading to ulceration. The eyes may be cleansed with cotton balls moistened with sterile normal saline to remove debris and discharge. If artificial tears are prescribed, they may be instilled every 2 hours. Periorbital edema often occurs after cranial surgery. If cold compresses are prescribed, care must be exerted to avoid contact with the cornea. Eye patches should be used cautiously because of the potential for corneal abrasion from contact with the patch. MAINTAINING BODY TEMPERATURE High fever in the patient who is unconscious may be caused by infection of the respiratory or urinary tract, drug reactions, or damage to the hypothalamic temperature-regulating center. A slight elevation of temperature may be caused by dehydration. The environment can be adjusted, depending on the patient's condition, to promote a normal body temperature. If body temperature is elevated, a minimum amount of bedding is used. The room may be cooled to 18.3°C (65°F). However, if the patient is an older adult and does not have an elevated temperature, a warmer environment is needed. Because of damage to the temperature-regulating center in the brain or severe intracranial infection, patients who are unconscious often develop very high temperatures. Such temperature elevations must be controlled, because the increased metabolic demands of the brain can exceed cerebral circulation and oxygen delivery, potentially resulting in cerebral deterioration (Hickey, 2014). Studies suggest that hyperthermia may contribute to poor outcome after brain injury but not through a decreased brain oxygen level (Madden & DeVon, 2015). Persistent hyperthermia with no identified clinical source of infection indicates brainstem damage and a poor prognosis. Quality and Safety Nursing Alert The body temperature of a patient who is unconscious is never taken by mouth. Rectal, tympanic (if not contraindicated), or core temperature measurement is preferred to the less accurate axillary temperature. Strategies for reducing fever include: Removing all bedding over the patient (with the possible exception of a light sheet, towel, or small drape) Administering acetaminophen or ibuprofen as prescribed Giving cool sponge baths Using a hypothermia blanket Monitoring temperature frequently to assess the patient's response to the therapy and to prevent an excessive decrease in temperature and shivering PREVENTING URINARY RETENTION The patient with an altered LOC is often incontinent or has urinary retention. The bladder is palpated or scanned at intervals to determine whether urinary retention is present, because a full bladder may be an overlooked cause of overflow incontinence. A portable bladder ultrasound instrument is a useful tool in bladder management and retraining programs. If the patient is not voiding, a program of intermittent catheterization should be devised in order to reduce the patient's risk of urinary tract infection. A catheter may be inserted during the acute phase of illness to monitor urinary output. Because catheters are a major cause of urinary tract infection, the patient is observed for fever and cloudy urine. The area around the urethral orifice is inspected for drainage and cleansed routinely. The urinary catheter is usually removed if the patient has a stable cardiovascular system and if no diuresis, sepsis, or voiding dysfunction existed before the onset of coma. Although many patients who are unconscious urinate spontaneously after catheter removal, the bladder should be palpated or scanned with a portable ultrasound device periodically for urinary retention (see Chapter 53, Fig. 53-8). An external catheter (condom catheter) for the male patient and absorbent pads for the female patient can be used for patients who are unconscious and can urinate spontaneously, although involuntarily. As soon as consciousness is regained, a bladder training program is initiated (Hickey, 2014). The patient who is incontinent is monitored frequently for skin irritation and skin breakdown. Appropriate skin care is implemented to prevent these complications. PROMOTING BOWEL FUNCTION The abdomen is assessed for distention by listening for bowel sounds and measuring the girth of the abdomen with a tape measure. There is a risk of diarrhea from infection, antibiotic agents, and hyperosmolar fluids. Frequent loose stools may also occur with fecal impaction. Commercial fecal collection bags are available for patients with fecal incontinence (see Chapter 47, Fig. 47-1). Immobility and lack of dietary fiber can cause constipation. The nurse monitors the number and consistency of bowel movements and performs a rectal examination for signs of fecal impaction. Stool softeners may be prescribed and can be given with tube feedings. To facilitate bowel emptying, a glycerin suppository may be indicated. The patient may require an enema every other day to empty the lower colon. RESTORING HEALTH MAINTENANCE Once increased ICP is not a problem, the nurse assists the patient and family to restore the health of the patient who is unconscious. This involves using auditory, visual, olfactory, gustatory, tactile, and kinesthetic activities to stimulate the patient emerging from coma (Megha, Harpreet, & Nayeem, 2013). Efforts are made to restore the sense of daily rhythm by maintaining usual day and night patterns for activity and sleep. The nurse touches and talks to the patient and encourages family members and friends to do so. Communication is extremely important and includes touching the patient and spending enough time with the patient to become sensitive to their needs. It is also important to avoid making any negative comments about the patient's status or prognosis in the patient's presence. The nurse orients the patient to time and place at least once every 8 hours. Sounds from the patient's usual environment may be introduced using a tape recorder. Family members can read to the patient from a favorite book and may suggest radio and television programs that the patient previously enjoyed as a means of enriching the environment and providing familiar input. When arousing from coma, many patients experience a period of agitation, indicating that they are becoming more aware of their surroundings but still cannot react or communicate in an appropriate fashion. Although this is disturbing for many family members, it is actually a positive clinical sign. At this time, it is necessary to minimize stimulation by limiting background noises, having only one person speak to the patient at a time, giving the patient a longer period of time to respond, and allowing for frequent rest or quiet times. After the patient has regained consciousness, videotaped family or social events may assist the patient in recognizing family and friends and allow him or her to experience missed events. Programs of sensory stimulation for patients with brain injury have been developed in an effort to improve outcomes. Although these are controversial programs with inconsistent results, some research supports the concept of providing structured stimulation (Megha et al., 2013). MEETING THE FAMILY'S NEEDS The family of the patient with altered LOC may be thrown into a sudden state of crisis and go through the process of severe anxiety, denial, anger, remorse, grief, and reconciliation. Depending on the disorder that caused the altered LOC and the extent of the patient's recovery, the family may be unprepared for the changes in the cognitive and physical status of their loved one. If the patient has significant residual deficits, the family may require considerable time, assistance, and support to come to terms with these changes. To help family members mobilize resources and coping skills, the nurse reinforces and clarifies information about the patient's condition, encourages the family to be involved in care, and listens to and encourages ventilation of feelings and concerns while supporting decision making about management and placement after hospitalization. Families may benefit from participation in support groups offered through the hospital, rehabilitation facility, or community organizations. The family may need to face the death of their loved one. The patient with a neurologic disorder is often pronounced brain dead before the heart stops beating. The term brain death describes irreversible loss of all functions of the entire brain and absence of brainstem reflexes (Wijdicks, 2013). The term may be misleading to the family because, although brain function has ceased, the patient appears to be alive, with the heart rate and blood pressure sustained by vasoactive medications and breathing continued by mechanical ventilation. When discussing a patient who is brain dead with family members, it is important to provide accurate, timely, understandable, and consistent information. See Chapter 16 for discussion of end-of-life care. MONITORING AND MANAGING POTENTIAL COMPLICATIONS Pneumonia, aspiration, and respiratory failure are potential complications in any patient who has a depressed LOC and who cannot protect the airway or turn, cough, and take deep breaths. The longer the period of unconsciousness, the greater the risk of pulmonary complications. Vital signs and respiratory function are monitored closely to detect any signs of respiratory failure or distress. Complete blood count and arterial blood gas measurements are assessed to determine whether there are adequate red blood cells to carry oxygen and whether ventilation is effective. Chest physiotherapy and suctioning are initiated to prevent respiratory complications such as pneumonia. Oral care interventions are performed for patients receiving mechanical ventilation to maintain oral health and decrease the incidence of pneumonia (Kiyoshi-Teo & Blegen, 2015). If pneumonia develops, cultures are obtained to identify the organism so that appropriate antibiotic agents can be given. The patient with altered LOC is monitored closely for evidence of impaired skin integrity, and strategies to prevent skin breakdown and pressure ulcers are continued through all phases of care, including hospitalization, rehabilitation, and home care. Factors that contribute to impaired skin integrity (e.g., incontinence, inadequate dietary intake, pressure on bony prominences, edema) are addressed. If pressure ulcers develop, strategies to promote healing are undertaken. Care is taken to prevent bacterial contamination of pressure ulcers, which may lead to sepsis and septic shock. See Chapter 10 for assessment and management of pressure ulcers. The patient should also be monitored for signs and symptoms of VTE, which may manifest as a deep vein thrombosis (DVT) or pulmonary embolism (PE). Prophylaxis with subcutaneous heparin or low-molecular-weight heparin (dalteparin [Fragmin], danaparoid [Orgaran]) as well as antiembolism stockings or pneumatic compression devices are prescribed according to the patient's risk factors for thrombosis and bleeding (Foreman, Schmalz, & Griessenauer, 2014). The nurse observes for signs and symptoms of DVT or PE. Patients with a prolonged decrease in LOC are at risk for developing contractures. During acute care, the patient is turned every 2 hours and passive range of motion performed at least twice a day. Splints, provided by occupational therapy, are applied to the hands and feet in a rotating manner to maintain functional joint alignment. Hand splints have been reported to be safe and beneficial for patients in decreasing spasticity and improving hand opening (Thibault, Deltombe, Wannez, et al., 2015). See Chapter 10 for further information about management of contractures.

