H

Head and neck cancer

When the patient can swallow, give small amounts of thickened liquids or pureed foods with the patient in high Fowler’s position. Close observation for choking is essential. Suctioning may be necessary to prevent aspiration.

Nursing management

Goals

The patient with head or neck cancer will have a patent airway, no complications related to therapy, adequate nutritional intake, minimal to no pain, the ability to communicate, and an acceptable body image.

Nursing diagnoses

■ Anxiety

■ Ineffective airway clearance

■ Risk for aspiration

■ Impaired verbal communication

■ Acute pain

Nursing interventions

Include information about risk factors in health teaching. Encourage good oral hygiene. Teach patients about safe sex practices to prevent HPV infection. If cancer has been diagnosed, tobacco and alcohol cessation is still important as the likelihood of a cure is diminished if these behaviors continue.

■ Interventions to reduce side effects of radiation therapy include measures to reduce dry mouth, teaching oral care to the patient, and encouraging patients to engage in regular exercise to reduce fatigue.

For procedures that involve a laryngectomy, teaching should include information about expected changes in speech. Establish a means of communication for the immediate postoperative period.

After surgery, maintenance of a patent airway is essential and a laryngectomy (tracheostomy) tube will be in place. Keep the patient in semi-Fowler’s position to decrease edema and tension on the suture lines. Monitor vital signs frequently because of the risk of hemorrhage and respiratory compromise. Immediately after surgery the postlaryngectomy patient requires frequent suctioning via the tracheostomy tube.

■ Encourage deep breathing and coughing and provide tracheostomy care as needed.

■ Depression and changes in sexuality patterns because of altered body image are common in the patient who has had radical neck dissection. Help the patient regain an acceptable self-concept.

■ A speech therapist should meet with the patient having a total laryngectomy to discuss voice restoration options.

Patient and caregiver teaching

■ Monitor patency of wound drainage tubes (if in place) every 4 hours to ensure proper functioning. After drainage tubes are removed, closely monitor the area to detect any swelling. If fluid continues to accumulate, aspiration may be necessary.

■ Instruct the patient and caregiver on how to manage tubes and whom to call if there are problems.

■ Provide pictorial instructions for tracheostomy care, suctioning, stoma care, and tube feedings as appropriate.

■ Teach the patient to cover the stoma before performing activities such as shaving and applying makeup to avoid inhalation of foreign materials.

■ Address measures to provide adequate humidity at home using a bedside humidifier and high oral fluid intake.

■ Encourage preparation of food that is colorful, attractive, and nutritious because taste may also be diminished secondary to the loss of smell and radiation therapy.

Head injury

Description

Head injury includes any trauma to the scalp, skull, or brain. A serious form of head injury is traumatic brain injury (TBI). In the United States in hospital emergency departments, an estimated 1.7 million people are treated and released with TBI.

■ Motor vehicle crashes and falls are the most common causes of head injury. Other causes of head injury include firearms, assaults, sports-related trauma, recreational injuries, and war-related injuries.

■ Males are twice as likely to sustain a TBI as females.

Deaths from head trauma occur at three time points after injury: immediately after injury, within 2 hours of injury, and approximately 3 weeks after injury.

■ The majority of deaths occur immediately after the injury, either from the direct head trauma or massive hemorrhage and shock.

■ Deaths occurring within a few hours of the trauma are caused by progressive worsening of the head injury or internal bleeding. Immediately recognizing changes in neurologic status and rapid surgical intervention are critical in the prevention of deaths.

■ Deaths occurring 3 weeks or more after the injury result from multisystem failure.

Types of head injuries

Scalp laceration

Because the scalp contains many blood vessels with poor constrictive abilities, even relatively small wounds can bleed profusely. The major complications of scalp lesions are blood loss and infection.

Skull fracture

Fractures frequently occur with head trauma. Fractures may be closed or open, depending on the presence of a scalp laceration or extension of the fracture into the air sinuses or dura.

■ The type and severity of a skull fracture depend on the velocity, momentum, and direction of the injuring agent, and the site of impact. Specific manifestations of a skull fracture are generally associated with the location of the injury (see Table 57-7, Lewis et al, Medical-Surgical Nursing, ed. 9, p. 1369).

Major potential complications of skull fracture are intracranial infections and hematoma, as well as meningeal and brain tissue damage.