increased intercranial pressure

The rigid cranial vault contains brain tissue (1400 g), blood (75 mL), and CSF (75 mL). The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP. ICP is usually measured in the lateral ventricles, with the normal pressure being 0 to 10 mm Hg, and 15 mm Hg being the upper limit of normal (Hickey, 2014). The Monro-Kellie hypothesis, also known as the Monro-Kellie doctrine, explains the dynamic equilibrium of cranial contents. The hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others. Because brain tissue has limited space to expand, compensation typically is accomplished by displacing or shifting CSF, increasing the absorption or diminishing the production of CSF, or decreasing cerebral blood volume. Without such changes, ICP begins to rise. Under normal circumstances, minor changes in blood volume and CSF volume occur constantly as a result of alterations in intrathoracic pressure (coughing, sneezing, straining), posture, blood pressure, and systemic oxygen and carbon dioxide levels (Hickey, 2014). Pathophysiology Increased ICP affects many patients with acute neurologic conditions because pathologic conditions alter the relationship between intracranial volume and ICP. Although elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies. Increased ICP from any cause decreases cerebral perfusion, stimulates further swelling (edema), and may shift brain tissue, resulting in herniation—a dire and frequently fatal event. Decreased Cerebral Blood Flow Increased ICP may reduce cerebral blood flow, resulting in ischemia and cell death. In the early stages of cerebral ischemia, the vasomotor centers are stimulated and the systemic pressure rises to maintain cerebral blood flow. Usually, this is accompanied by a slow bounding pulse and respiratory irregularities. These changes in blood pressure, pulse, and respiration are important clinically because they suggest increased ICP. The concentration of carbon dioxide in the blood and in the brain tissue also plays a role in the regulation of cerebral blood flow. An increase in the partial pressure of arterial carbon dioxide (PaCO2) causes cerebral vasodilation, leading to increased cerebral blood flow and increased ICP. A decrease in PaCO2 has a vasoconstrictive effect, limiting blood flow to the brain. Decreased venous outflow may also increase cerebral blood volume, thus raising ICP. Cerebral Edema Cerebral edema or swelling is defined as an abnormal accumulation of water or fluid in the intracellular space, extracellular space, or both, associated with an increase in the volume of brain tissue. Edema can occur in the gray, white, or interstitial matter. As brain tissue swells within the rigid skull, several mechanisms attempt to compensate for the increasing ICP. These compensatory mechanisms include autoregulation as well as decreased production and flow of CSF. Autoregulation refers to the brain's ability to change the diameter of its blood vessels to maintain a constant cerebral blood flow during alterations in systemic blood pressure. This mechanism can be impaired in patients who are experiencing a pathologic and sustained increase in ICP. Cerebral Response to Increased Intracranial Pressure As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage. The brain can maintain a steady perfusion pressure if the arterial systolic blood pressure is 50 to 150 mm Hg and the ICP is less than 40 mm Hg. Changes in ICP are closely linked with cerebral perfusion pressure (CPP). The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP). For example, if the MAP is 100 mm Hg and the ICP is 15 mm Hg, then the CPP is 85 mm Hg. The normal CPP is 70 to 100 mm Hg (Hickey, 2014). As ICP rises and the autoregulatory mechanism of the brain is overwhelmed, the CPP can increase to greater than 100 mm Hg or decrease to less than 50 mm Hg. Patients with a CPP of less than 50 mm Hg experience irreversible neurologic damage. Therefore, the CPP must be maintained at 70 to 80 mm Hg to ensure adequate blood flow to the brain. If ICP is equal to MAP, cerebral circulation ceases. A clinical phenomenon known as the Cushing's response (or Cushing's reflex) is seen when cerebral blood flow decreases significantly. When ischemic, the vasomotor center triggers an increase in arterial pressure in an effort to overcome the increased ICP. A sympathetically mediated response causes an increase in the systolic blood pressure with a widening of the pulse pressure and cardiac slowing. This response is seen clinically as an increase in systolic blood pressure, widening of the pulse pressure, and reflex slowing of the heart rate. It is a late sign requiring immediate intervention; however, perfusion may be recoverable if the Cushing's response is treated rapidly. At a certain point, the brain's ability to autoregulate becomes ineffective and decompensation (ischemia and infarction) begins. When this occurs, the patient exhibits significant changes in mental status and vital signs. The bradycardia, hypertension, and bradypnea associated with this deterioration are known as Cushing's triad, which is a grave sign. At this point, herniation of the brainstem and occlusion of the cerebral blood flow occur if therapeutic intervention is not initiated. Herniation refers to the shifting of brain tissue from an area of high pressure to an area of lower pressure (see Fig. 66-2). The herniated tissue exerts pressure on the brain area into which it has shifted, which interferes with the blood supply in that area. Cessation of cerebral blood flow results in cerebral ischemia, infarction, and brain death. Figure 66-2 • Cross-section of the brain showing herniation of part of the temporal lobe through the tentorium as a result of a temporoparietal epidural hematoma. Reprinted with permission from Hickey, J. V. (2014). The clinical practice of neurological & neurosurgical nursing (7th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. Clinical Manifestations If ICP increases to the point at which the brain's ability to adjust has reached its limits, neural function is impaired; this may be manifested at first by clinical changes in LOC and later by abnormal respiratory and vasomotor responses. Quality and Safety Nursing Alert The earliest sign of increasing ICP is a change in LOC. Agitation, slowing of speech, and delay in response to verbal suggestions may be early indicators. Any sudden change in the patient's condition, such as restlessness (without apparent cause), confusion, or increasing drowsiness, has neurologic significance. These signs may result from compression of the brain due to swelling from hemorrhage or edema, an expanding intracranial lesion (hematoma or tumor), or a combination of both. As ICP increases, the patient becomes stuporous, reacting only to loud or painful stimuli. At this stage, serious impairment of brain circulation is probably taking place, and immediate intervention is required. As neurologic function deteriorates further, the patient becomes comatose and exhibits abnormal motor responses in the form of decortication (abnormal flexion of the upper extremities and extension of the lower extremities), decerebration (extreme extension of the upper and lower extremities), or flaccidity (see Fig. 66-1). If the coma is profound and irreversible with no known confounding factors, brainstem reflexes are absent, and respirations are impaired or absent, the patient may be evaluated for brain death (Wijdicks, 2013). Assessment and Diagnostic Findings The diagnostic studies used to determine the underlying cause of increased ICP are discussed in detail in Chapter 65. The most common diagnostic tests are CT scanning and MRI. The patient may also undergo cerebral angiography, PET, or SPECT. Transcranial Doppler studies provide information about cerebral blood flow. The patient with increased ICP may also undergo electrophysiologic monitoring to observe cerebral blood flow indirectly. Evoked potential monitoring measures the electrical potentials produced by nerve tissue in response to external stimulation (auditory, visual, or sensory). Lumbar puncture is avoided in patients with increased ICP, because the sudden release of pressure in the lumbar area can cause the brain to herniate (Hickey, 2014). See Chapter 65 for further discussion of lumbar puncture and other diagnostic tests. Complications Complications of increased ICP include brainstem herniation, diabetes insipidus, and syndrome of inappropriate antidiuretic hormone (SIADH). Brainstem herniation results from an excessive increase in ICP in which the pressure builds in the cranial vault and the brain tissue presses down on the brainstem. This increasing pressure on the brainstem results in cessation of blood flow to the brain, leading to irreversible brain anoxia and brain death. Neurogenic diabetes insipidus is the result of decreased secretion of antidiuretic hormone (ADH). The patient has excessive urine output, decreased urine osmolality, and serum hyperosmolarity (Grossman & Porth, 2014). Therapy consists of administration of fluids, electrolyte replacement, and administration of a synthetic vasopressin (desmopressin [DDAVP]). See Chapters 13 and 52 for a discussion of diabetes insipidus. SIADH is the result of increased secretion of ADH. The patient becomes volume overloaded, urine output diminishes, and serum sodium concentration becomes dilute. Treatment of SIADH includes fluid restriction (less than 800 mL/day with no free water), which is usually sufficient to correct the hyponatremia. In severe cases, careful administration of a 3% hypertonic saline solution may be therapeutic (Aylwin, Burst, Peri, et al., 2015). The change in serum sodium concentration should not exceed a correction rate of approximately 1.3 mEq/L/hr. See Chapters 13 and 52 for further discussion of SIADH. Medical Management Increased ICP is a true emergency and must be treated promptly. Invasive monitoring of ICP is an important component of management. Immediate management to relieve increased ICP requires decreasing cerebral edema, lowering the volume of CSF, or decreasing cerebral blood volume while maintaining cerebral perfusion. These goals are accomplished by administering osmotic diuretics, restricting fluids, draining CSF, controlling fever, maintaining systemic blood pressure and oxygenation, and reducing cellular metabolic demands. See Chapter 68 for a discussion of the management of increased ICP. Monitoring Intracranial Pressure and Cerebral Oxygenation The purposes of ICP monitoring are to identify increased pressure early in its course (before cerebral damage occurs), to quantify the degree of elevation, to initiate appropriate treatment, to provide access to CSF for sampling and drainage, and to evaluate the effectiveness of treatment. ICP can be monitored with the use of an intraventricular catheter (ventriculostomy), a subarachnoid bolt, an epidural or subdural catheter, or a fiberoptic transducer-tipped catheter placed in the subdural space or in the ventricle (see Fig. 66-3). When a ventriculostomy or intraventricular catheter monitoring device is used for monitoring ICP, a fine-bore catheter is inserted into a lateral ventricle, preferably in the nondominant hemisphere of the brain (American Association of Neuroscience Nurses [AANN], 2012). The catheter is connected by a fluid-filled system to a transducer, which records the pressure in the form of an electrical impulse. In addition to obtaining continuous ICP recordings, the ventricular catheter allows CSF to drain, particularly during acute increases in pressure. The ventriculostomy can also be used to drain blood from the ventricle. Continuous drainage of CSF under pressure control is an effective method of treating intracranial hypertension. Another advantage of a ventricular catheter is access for the intraventricular administration of medications and the occasional instillation of air or a contrast agent for ventriculography. Complications associated with its use include infection, meningitis, ventricular collapse, occlusion of the catheter by brain tissue or blood, and problems with the monitoring system. Figure 66-3 • Intracranial pressure monitoring. A device may be placed in the ventricle (A), the subarachnoid space (B), the intraparenchymal space (C), or the subdural space (D). p. 1981 The subarachnoid screw or bolt is a hollow device that is inserted through the skull and dura mater into the cranial subarachnoid space (Hickey, 2014). It has the advantage of not requiring a ventricular puncture. The subarachnoid screw is attached to a pressure transducer, and the output is recorded on an oscilloscope. The hollow screw technique also has the advantage of avoiding complications from brain shift and small ventricle size. Complications include infection and blockage of the screw by clot or brain tissue, which leads to a loss of pressure tracing and a decrease in accuracy at high ICP readings. An epidural monitor uses a pneumatic flow sensor to detect ICP. The epidural ICP monitoring system has a low incidence of infection and complications and appears to read pressures accurately. Calibration of the system is maintained automatically, and abnormal pressure waves trigger an alarm system. One disadvantage of the epidural catheter is the inability to withdraw CSF for analysis. A fiberoptic monitor, or transducer-tipped catheter, is an alternative to other intraventricular, subarachnoid, and subdural systems (Sandsmark, Kumar, Park, et al., 2012). The miniature transducer reflects pressure changes, which are converted to electrical signals in an amplifier and displayed on a digital monitor. The catheter can be inserted into the ventricle, subarachnoid space, subdural space, or brain parenchyma or under a bone flap. If inserted into the ventricle, it can also be used in conjunction with a CSF drainage device. Interpreting Intracranial Pressure Waveforms Waves of high pressure and troughs of relatively normal pressure indicate changes in ICP. Waveforms are captured and recorded on an oscilloscope. These waves have been classified as A waves (plateau waves), B waves, and C waves (see Fig. 66-4). The plateau waves (A waves) are transient, paroxysmal, recurring elevations of ICP that may last 5 to 20 minutes and range in amplitude from 40 to 100 mm Hg (Dias, Maia, Cerejo, et al., 2014). Plateau waves have clinical significance and indicate changes in vascular volume within the intracranial compartment that are beginning to compromise cerebral perfusion. The A waves may increase in amplitude and frequency, reflecting cerebral ischemia and brain damage that can occur before overt signs and symptoms of raised ICP are seen clinically. B waves are shorter (30 seconds to 2 minutes) and have smaller amplitude (up to 50 mm Hg). They have less clinical significance, but if seen in a series in a patient with depressed consciousness, they may precede the appearance of A waves. B waves may be seen in patients with intracranial hypertension and decreased intracranial compliance. C waves are small, rhythmic oscillations with frequencies of 4 to 8 per minute and appear to be related to rhythmic variations of the systemic arterial blood pressure and respirations (Hickey, 2014). Figure 66-4 • Intracranial pressure waves. Composite diagram of A (plateau) waves, which indicate cerebral ischemia; B waves, which indicate intracranial hypertension and variations in the respiratory cycle; and C waves, which relate to variations in systemic arterial pressure and respirations. Other Neurologic Monitoring Systems Another trend in neurologic monitoring is microdialysis of the patient with a brain injury (de Lima Oliveira, Kairalla, Fonoff, et al., 2014). Cortical probes are placed near the injured area and are used to measure levels of glutamate, lactate, pyruvate, and glucose, substances that reflect the metabolic function of the brain. Some researchers theorize that direct measurements of glucose and energy by-products in the brain will lead to better management of these patients. Although cerebral microdialysis has reduced the mortality of patients who are brain injured, more study is needed to link it to improved outcomes (de Lima Oliveira et al., 2014). An additional trend is monitoring of cerebral oxygenation through monitoring of the oxygen saturation in the jugular venous bulb (SjvO2) or via a catheter in the brain. Cerebral oxygenation is thought to be important because changes in cerebral perfusion may reflect an increase in ICP. Readings taken from a catheter residing in the jugular outflow tract allow for a comparison of arterial and venous oxygen saturation, and the balance of cerebral oxygen supply and demand is demonstrated. Venous jugular desaturations can reflect early cerebral ischemia, alerting the clinician before an increase in ICP occurs. Minimizing cerebral desaturations can potentially improve outcomes (Sandsmark et al., 2012). This type of monitoring is now widely available and has been successfully used to identify secondary brain insults. A limiting factor is that this saturation reflects overall perfusion of the brain rather than that of a specific injured area (Oddo, Bosel, & Participants in the International Multidisciplinary Consensus Conference on Multimodality Monitoring, 2014). Another method of measuring cerebral oxygenation and temperature is by inserting a fiberoptic catheter into the brain matter (Oddo et al., 2014). The most common system is Licox (see Fig. 66-5). The system includes a monitor with a screen for the display of oxygen and temperature values and cables that connect to the monitoring probes in the brain (Hickey, 2014). Decreasing Cerebral Edema Osmotic diuretics such as mannitol and hypertonic saline (3%) may be given to dehydrate the brain tissue and reduce cerebral edema (Ong, Keyrouz, & Diringer, 2015). They act by drawing water across intact membranes, thereby reducing the volume of the brain and extracellular fluid. An indwelling urinary catheter is usually inserted to monitor urinary output and to manage the resulting diuresis. If the patient is receiving osmotic diuretics, serum osmolality and electrolytes should be determined to assess hydration status. If a brain tumor is the cause of the increased ICP, corticosteroids (e.g., dexamethasone) help reduce the edema surrounding the tumor. Figure 66-5 • Licox catheter system. A. The brain tissue oxygen catheter and monitor. B. Placement of the catheter in brain white matter. Redrawn with permission of Integra NeuroSciences, Plainsboro, NJ. Another method for decreasing cerebral edema is fluid restriction (Hickey, 2014). Limiting overall fluid intake leads to dehydration and hemoconcentration, which draws fluid across the osmotic gradient and decreases cerebral edema. Conversely, overhydration of the patient with increased ICP is avoided, because it increases cerebral edema. Researchers have long hypothesized that lowering body temperature would decrease cerebral edema by reducing the oxygen and metabolic requirements of the brain, thus protecting the brain from continued ischemia. If body metabolism can be reduced by lowering the body temperature, the collateral circulation in the brain may be able to provide an adequate blood supply to the brain. The effect of hypothermia on ICP requires more study; thus far, induced hypothermia has not consistently been shown to be beneficial for patients with brain injury. Inducing and maintaining hypothermia is a major clinical treatment and requires knowledge and skilled nursing observation and management. The type and length of rewarming techniques after hypothermia may also be factors in the outcome of patients with neurologic injuries (Andrews, Sinclair, Rodriguez, et al., 2015; Madden & DeVon, 2015). Maintaining Cerebral Perfusion Cardiac output may be manipulated to provide adequate perfusion to the brain. Improvements in cardiac output are made using fluid volume and inotropic agents such as dobutamine (Dobutrex) and norepinephrine (Levophed). The effectiveness of the cardiac output is reflected in the CPP, which is maintained at greater than 70 mm Hg (Oddo et al., 2014). A lower CPP indicates that the cardiac output is insufficient to maintain adequate cerebral perfusion. SjvO2 and Licox, described earlier, assist in monitoring cerebral perfusion. Decompressive hemicraniectomy may also be considered as a surgical strategy to assist in the management of refractory intracranial hypertension. The removal of a part of the skull allows the brain to expand without the pressure constraints exerted by the cranial vault. Complications of this procedure include infection and increased potential for injury to the unprotected underlying brain structures. Once the patient is no longer at risk for increased ICP, the bone flap may be surgically replaced (Alali, Naimark, Wilson, et al., 2014). Reducing Cerebrospinal Fluid and Intracranial Blood Volume CSF drainage is frequently performed, because the removal of CSF with a ventriculostomy drain can dramatically reduce ICP and restore CPP. Caution should be used in draining CSF, however, because excessive drainage may result in collapse of the ventricles and herniation. The reduction in PaCO2 may result in hypoxia, ischemia, and an increase in cerebral lactate levels. Maintaining the PaCO2 at greater than 30 mm Hg may prove beneficial (Hickey, 2014). Controlling Fever Preventing a temperature elevation is critical, because fever increases cerebral metabolism and the rate at which cerebral edema forms. Strategies to reduce body temperature include administration of antipyretic medications, as prescribed, and the use of a hypothermia blanket. Additional strategies for reducing fever were discussed previously in the Nursing Process section on altered LOC. The patient's temperature is monitored closely, and the patient is observed for shivering, which should be avoided because it is associated with increased oxygen consumption, increased levels of circulating catecholamines, and increased vasoconstriction. Shivering is associated with decreased levels of brain oxygenation; however, the association between shivering and neurologic outcome is unknown. Maintaining Oxygenation and Reducing Metabolic Demands Arterial blood gases and pulse oximetry are monitored to ensure that systemic oxygenation remains optimal. Metabolic demands may be reduced through the administration of high doses of barbiturates if the patient is unresponsive to conventional treatment. The mechanism by which barbiturates decrease ICP and protect the brain is uncertain, but the resultant comatose state is thought to reduce the metabolic requirements of the brain, thus providing cerebral protection (Alali et al., 2014). Another method of reducing cellular metabolic demand and improving oxygenation is the administration of medications causing sedation. The patient who receives these agents cannot move; this decreases the metabolic demands and results in a decrease in cerebral oxygen demand. The patient cannot respond to or report pain either. The most common agents used for sedation are pentobarbital (Nembutal), thiopental (Pentothal), propofol (Diprivan), and dexmedetomidine (Precedex) (Majdan, Mauritz, Wilbacher, et al., 2013; Wang, Ji, Fen, et al., 2013). If sedative agents are used, the ability to perform serial neurologic assessments is lost. Therefore, other monitoring tools are needed to assess the patient's status and response to therapy. Important parameters that must be assessed include ICP, blood pressure, heart rate, respiratory rate, and the patient's response to ventilator therapy (e.g., "fighting or bucking the ventilator"). The level of pharmacologic paralysis is adjusted based on serum levels of the medications given and the assessed parameters. Potential complications of these medications include hypotension caused by decreased sympathetic tone and myocardial depression. Patients receiving high doses of barbiturates or pharmacologic sedatives require continuous cardiac monitoring, endotracheal intubation, mechanical ventilation, and arterial pressure monitoring, as well as ICP monitoring.