Head trauma

Brain injuries are categorized as diffuse (generalized) or focal (localized). In diffuse injury (i.e., concussion, diffuse axonal), damage to the brain cannot be localized to one particular area of the brain, whereas a focal injury (e.g., contusion, hematoma) can be localized to a specific area of the brain.

Diffuse injury

Concussion is a minor, sudden, transient, and diffuse head injury associated with a disruption in neural activity and a change in the level of consciousness (LOC). The patient may not lose total consciousness. Signs include a brief disruption in LOC, amnesia for the event (retrograde amnesia), and headache. Manifestations are generally of short duration.

■ Postconcussion syndrome may develop in some patients and is usually seen anywhere from 2 weeks to 2 months after the injury. Symptoms include persistent headache, lethargy, behavior changes, decreased short-term memory, and changes in intellectual ability.

Although concussion is generally considered benign and usually resolves spontaneously, the symptoms may be the beginning of a more serious, progressive problem. At the time of discharge it is important to give the patient and caregiver instructions for observation and accurate reporting of symptoms or changes in neurologic status.

Diffuse axonal injury (DAI) is widespread axonal damage occurring after a mild, moderate, or severe TBI.

■ Clinical signs of DAI include decreased LOC, increased intracranial pressure (ICP), decortication or decerebration, and global cerebral edema. Approximately 90% of patients with DAI remain in a persistent vegetative state.

■ Patients who survive the initial event are rapidly triaged to an ICU where they will be vigilantly watched for signs of increased ICP and treated for increased ICP (see Increased Intracranial Pressure, p. 346).

Focal injury

Focal injury can be minor to severe and can be localized to an area of injury. Focal injury consists of lacerations, contusions, hematomas, and cranial nerve injuries.

Lacerations involve actual tearing of brain tissue and often occur with compound fractures and penetrating injuries. Tissue damage is severe, and surgical repair of the laceration is impossible because of the nature of brain tissue. If bleeding is deep into the brain parenchyma, focal and generalized signs develop. Prognosis is generally poor for the patient with a large intracerebral hemorrhage.

A contusion is the bruising of brain tissue within a focal area. It is usually associated with a closed head injury. A contusion may contain areas of hemorrhage, infarction, necrosis, and edema and frequently occurs at a fracture site.

■ Contusions or lacerations may occur both at the site of the direct impact of the brain on the skull (coup) and at a secondary area of damage on the opposite side away from injury (contrecoup), leading to multiple contused areas.

■ Neurologic assessment may demonstrate focal findings as well as generalized findings depending on the size and location of the contusion. Seizures are a common complication.

Complications

Epidural hematoma

An epidural hematoma results from bleeding between the dura and inner surface of the skull. An epidural hematoma is a neurologic emergency and is usually associated with a linear fracture crossing a major artery in the dura, causing a tear. It can have a venous or an arterial origin.

■ Venous epidural hematomas are associated with a tear of the dural venous sinus and develop slowly.

■ With arterial hematomas, the middle meningeal artery lying under the temporal bone is often torn. Because this is an arterial hemorrhage, the hematoma develops rapidly.

Manifestations typically include an initial period of unconsciousness at the scene, with a brief lucid interval followed by a decrease in LOC. Other symptoms may be headache, nausea and vomiting, or focal findings. Rapid surgical intervention to evacuate the hematoma and prevent cerebral herniation, along with medical management for increasing ICP, can dramatically improve outcomes.

Subdural hematoma

A subdural hematoma occurs from bleeding between the dura mater and the arachnoid layer of the meninges. The hematoma usually results from injury to the brain tissue and its blood vessels. A subdural hematoma is usually venous in origin, with a slow development of the hematoma, but rapid development can occur if the hematoma is of arterial origin. Subdural hematomas may be acute, subacute, or chronic (Table 40).

■ An acute subdural hematoma manifests within 24 to 48 hours of the injury. Manifestations are similar to those associated with brain tissue compression in increased ICP (see Increased Intracranial Pressure, p. 346). The patient’s appearance may range from drowsy and confused to unconscious. The ipsilateral pupil dilates and becomes fixed if ICP is significantly elevated.

■ A subacute subdural hematoma usually occurs within 2 to 14 days of the injury. After the initial bleeding, a subdural hematoma may appear to enlarge over time as the breakdown products of the blood draw fluid into the subdural space.