intracranial surgery

A craniotomy involves opening the skull surgically to gain access to intracranial structures. This procedure is performed to remove a tumor, relieve elevated ICP, evacuate a blood clot, or control hemorrhage. The surgeon cuts the skull to create a bony flap, which can be repositioned after surgery and held in place by periosteal or wire sutures. One of two approaches through the skull is used: (1) above the tentorium (supratentorial craniotomy) into the supratentorial compartment, or (2) below the tentorium into the infratentorial (posterior fossa) compartment. A third approach, the transsphenoidal approach (through the mouth and nasal sinuses) is often used to gain access to the pituitary gland (Bader et al., 2016). Table 66-3 compares these three different surgical approaches. Alternatively, intracranial structures may be approached through burr holes (see Fig. 66-8), which are circular openings made in the skull by either a hand drill or an automatic craniotome (which has a self-controlled system to stop the drill when the bone is penetrated). Burr holes may be used to determine the presence of cerebral swelling and injury and the size and position of the ventricles. They are also a means of evacuating an intracranial hematoma or abscess and for making a bone flap in the skull that allows access to the ventricles for decompression, ventriculography, or shunting procedures. Other cranial procedures include craniectomy (excision of a portion of the skull) and cranioplasty (repair of a cranial defect using a plastic or metal plate).

altered level of consciousness

An altered level of consciousness (LOC) is present when the patient is not oriented, does not follow commands, or needs persistent stimuli to achieve a state of alertness. LOC is gauged on a continuum, with a normal state of alertness and full cognition (consciousness) on one end and coma on the other end. Coma is a clinical state of unarousable unresponsiveness in which there are no purposeful responses to internal or external stimuli, although nonpurposeful responses to painful stimuli and brainstem reflexes may be present. The usual duration of coma is variable. Akinetic mutism is a state of unresponsiveness to the environment in which the patient makes no voluntary movement. Persistent vegetative state is a condition in which the unresponsive patient resumes sleep-wake cycles after coma but is devoid of cognitive or affective mental function. A minimally conscious state differs from persistent vegetative state in that the patient has inconsistent but reproducible signs of awareness (Bruno, Laureys, & Demertzi, 2013). Locked-in syndrome results from a lesion affecting the pons and results in paralysis and the inability to speak, but vertical eye movements and lid elevation remain intact and are used to indicate responsiveness (Bruno et al., 2013). The level of responsiveness and consciousness is the most important indicator of the patient's condition. Pathophysiology Altered LOC is not a disorder itself; rather, it is a result of multiple pathophysiologic phenomena. The cause may be neurologic (head injury, stroke), toxicologic (drug overdose, alcohol intoxication), or metabolic (hepatic or kidney injury, diabetic ketoacidosis). The underlying cause of neurologic dysfunction is disruption in the cells of the nervous system, neurotransmitters, or brain anatomy (see Chapter 65). Disruptions result from cellular edema or other mechanisms, such as disruption of chemical transmission at receptor sites by antibodies. Intact anatomic structures of the brain are needed for normal function. The two hemispheres of the cerebrum must communicate, via an intact corpus callosum, and the lobes of the brain (frontal, parietal, temporal, and occipital) must communicate and coordinate their specific functions (see Chapter 65). Other anatomic structures of importance are the cerebellum and the brainstem. The cerebellum has both excitatory and inhibitory actions and is largely responsible for coordination of movement. The brainstem contains areas that control the heart rate, respiration, and blood pressure. Disruptions in the anatomic structures result from trauma, edema, pressure from tumors, or other mechanisms, such as an increase or decrease in the circulation of blood or CSF. Clinical Manifestations Alterations in LOC occur along a continuum, and the clinical manifestations depend on where the patient is on this continuum. As the patient's state of alertness and consciousness decreases, changes occur in the pupillary response, eye opening response, verbal response, and motor response. However, initial alterations in LOC may be reflected by subtle behavioral changes, such as restlessness or increased anxiety. The pupils, normally round and quickly reactive to light, become sluggish (response is slower); as the patient becomes comatose, the pupils become fixed (no response to light). The patient in a coma does not open the eyes to voice or command, respond verbally, or move the extremities in response to a request to do so. Assessment and Diagnostic Findings The patient with an altered LOC is at risk for alterations in every body system. A complete assessment is performed, with particular attention to the neurologic system. The neurologic examination should be as complete as the LOC allows. It includes an evaluation of mental status, cranial nerve function, cerebellar function (balance and coordination), reflexes, and motor and sensory function. LOC, a sensitive indicator of neurologic function, is assessed based on the criteria in the Glasgow Coma Scale: eye opening, verbal response, and motor response (Hickey, 2014). The patient's responses are rated on a scale from 3 to 15. A score of 3 indicates severe impairment of neurologic function, brain death, or pharmacologic inhibition of the neurologic response. A score of 15 indicates that the patient is fully responsive (see Chapter 68). If the patient is comatose and has localized signs such as abnormal pupillary and motor responses, it is assumed that neurologic disease is present until proven otherwise. If the patient is comatose but pupillary light reflexes are preserved, a toxic or metabolic disorder is suspected. Common diagnostic procedures used to identify the cause of unconsciousness include computed tomography (CT) scanning, perfusion CT (PCT), magnetic resonance imaging (MRI), magnetic resonance spectroscopy (MRS), and electroencephalography (EEG). Additional procedures include positron emission tomography (PET) and single-photon emission computed tomography (SPECT) (see Chapter 65). Emerging research identifies EEG, MRI, and PET as important technologies in determining brain function through the evaluation of metabolic and electrical activity (Van Der Naalt, 2015). Laboratory tests include analysis of blood glucose, electrolytes, serum ammonia, and liver function tests; blood urea nitrogen (BUN) levels; serum osmolality; calcium level; and partial thromboplastin and prothrombin times. Other studies may be used to evaluate serum ketones, alcohol and drug concentrations, and arterial blood gases. Medical Management The first priority of treatment for the patient with altered LOC is to obtain and maintain a patent airway. The patient may be orally or nasally intubated, or a tracheostomy may be performed. Until the ability of the patient to breathe is determined, a mechanical ventilator is used to maintain adequate oxygenation and ventilation. The circulatory status (blood pressure, heart rate) is monitored to ensure adequate perfusion to the body and brain. An intravenous (IV) catheter is inserted to provide access for IV fluids and medications. Neurologic care focuses on the specific neurologic pathology, if known. Nutritional support, via a feeding tube or a gastrostomy tube, is initiated as soon as possible. In addition to measures designed to determine and treat the underlying causes of altered LOC, other medical interventions are aimed at pharmacologic management and prevention of complications.

things that can cause a headache

Antihypertensive agents, diuretic medications, anti-inflammatory agents, and monoamine oxidase (MAO) inhibitors are a few of the categories of medications that can provoke headaches. Daily use of over-the-counter or prescribed pain medications for 8 to 10 days out of a month can lead to a chronic headache due to medication overuse (Becker, Findlay, Moga, et al., 2015). Emotional factors can play a role in precipitating headaches. Stress is thought to be a major initiating factor in migraine headaches; therefore, sleep patterns, level of stress, recreational interests, appetite, emotional problems, and family stressors are relevant. There is a strong familial tendency for headache disorders, and a positive family history may help in making a diagnosis.