■ A chronic subdural hematoma develops over weeks or months after a seemingly minor head injury. Chronic subdural hematomas are more common in older adults because of a potentially larger subdural space as a result of brain atrophy. The presenting complaints are focal symptoms, rather than signs of increased ICP.

Table 40

Types of Subdural Hematomas

Occurrence After Injury	Progression of Symptoms	Treatment
Acute
24-48 hr after severe trauma	Immediate deterioration	Craniotomy, evacuation and decompression
Subacute
48 hr–2 wk after severe trauma	Alteration in mental status as hematoma develops Progression dependent on size and location of hematoma	Evacuation and decompression
Chronic
Weeks or months, usually >20 days after injury Often injury seemed trivial or was forgotten by patient	Nonspecific, nonlocalizing progression Progressive alteration in LOC	Evacuation and decompression, membranectomy

LOC, Level of consciousness.

Intracerebral hematoma

An intracerebral hematoma occurs from bleeding within the brain tissue. It usually occurs within the frontal and temporal lobes, possibly from the rupture of intracerebral vessels at the time of injury.

Diagnostic studies

■ CT scan is the best diagnostic test to evaluate for craniocerebral trauma.

■ MRI, positron emission therapy (PET), and evoked potential studies assist in diagnosis and differentiation of head injuries.

■ Transcranial Doppler studies are used to measure cerebral blood flow velocity.

■ Cervical spine x-ray series, CT scan, or MRI of the spine may be done.

Collaborative care

Emergency management of the patient with head injury includes measures to prevent secondary injury by treating cerebral edema and managing increased ICP (see Table 57-9, Lewis et al, Medical-Surgical Nursing, ed. 9, p. 1372). The principal treatment of head injuries is timely diagnosis and surgery if necessary. For the patient with a concussion or contusion, observation and management of increased ICP are primary management strategies.

■ The treatment of skull fractures is usually conservative. For depressed fractures and fractures with loose fragments, a craniotomy is necessary to elevate depressed bone and remove free fragments. If large amounts of bone are destroyed, the bone may be removed (craniectomy) and a cranioplasty will be needed at a later time (see the section on cranial surgery, Lewis et al, Medical-Surgical Nursing, ed. 9, pp. 1379 to 1381).

■ In cases of large acute subdural and epidural hematomas or those associated with significant neurologic impairment, the blood must be removed. A craniotomy is generally performed to visualize and allow control of the bleeding vessels. Burr-hole openings may be used in an extreme emergency for more rapid decompression, followed by a craniotomy. A drain may be placed postoperatively for several days to prevent reaccumulation of blood.

Nursing management

Goals

The patient with an acute head injury will maintain adequate cerebral oxygenation and perfusion; remain normothermic; achieve control of pain and discomfort; be free from infection; have adequate nutrition; and attain maximal cognitive, motor, and sensory function.

Nursing diagnoses/collaborative problems

■ Risk for ineffective cerebral tissue perfusion

■ Hyperthermia

■ Impaired physical mobility

■ Anxiety

■ Potential complication: increased ICP

Nursing interventions

One of the best ways to prevent head injuries is to prevent car and motorcycle crashes.

■ Be active in campaigns that promote driving safety, and speak to driver education classes regarding the dangers of unsafe driving and driving after drinking alcohol and using drugs.

■ The use of seat belts in cars and the use of helmets for riding on motorcycles are the most effective measures for increasing survival after crashes.

Acute intervention.

The general goal of nursing management of the head-injured patient is to maintain cerebral oxygenation and perfusion and prevent secondary cerebral ischemia. Surveillance or monitoring for changes in neurologic status is critically important because the patient’s condition may deteriorate rapidly, necessitating emergency surgery.

■ Explain the need for frequent neurologic assessments to both the patient and caregiver.

■ Behavioral manifestations associated with head injury can result in a frightened, disoriented patient who is combative and resists help.

The Glasgow Coma Scale (GCS) is useful in assessing the LOC (see Glasgow Coma Scale, p. 766). Indications of a deteriorating neurologic state, such as a decreasing LOC or lessening of motor strength, should be reported to the health care provider, and the patient’s condition should be closely monitored.

The major focus of nursing care for the brain-injured patient relates to increased ICP (seeIncreased Intracranial Pressure: Nursing Management, p. 346).

■ Loss of the corneal reflex may necessitate administering lubricating eye drops or taping the eyes shut to prevent abrasion.

■ Periorbital ecchymosis and edema disappear spontaneously, but cold and, later, warm compresses provide comfort and hasten the process.