nursing process icp

Assessment Initial assessment of the patient with increased ICP includes obtaining a history of events leading to the present illness and the pertinent past medical history. It is usually necessary to obtain this information from family or friends. The neurologic examination should be as complete as the patient's condition allows. It includes an evaluation of mental status, LOC, cranial nerve function, cerebellar function (balance and coordination), reflexes, and motor and sensory function. Because the patient is critically ill, ongoing assessment is more focused, including pupil checks, assessment of selected cranial nerves, frequent measurements of vital signs and ICP, and the use of the Glasgow Coma Scale (see Table 66-1). Diagnosis NURSING DIAGNOSES Based on the assessment data, major nursing diagnoses include the following: Ineffective airway clearance related to diminished protective reflexes (cough, gag) Ineffective breathing patterns related to neurologic dysfunction (brainstem compression, structural displacement) Risk for ineffective cerebral tissue perfusion related to the effects of increased ICP Deficient fluid volume related to fluid restriction Risk for infection related to ICP monitoring system (fiberoptic or intraventricular catheter) Other relevant nursing diagnoses are included in the earlier section on altered LOC. COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS Potential complications may include the following: Brainstem herniation Diabetes insipidus SIADH Planning and Goals The goals for the patient include maintenance of a patent airway, normalization of respiration, adequate cerebral tissue perfusion through reduction in ICP, restoration of fluid balance, absence of infection, and absence of complications. Nursing Interventions MAINTAINING A PATENT AIRWAY The patency of the airway is assessed. Secretions that are obstructing the airway must be suctioned with care, because transient elevations of ICP occur with suctioning (Hickey, 2014). Hypoxia caused by poor oxygenation leads to cerebral ischemia and edema. Coughing is discouraged because it increases ICP. The lung fields are auscultated at least every 8 hours to determine the presence of adventitious sounds or any areas of congestion. Elevating the head of the bed may aid in clearing secretions and improve venous drainage of the brain. ACHIEVING AN ADEQUATE BREATHING PATTERN The patient must be monitored constantly for respiratory irregularities. Increased pressure on the frontal lobes or deep midline structures may result in Cheyne-Stokes respirations, whereas pressure in the midbrain can cause hyperventilation. If the lower portion of the brainstem (the pons and medulla) is involved, respirations become irregular and eventually cease. Hyperventilation therapy is a controversial therapy in traumatic brain injury used in some centers to reduce ICP by causing cerebral vasoconstriction and a decrease in cerebral blood volume. The nurse collaborates with the respiratory therapist in monitoring the PaCO2, which is usually maintained at less than 30 mm Hg. Patients undergoing hyperventilation therapy also benefit from multimodality monitoring to determine the overall effect of this therapy on brain perfusion (de Lima Oliveira et al., 2014). A neurologic observation record (see Fig. 66-6) is maintained, and all observations are made in relation to the patient's baseline condition. Repeated assessments of the patient are made (sometimes minute by minute) so that improvement or deterioration may be noted immediately. If the patient's condition deteriorates, the primary provider is notified emergently and preparations are made for surgical intervention. OPTIMIZING CEREBRAL TISSUE PERFUSION In addition to ongoing nursing assessment, strategies are initiated to reduce factors contributing to the elevation of ICP (see Table 66-2). Proper positioning helps reduce ICP. The patient's head is kept in a neutral (midline) position, maintained with the use of a cervical collar if necessary, to promote venous drainage. Elevation of the head is maintained at 30 to 45 degrees unless contraindicated. Extreme rotation of the neck and flexion of the neck are avoided, because compression or distortion of the jugular veins increases ICP. Extreme hip flexion is also avoided, because this position causes an increase in intra-abdominal and intrathoracic pressures, which can produce an increase in ICP. Relatively minor changes in position can significantly affect ICP. If monitoring reveals that turning the patient raises ICP, rotating beds, turning sheets, and holding the patient's head during turning may minimize the stimuli that increase ICP. Research suggests that patient response to position change is highly variable and requires close hemodynamic monitoring and individualized care (Mitchell, Kirkness, & Blissitt, 2015). The Valsalva maneuver, which can be produced by straining at defecation or even moving in bed, raises ICP and is to be avoided. Stool softeners may be prescribed. If the patient is alert and able to eat, a diet high in fiber may be indicated. Abdominal distention, which increases intra-abdominal and intrathoracic pressure and ICP, should be noted. Enemas and cathartics are avoided if possible. When moving or being turned in bed, the patient can be instructed to exhale (which opens the glottis) to avoid the Valsalva maneuver. Mechanical ventilation presents unique problems for the patient with increased ICP. Before suctioning, the patient should be preoxygenated and briefly hyperventilated using 100% oxygen on the ventilator. Suctioning should not last longer than 15 seconds. High levels of positive end-expiratory pressure (PEEP) must be utilized cautiously, because they may decrease venous return to the heart and decrease venous drainage from the brain through increased intrathoracic pressure (Nemer, Caldeira, Santos, et al., 2015). Activities that increase ICP, as indicated by changes in waveforms, should be avoided if possible. Spacing of nursing interventions may prevent transient increases in ICP. During nursing interventions, the ICP should not increase above 25 mm Hg, and it should return to baseline levels within 5 minutes. Patients with increased ICP should not demonstrate a significant increase in pressure or change in the ICP waveform. Patients with the potential for a significant increase in ICP may need sedation before initiation of nursing activities (Bader, Littlejohns, & Olson, 2016). Emotional stress and frequent arousal from sleep are avoided. A calm atmosphere is maintained. Environmental stimuli (e.g., noise, conversation) should be minimal. MAINTAINING NEGATIVE FLUID BALANCE The administration of osmotic and loop diuretics is part of the treatment protocol to reduce ICP. Corticosteroids may be used to reduce cerebral edema (except when it results from trauma), and fluids may be restricted. All of these treatment modalities promote dehydration. Skin turgor, mucous membranes, urine output, and serum and urine osmolality are monitored to assess fluid status. If IV fluids are prescribed, the nurse ensures that they are given at a slow to moderate rate with an IV infusion pump, to prevent too-rapid administration and avoid overhydration. For the patient receiving mannitol, the nurse observes for the possible development of heart failure and pulmonary edema. The intent of treatment is to promote a shift of fluid from the intracellular to the intravascular compartment and to control cerebral edema. However, this shift of fluid volume to the intravascular compartment may overwhelm the ability of the myocardium to increase workload sufficient to meet these demands, which may cause failure and pulmonary edema. For patients undergoing dehydrating procedures, vital signs, including blood pressure, must be monitored to assess fluid volume status. An indwelling urinary catheter is inserted to permit assessment of renal function and fluid status. During the acute phase, urine output is monitored hourly. An output greater than 200 mL per hour for 2 consecutive hours may indicate the onset of diabetes insipidus (Hickey, 2014). These patients need careful oral hygiene, because mouth dryness occurs with dehydration. Frequently rinsing the mouth with nondrying solutions, lubricating the lips, and removing encrustations relieve dryness and promote comfort. PREVENTING INFECTION The risk of infection is greatest when ICP is monitored with an intraventricular catheter and increases with the duration of the monitoring. Most health care facilities have written protocols for managing these systems and maintaining their sterility; strict adherence to the protocols is essential. Aseptic technique must be used when managing the system and changing the ventricular drainage bag. The drainage system is also checked for loose connections, because they can cause leakage and contamination of the CSF as well as inaccurate readings of ICP. The nurse observes the character of the CSF drainage and reports increasing cloudiness or blood. The patient is monitored for signs and symptoms of meningitis: fever, chills, nuchal (neck) rigidity, and increasing or persistent headache. See Chapter 69 for a discussion of meningitis. MONITORING AND MANAGING POTENTIAL COMPLICATIONS The primary complication of increased ICP is brain herniation resulting in death (see Fig. 66-2). Nursing management focuses on detecting early signs of increasing ICP, because medical interventions are usually ineffective once later signs develop (Bader et al., 2016). Frequent neurologic assessments and documentation and analysis of trends will reveal the subtle changes that may indicate increasing ICP. Detecting Indications of Increasing Intracranial Pressure. The nurse assesses for and immediately reports any signs or symptoms of increasing ICP (see Chart 66-1). The focus is on detecting early signs of increasing ICP. Monitoring Intracranial Pressure. Because clinical assessment is not always a reliable guide in recognizing increased ICP, especially in patients who are comatose, monitoring of ICP and cerebral oxygenation is an essential part of management. ICP is monitored closely for continuous elevation or significant increase over baseline. The trend of ICP measurements over time is an important indication of the patient's underlying status. Vital signs are assessed when an increase in ICP is noted (Bader et al., 2016). Careful attention to aseptic technique is needed when handling any part of the monitoring system. The insertion site is inspected for signs of infection. Temperature, pulse, and respirations are closely monitored for systemic signs of infection. All connections and stopcocks are checked for leaks, because even small leaks can distort pressure readings and lead to infection (AANN, 2012). When ICP is monitored with a fluid system, the transducer is calibrated at a particular reference point, usually 2.5 cm (1 inch) above the ear with the patient in the supine position; this point corresponds to the level of the foramen of Monro (see Fig. 66-7). CSF pressure readings depend on the patient's position. For subsequent pressure readings, the head should be in the same position relative to the transducer. Fiberoptic catheters are calibrated before insertion and do not require further referencing; they do not require the head of the bed to be at a specific position to obtain an accurate reading. When technology is associated with patient management, the nurse must be certain that the technologic equipment is functioning properly. The most important concern must be the patient to whom equipment is attached. The patient and family must be informed about the technology and the goals of its use. The patient's response is monitored, and appropriate comfort measures are implemented to ensure that the patient's stress is minimized. Figure 66-7 • Location of the foramen of Monro for calibration of the intracranial pressure monitoring system. ICP measurement is only one parameter; repeated neurologic checks and clinical examinations remain important measures. Astute observation, comparison of findings with previous observations, and interventions can assist in preventing life-threatening ICP elevations. Monitoring for Secondary Complications. The nurse also assesses for complications of increased ICP, including diabetes insipidus and SIADH (see Chapters 13 and 52). Urine output should be monitored closely. Diabetes insipidus requires fluid and electrolyte replacement, along with the administration of vasopressin, to replace and slow the urine output. Serum electrolyte levels are monitored for imbalances. SIADH requires fluid restriction and monitoring of serum electrolyte levels.