■ Diplopia can be relieved by use of an eye patch.

■ Hyperthermia can result in increased metabolism, cerebral blood flow, cerebral blood volume, and ICP. Increased metabolic waste also produces further cerebral vasodilation. Avoid hyperthermia, with a goal of 36° C to 37° C as the standard of care.

■ If cerebrospinal fluid (CSF) rhinorrhea or otorrhea occurs, inform the physician immediately. The head of the bed may be elevated to decrease the CSF pressure. A loose collection pad may be placed under the nose or over the ear. Instruct the patient not to sneeze or blow the nose.

■ Nausea and vomiting may be a problem and can be alleviated by antiemetic drugs.

■ Headache can usually be controlled with acetaminophen or small doses of codeine.

If the patient’s condition deteriorates, intracranial surgery may be necessary. A burr-hole opening or craniotomy may be indicated, depending on the underlying injury. The patient is often unconscious before surgery, making it necessary for a family member to sign the consent form for surgery. This is a difficult and frightening time for the patient’s caregiver and family and requires sensitive nursing management. The suddenness of the situation makes it especially difficult for the family to cope.

Rehabilitation.

Once the condition has stabilized, the patient is usually transferred for acute rehabilitation management. There may be chronic problems related to motor and sensory deficits, communication, memory, and intellectual functioning.

■ The patient’s outward appearance is not a good indicator of how well the patient will function in the home or work environment given recovery time and rehabilitation.

■ The mental and emotional sequelae of brain trauma are often the most incapacitating problems. Many of the patients with head injuries who have been comatose for more than 6 hours undergo some personality change. The patient’s behavior may indicate a loss of social restraint, judgment, tact, and emotional control.

Progressive recovery may continue for 6 months or more before a plateau is reached and a prognosis for recovery can be made. Nursing management depends on specific residual deficits. In all cases the family must be given special consideration. They need to understand what is happening and be taught appropriate interaction patterns.

■ The family often has unrealistic expectations of the patient as the coma begins to recede. The family expects full return to pretrauma status. In reality, the patient usually experiences a reduced awareness and ability to interpret environmental stimuli.

■ Prepare the family for the emergence of the patient from coma and explain that the process of awakening often takes several weeks. Arrange for social work and chaplain consultations for the family in addition to providing open visitation and frequent status updates.

■ Family members, particularly spouses, go through role transition as the role changes from one of spouse to that of caregiver.

Headache

Description

Headache is probably the most common type of pain experienced by humans. The majority of people have functional headaches, such as migraine or tension type, whereas others have organic headaches caused by intracranial or extracranial disease.

■ Primary headaches are those not caused by a disease or another medical condition. They include tension-type, migraine, and cluster headaches. Characteristics of primary headaches are shown in Table 41.

■ Secondary headaches are caused by another condition or disorder, such as sinus infection, neck injury, and stroke.

Table 41

Comparison of Types of Headaches

Pattern	Tension-Type Headache	Migraine Headache	Cluster Headache
Site (see Fig. 59-1, Lewis et al, Medical-Surgical Nursing, ed 9, p. 1414)	Bilateral, bandlike pressure at base of skull	Unilateral (in 60%), may switch sides, commonly anterior	Unilateral, radiating up or down from one eye
Quality	Constant, squeezing tightness	Throbbing, synchronous with pulse	Severe, bone-crushing
Frequency	Cycles for many years	Periodic, cycles of several months to years	May have months or years between attacks Attacks occur in clusters over a period of 2 to 12 wk
Duration	30 min to 7 days	4 to 72 hr	5 min to 3 hr
Time and mode of onset	Not related to time	May be preceded by prodrome Onset after awakening Gets better with sleep	Nocturnal, commonly awakens patient from sleep
Associated symptoms	Palpable neck and shoulder muscle tension, stiff neck, tenderness	Nausea, vomiting Irritability, sweating Photophobia Phonophobia Prodrome of sensory, motor, or psychic phenomena Family history (in 65%)	Facial flushing or pallor Unilateral lacrimation, ptosis, and rhinitis

Tension-type headache

Tension-type headache, also called stress headache, is the most common type of headache and is characterized by its bilateral location and pressing/tightening quality. It is usually of mild or moderate intensity and can last from minutes to days. It is likely that neurovascular factors similar to those involved in migraine headaches play a role in the development of tension-type headaches.

Clinical manifestations.

Patients usually present with a bilateral frontal-occipital headache described as a constant, dull pressure, or bandlike headache associated with neck pain and increased tone in the cervical and neck muscles. There is no prodrome (early manifestation of impending disease) in tension-type headache. The headache does not involve nausea or vomiting, but may involve sensitivity to light (photophobia) or sound (phonophobia).

■ Headaches may occur intermittently for weeks, months, or years. Many patients can have a combination of migraine and tension-type headaches with features of both headaches occurring simultaneously.

Diagnostic studies.

Careful history taking is the most important diagnostic tool. Electromyography (EMG) may reveal sustained contraction of the neck, scalp, or facial muscles. If tension-type headache is present during physical examination, increased resistance to passive movement of the head and tenderness of head and neck may be present.

Migraine headache

Migraine headache is a recurring headache characterized by unilateral or bilateral throbbing pain, a triggering event or factor, and manifestations associated with neurologic and autonomic nervous system dysfunction. The most common age for migraine onset is between ages 20 and 30 years, with women being affected more than men. Risk factors for migraine include family history, low level of education, low socioeconomic status, high workload, and frequent tension-type headaches.

Pathophysiology.

The current theory is that a complex series of neurovascular events initiates a migraine headache. People who have migraines have a state of neuronal hyperexcitability in the cerebral cortex, especially in the occipital cortex. Approximately 70% of those with migraine have a first-degree relative who also had migraine headaches.

Migraines can be preceded by prodrome and aura. The prodrome may precede the headache by several hours or several days.

■ The prodrome may include neurologic (e.g., photophobia), psychologic (e.g., hyperactivity, irritability), and other (e.g., food craving) manifestations.

■ An aura is a complex experience of neurologic symptoms characterized by visual (e.g., bright lights, scotomas [patchy blindness], visual distortions [zig-zag lines]) and sensory (hearing voices or sounds that do not exist, strange smells) and/or motor (e.g., weakness, paralysis, feeling that limbs are moving) phenomena.

In many cases, migraine headaches have no known precipitating events. However, for other patients, the headache may be precipitated or triggered by foods, hormonal fluctuation, head trauma, physical exertion, fatigue, stress, and drugs.

Clinical manifestations.

Migraine without aura is the most common type of migraine headache. Migraine with aura occurs in only 10% of migraine headache episodes.

The headache may last 4 to 72 hours. During the headache phase, some patients may tend to “hibernate”; that is, they seek shelter from noise, light, odors, people, and problems. The headache is described as a steady, throbbing pain that is synchronous with the pulse. Although the headache is usually unilateral, it may switch to the opposite side in another episode. In some patients, the symptoms of the migraine headaches may become progressively worse over time.

Diagnostic studies.

There are no specific laboratory or radiologic tests for migraine headache. The diagnosis is usually made from the history. Neurologic and other diagnostic examinations are often normal.

Cluster headache

Cluster headache, a rare form of headache, involves repeated headaches that typically last 2 weeks to 3 months, and then the patient goes into remission for months to years. The clusters occur with regularity, usually occurring at the same time each day, during the same seasons of the year.

Pathophysiology.

Neither the cause nor pathophysiology of cluster headache is fully known. The trigeminal nerve has a role in the production of pain, but cluster headaches also involve dysfunction of intracranial blood vessels, the sympathetic nervous system, and pain modulation systems. Imaging studies show hypothalamic activation at the onset of cluster headache. Alcohol is the only dietary trigger. Strong odors, weather changes, and napping are other triggers.

Clinical manifestations.

The cluster headache is one of the most severe forms of headache, with intense pain lasting from a few minutes to 3 hours.

■ The pain is generally located around the eye, radiating to the temple, forehead, cheek, nose, or gums.

■ Other manifestations include swelling around the eye, lacrimation (tearing), facial flushing or pallor, rhinitis, and constriction of the pupil.

■ During the headache, the patient is often agitated and restless, unable to sit still or relax.

Diagnostic studies.

Diagnosis is primarily based on the history. Asking patients to keep a headache diary can be useful. CT scan, MRI, or magnetic resonance angiography (MRA) may rule out an aneurysm, a tumor, or an infection. A lumbar puncture may rule out other disorders.