headache

Headache, or cephalalgia, is one of the most common of all human physical complaints. Headache is a symptom rather than a disease entity; it may indicate organic disease (neurologic or other disease), a stress response, vasodilation (migraine), skeletal muscle tension (tension headache), or a combination of factors. A primary headache is one for which no organic cause can be identified. This type of headache includes migraine, tension-type, and cluster headaches (Hickey, 2014). Cranial arteritis is another common cause of headache. A classification of headaches was issued first by the Headache Classification Committee of the International Headache Society in 1988. The International Headache Society revised the headache classification in 2013; an abbreviated list is shown in Chart 66-7. Migraine is a complex of symptoms characterized by periodic and recurrent attacks of severe headache lasting from hours to days in adults. The cause of migraine has not been clearly demonstrated, but it is primarily a vascular disturbance that has a strong familial tendency. The typical time of onset is at puberty, and the incidence is higher in women than men (D'Arcy, 2014). There are many subtypes of migraine headache, including migraine with and without aura. Most patients have migraine without an aura. Tension-type headaches tend to be chronic and less severe and are probably the most common type of headache. Trigeminal autonomic cephalalgias include cluster headaches and paroxysmal hemicrania. Cluster headaches are relatively uncommon and seen more frequently in men than in women (Grossman & Porth, 2014). Types of headaches not subsumed under these categories fall into the other primary headache group and include headaches triggered by cough, exertion, and sexual activity. Chart 66-7 International Headache Society Classification of Headache Migraine Tension-type headache Trigeminal autonomic cephalalgias Other primary disorders Headache attributed to trauma or injury to the head and/or neck Headache attributed to cranial or cervical vascular disorder Headache attributed to nonvascular intracranial disorder Headache attributed to a substance or its withdrawal Headache attributed to infection Headache attributed to disorder of homeostasis Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures Headache attributed to psychiatric disorder Painful cranial neuropathies and other facial pains Other headache disorders Adapted from Headache Classification Subcommittee of the International Headache Society. (2013). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia, 33(9), 629-808. Cranial arteritis is a cause of headache in the older population, reaching its greatest incidence in those older than 70 years of age. Inflammation of the cranial arteries is characterized by a severe headache localized in the region of the temporal arteries. The inflammation may be generalized (in which case cranial arteritis is part of a vascular disease) or focal (in which case only the cranial arteries are involved). A secondary headache is a symptom associated with other causes, such as a brain tumor, an aneurysm, or lumbar puncture (Destrebecq, Terzoni, & Sala, 2014). Although most headaches do not indicate serious disease, persistent headaches require further investigation. Serious disorders related to headache include brain tumors, subarachnoid hemorrhage, stroke, severe hypertension, meningitis, and head injuries. Pathophysiology The cerebral signs and symptoms of migraine result from a hyperexcitable brain that is susceptible to a phenomenon known as cortical spreading depression, a wave of depolarization over the cerebral cortex, cerebellum, and hippocampus. This depolarization activates inflammatory neuropeptides and other neurotransmitters (including serotonin), resulting in the stimulation of meningeal nociceptors. Vascular changes, inflammation, and a continuation of pain signal stimulation occur (Charles, 2015). The initial phase of this process is known as the premonitory phase and may include light, sound, and smell sensitivity. If treatment is initiated at this point, the migraine may be fully terminated. As the attack progresses, central sensitization occurs, and the migraine becomes much harder to treat. Attacks can be triggered by hormonal changes associated with menstrual cycles, bright lights, stress, depression, sleep deprivation, fatigue, or odors. Certain foods containing tyramine (especially aged cheese), monosodium glutamate, and chocolate may be food triggers (Grossman & Porth, 2014). The use of oral contraceptives may be associated with increased frequency and severity of attacks in some women. Emotional or physical stress may cause contraction of the muscles in the neck and scalp, resulting in tension headache. The pathophysiology of cluster headache is not fully understood. One theory is that it is caused by dilation of orbital and nearby extracranial arteries. Cranial arteritis is thought to represent an immune vasculitis in which immune complexes are deposited within the walls of affected blood vessels, producing vascular injury and inflammation. A biopsy may be performed on the involved artery to make the diagnosis. Clinical Manifestations Migraine The migraine with aura can be divided into four phases: premonitory, aura, the headache, and recovery (headache termination and postdrome). Premonitory Phase The premonitory phase is experienced by more than 80% of adult migraine sufferers, with symptoms that occur hours to days before a migraine headache (Charles, 2013). Symptoms may include depression, irritability, feeling cold, food cravings, anorexia, change in activity level, increased urination, diarrhea, or constipation. Patients may experience the same prodrome with each migraine headache. A current theory regarding premonitory symptoms is that they involve the neurotransmitter dopamine. Aura Phase An aura may be a variable feature for patients who experience migraines (Charles & Hansen, 2015). An aura is characterized by focal neurologic symptoms. Visual disturbances (i.e., light flashes and bright spots) are most common and may be hemianopic (affecting only half of the visual field). Other symptoms that may follow include numbness and tingling of the lips, face, or hands; mild confusion; slight weakness of an extremity; drowsiness; and dizziness. This period of aura was thought to correspond to the phenomenon of cortical spreading depression that is associated with reduced metabolic demand in abnormally functioning neurons. This can be associated with decreased blood flow; however, cerebral blood flow studies performed during migraine headaches demonstrate that although changes in blood vessels occur during phases of migraine, cerebral blood flow is not the main abnormality. In fact, some studies suggest that the aura and headache phases may occur simultaneously (Charles, 2013). Headache Phase Migraine headache is severe and incapacitating and is often associated with photophobia (light sensitivity), phonophobia (sound sensitivity), or allodynia (abnormal perception of innocuous stimuli) (Charles, 2013). Research differs in the role of vascular changes (either vasodilatory or vasoconstrictive) with respect to migraine pathophysiology and the experience of migraine headache. Symptoms of migraine can also include nausea and vomiting. Postdrome Phase In the postdrome phase, the pain gradually subsides, but patients may experience tiredness, weakness, cognitive difficulties, and mood changes for hours to days. Muscle contraction in the neck and scalp is common, with associated muscle ache and localized tenderness. Physical exertion may exacerbate the headache pain. During this postheadache phase, patients may sleep for extended periods. Other Headache Types The tension-type headache is characterized by a steady, constant feeling of pressure that usually begins in the forehead, temple, or back of the neck. It is often bandlike or may be described as "a weight on top of my head." Cluster headaches are unilateral and come in clusters of one to eight daily, with excruciating pain localized to the eye and orbit and radiating to the facial and temporal regions. The pain is accompanied by watering of the eye and nasal congestion. Each attack lasts 15 minutes to 3 hours and may have a crescendo-decrescendo pattern (Hickey, 2014). The headache is often described as penetrating. Cranial arteritis often begins with general manifestations, such as fatigue, malaise, weight loss, and fever. Clinical manifestations associated with inflammation (heat, redness, swelling, tenderness, or pain over the involved artery) usually are present. Sometimes a tender, swollen, or nodular temporal artery is visible. Visual problems are caused by ischemia of the involved structures. Assessment and Diagnostic Findings The diagnostic evaluation includes a detailed history, a physical assessment of the head and neck, and a complete neurologic examination. Headaches may manifest differently in the same person over the course of a lifetime, and the same type of headache may manifest differently from patient to patient. The health history focuses on assessing the headache itself, with emphasis on the factors that precipitate or provoke it. The patient is asked to describe the headache in their own words. Because headache is often the presenting symptom of a wider variety of physiologic and psychological disturbances, a general health history is an essential component of the patient database. Therefore, questions addressed in the health history should cover major medical and surgical illness as well as a body systems review. The medication history can provide insight into the patient's overall health status and indicate medications that may be provoking headaches. Antihypertensive agents, diuretic medications, anti-inflammatory agents, and monoamine oxidase (MAO) inhibitors are a few of the categories of medications that can provoke headaches. Daily use of over-the-counter or prescribed pain medications for 8 to 10 days out of a month can lead to a chronic headache due to medication overuse (Becker, Findlay, Moga, et al., 2015). Emotional factors can play a role in precipitating headaches. Stress is thought to be a major initiating factor in migraine headaches; therefore, sleep patterns, level of stress, recreational interests, appetite, emotional problems, and family stressors are relevant. There is a strong familial tendency for headache disorders, and a positive family history may help in making a diagnosis. A direct relationship may exist between exposure to toxic substances and headache. Careful questioning may uncover chemicals to which a worker has been exposed. Under the Right-to-Know Law, employees have access to the material safety data sheets (commonly referred to as MSDS) for all substances with which they come in contact in the workplace (see Chapter 72). The occupational history also includes assessment of the workplace as a possible source of stress and for a possible ergonomic basis of muscle strain and headache. A complete description of the headache itself is crucial. The nurse reviews the age at onset of headaches; this particular headache's frequency, location, and duration; the type of pain; factors that relieve and precipitate the event; and associated symptoms. The data obtained should include the patient's own words about the headache in response to the following questions: What is the location? Is it unilateral or bilateral? Does it radiate? What is the quality—dull, aching, steady, boring, burning, intermittent, continuous, paroxysmal? How many headaches occur during a given period of time? What are the precipitating factors, if any—environmental (e.g., sunlight, weather change), foods, exertion, other? p. 2005 p. 2006 What makes the headache worse (e.g., coughing, straining)? What time (day or night) does it occur? How long does a typical headache last? Are there any associated symptoms, such as facial pain, lacrimation (excessive tearing), or scotomas (blind spots in the field of vision)? What usually relieves the headache (aspirin, nonsteroidal anti-inflammatory drugs, ergot preparation, food, heat, rest, neck massage)? Does nausea, vomiting, weakness, or numbness in the extremities accompany the headache? Does the headache interfere with daily activities? Do you have any allergies? Do you have insomnia, poor appetite, loss of energy? Is there a family history of headache? What is the relationship of the headache to your lifestyle or physical or emotional stress? What medications are you taking? Diagnostic testing often is not helpful in the investigation of headache, because usually there are few objective findings. In patients who demonstrate abnormalities on the neurologic examination, CT scan, cerebral angiography, or MRI scan may be used to detect underlying causes, such as tumor or aneurysm. Electromyography (EMG) may reveal a sustained contraction of the neck, scalp, or facial muscles. Laboratory tests may include complete blood count, erythrocyte sedimentation rate, electrolytes, glucose, creatinine, and thyroid hormone levels. Prevention Prevention begins by having the patient avoid specific triggers that are known to initiate the headache syndrome. Preventive medical management of migraine involves the daily use of one or more agents that are thought to block the physiologic events leading to an attack. Treatment regimens vary greatly, as do patient responses; therefore, close monitoring is indicated. Alcohol, nitrites, vasodilators, and histamines may precipitate cluster headaches. Elimination of these factors helps prevent the headaches. Medical Management Therapy for migraine headache is divided into abortive (symptomatic) and preventive approaches. The abortive approach, best used in those patients who have less frequent attacks, is aimed at relieving or limiting a headache at the onset or while it is in progress. The preventive approach is used in patients who experience more frequent attacks at regular or predictable intervals and may have a medical condition that precludes the use of abortive therapies (Becker et al., 2015). Medical management of migraine during pregnancy and lactation includes nonpharmacologic strategies in addition to safe medication practices (Wells, Turner, Lee, et al., 2016). Nonpharmacologic treatments include mainly avoidance of triggers (Grossman & Porth, 2014) (see Chart 66-8). The triptans, which are serotonin receptor agonists, are the most specific antimigraine agents available. These agents cause vasoconstriction, reduce inflammation, and may reduce pain transmission. The five triptans in routine clinical use include sumatriptan (Imitrex), naratriptan (Amerge), rizatriptan (Maxalt), zolmitriptan (Zomig), and almotriptan (Axert) (D'Arcy, 2014). Numerous serotonin receptor agonists are under study. Many of the triptan medications are available in a variety of formulations, such as nasal sprays, inhalers, conventional tablet, disintegrating tablet, suppositories, or injections. The nasal sprays are useful for patients experiencing nausea and vomiting (Dahlöf & Van Den Brink, 2012).

pathophysiology of hepatic encephalopothy

Increased ICP affects many patients with acute neurologic conditions because pathologic conditions alter the relationship between intracranial volume and ICP. Although elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies. Increased ICP from any cause decreases cerebral perfusion, stimulates further swelling (edema), and may shift brain tissue, resulting in herniation—a dire and frequently fatal event. Decreased Cerebral Blood Flow Increased ICP may reduce cerebral blood flow, resulting in ischemia and cell death. In the early stages of cerebral ischemia, the vasomotor centers are stimulated and the systemic pressure rises to maintain cerebral blood flow. Usually, this is accompanied by a slow bounding pulse and respiratory irregularities. These changes in blood pressure, pulse, and respiration are important clinically because they suggest increased ICP. The concentration of carbon dioxide in the blood and in the brain tissue also plays a role in the regulation of cerebral blood flow. An increase in the partial pressure of arterial carbon dioxide (PaCO2) causes cerebral vasodilation, leading to increased cerebral blood flow and increased ICP. A decrease in PaCO2 has a vasoconstrictive effect, limiting blood flow to the brain. Decreased venous outflow may also increase cerebral blood volume, thus raising ICP. Cerebral Edema Cerebral edema or swelling is defined as an abnormal accumulation of water or fluid in the intracellular space, extracellular space, or both, associated with an increase in the volume of brain tissue. Edema can occur in the gray, white, or interstitial matter. As brain tissue swells within the rigid skull, several mechanisms attempt to compensate for the increasing ICP. These compensatory mechanisms include autoregulation as well as decreased production and flow of CSF. Autoregulation refers to the brain's ability to change the diameter of its blood vessels to maintain a constant cerebral blood flow during alterations in systemic blood pressure. This mechanism can be impaired in patients who are experiencing a pathologic and sustained increase in ICP. Cerebral Response to Increased Intracranial Pressure As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage. The brain can maintain a steady perfusion pressure if the arterial systolic blood pressure is 50 to 150 mm Hg and the ICP is less than 40 mm Hg. Changes in ICP are closely linked with cerebral perfusion pressure (CPP). The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP). For example, if the MAP is 100 mm Hg and the ICP is 15 mm Hg, then the CPP is 85 mm Hg. The normal CPP is 70 to 100 mm Hg (Hickey, 2014). As ICP rises and the autoregulatory mechanism of the brain is overwhelmed, the CPP can increase to greater than 100 mm Hg or decrease to less than 50 mm Hg. Patients with a CPP of less than 50 mm Hg experience irreversible neurologic damage. Therefore, the CPP must be maintained at 70 to 80 mm Hg to ensure adequate blood flow to the brain. If ICP is equal to MAP, cerebral circulation ceases. A clinical phenomenon known as the Cushing's response (or Cushing's reflex) is seen when cerebral blood flow decreases significantly. When ischemic, the vasomotor center triggers an increase in arterial pressure in an effort to overcome the increased ICP. A sympathetically mediated response causes an increase in the systolic blood pressure with a widening of the pulse pressure and cardiac slowing. This response is seen clinically as an increase in systolic blood pressure, widening of the pulse pressure, and reflex slowing of the heart rate. It is a late sign requiring immediate intervention; however, perfusion may be recoverable if the Cushing's response is treated rapidly. At a certain point, the brain's ability to autoregulate becomes ineffective and decompensation (ischemia and infarction) begins. When this occurs, the patient exhibits significant changes in mental status and vital signs. The bradycardia, hypertension, and bradypnea associated with this deterioration are known as Cushing's triad, which is a grave sign. At this point, herniation of the brainstem and occlusion of the cerebral blood flow occur if therapeutic intervention is not initiated. Herniation refers to the shifting of brain tissue from an area of high pressure to an area of lower pressure (see Fig. 66-2). The herniated tissue exerts pressure on the brain area into which it has shifted, which interferes with the blood supply in that area. Cessation of cerebral blood flow results in cerebral ischemia, infarction, and brain death.

phases of migraine

Migraine The migraine with aura can be divided into four phases: premonitory, aura, the headache, and recovery (headache termination and postdrome). Premonitory Phase The premonitory phase is experienced by more than 80% of adult migraine sufferers, with symptoms that occur hours to days before a migraine headache (Charles, 2013). Symptoms may include depression, irritability, feeling cold, food cravings, anorexia, change in activity level, increased urination, diarrhea, or constipation. Patients may experience the same prodrome with each migraine headache. A current theory regarding premonitory symptoms is that they involve the neurotransmitter dopamine. Aura Phase An aura may be a variable feature for patients who experience migraines (Charles & Hansen, 2015). An aura is characterized by focal neurologic symptoms. Visual disturbances (i.e., light flashes and bright spots) are most common and may be hemianopic (affecting only half of the visual field). Other symptoms that may follow include numbness and tingling of the lips, face, or hands; mild confusion; slight weakness of an extremity; drowsiness; and dizziness. This period of aura was thought to correspond to the phenomenon of cortical spreading depression that is associated with reduced metabolic demand in abnormally functioning neurons. This can be associated with decreased blood flow; however, cerebral blood flow studies performed during migraine headaches demonstrate that although changes in blood vessels occur during phases of migraine, cerebral blood flow is not the main abnormality. In fact, some studies suggest that the aura and headache phases may occur simultaneously (Charles, 2013). Headache Phase Migraine headache is severe and incapacitating and is often associated with photophobia (light sensitivity), phonophobia (sound sensitivity), or allodynia (abnormal perception of innocuous stimuli) (Charles, 2013). Research differs in the role of vascular changes (either vasodilatory or vasoconstrictive) with respect to migraine pathophysiology and the experience of migraine headache. Symptoms of migraine can also include nausea and vomiting. Postdrome Phase In the postdrome phase, the pain gradually subsides, but patients may experience tiredness, weakness, cognitive difficulties, and mood changes for hours to days. Muscle contraction in the neck and scalp is common, with associated muscle ache and localized tenderness. Physical exertion may exacerbate the headache pain. During this postheadache phase, patients may sleep for extended periods. Other Headache Types The tension-type headache is characterized by a steady, constant feeling of pressure that usually begins in the forehead, temple, or back of the neck. It is often bandlike or may be described as "a weight on top of my head." Cluster headaches are unilateral and come in clusters of one to eight daily, with excruciating pain localized to the eye and orbit and radiating to the facial and temporal regions. The pain is accompanied by watering of the eye and nasal congestion. Each attack lasts 15 minutes to 3 hours and may have a crescendo-decrescendo pattern (Hickey, 2014). The headache is often described as penetrating. Cranial arteritis often begins with general manifestations, such as fatigue, malaise, weight loss, and fever. Clinical manifestations associated with inflammation (heat, redness, swelling, tenderness, or pain over the involved artery) usually are present. Sometimes a tender, swollen, or nodular temporal artery is visible. Visual problems are caused by ischemia of the involved structures.