Collaborative care

If no systemic underlying disease is found, the type of headache guides the therapy. Table 59-3, Lewis et al, Medical-Surgical Nursing, ed. 9, p. 1417 summarizes current therapies for prophylaxis and symptomatic relief of headaches. These therapies include drugs, meditation, yoga, biofeedback, cognitive-behavioral therapy, and relaxation training.

Drug therapy

Tension-type headache.

Drug treatment usually involves aspirin, acetaminophen, or nonsteroidal antiinflammatory drugs (NSAIDs) used alone or in combination with a sedative, muscle relaxant, or tranquilizer. However, many of these drugs have serious side effects.

Migraine headache.

Drug treatment is aimed at terminating or decreasing the symptoms of the acute attack. Many people with mild or moderate migraine can obtain relief with NSAIDs, aspirin, or caffeine-containing combination analgesics. For moderate to severe headaches, the triptans have become the first line of therapy.

■ Triptans affect selected serotonin receptors, reducing the neurogenic inflammation of the cerebral blood vessels and producing vasoconstriction. They include sumatriptan (Imitrex), naratriptan (Amerge), rizatriptan (Maxalt), almotriptan (Axert), frovatriptan (Frova), zolmitriptan (Zomig), and eletriptan (Relpax). The combination drug sumatriptan/naproxen (Treximet) combines a triptan with an antiinflammatory drug. Because these drugs cause vasoconstriction, they are avoided in patients with heart disease or stroke. Triptan medications should be taken at the first symptom of migraine headache.

■ Topiramate (Topamax), taken daily, has been shown to be an effective therapy for migraine prevention in adults. It must be used for 2 to 3 months to determine its effectiveness. Other preventive drugs for migraine headaches can include β-adrenergic blockers (e.g., propranolol [Inderal], atenolol [Tenormin]), tricyclic antidepressants (e.g., amitriptyline [Elavil]), selective serotonin reuptake inhibitors (e.g., fluoxetine [Prozac]), and calcium channel blockers (e.g., verapamil (Calan), flunarizine (Sibelium).

■ Botulinum toxin (Botox) may be an effective prophylactic treatment for patients who have chronic migraines or migraines that do not respond to other medications.

Cluster headache.

Because these headaches occur suddenly, often at night, and are not long lasting, drug therapy is not as useful as it is for other types of headache. Prophylactic medications may include verapamil (Isoptin), lithium, ergotamine, melatonin, or divalproex (Depakote).

■ Acute treatment of cluster headache is inhalation of 100% oxygen (O₂) delivered at a rate of 6 to 8 L/min for 10 minutes, which may relieve headache by causing vasoconstriction. The triptans (e.g., sumatriptan) are also effective in treating acute cluster headache. Intranasal administration of lidocaine is useful as an adjunctive therapy.

■ Methysergide may be used prophylactically when the cluster headache recurs at a known time.

Nursing management

Goals

The patient with a headache will have reduced or no pain, experience increased comfort and decreased anxiety, demonstrate understanding of triggering events and treatment strategies, use positive coping strategies to deal with pain, and experience increased quality of life and decreased disability.

Nursing diagnoses

■ Acute pain

■ Ineffective self-health management

Nursing interventions

Headaches may result from an inability to cope with daily stresses. An effective therapy may be to help patients examine their lifestyle, recognize stressful situations, and learn to cope with them more appropriately. Help the patient identify precipitating factors and develop ways to avoid them. Encourage daily exercise, relaxation periods, and socializing because each can help decrease the recurrence of headache.

■ Suggest alternative ways of handling the pain of headache through techniques such as relaxation, meditation, yoga, and self-hypnosis. Massage and moist hot packs to the neck and head can help a patient with tension-type headaches.

■ The patient should learn about drugs prescribed for prophylactic and symptomatic treatment of headache and should be able to describe the purpose, action, dosage, and side effects.

■ For the patient whose headaches are triggered by food, provide dietary counseling. The patient needs to be encouraged to eliminate foods that may provoke headaches (e.g., chocolate, alcohol, excessive caffeine, cheese, fermented foods, monosodium glutamate).

■ Cluster headache attacks may occur at high altitudes with low oxygen levels during air travel. Ergotamine, taken before the plane takes off, may decrease the likelihood of these attacks.

Patient and caregiver teaching

A teaching guide for the patient with a headache is provided in Table 42.

Table 42

Patient and Caregiver Teaching Guide
Headaches

For the patient with a headache, include the following instructions when teaching the patient and caregiver.

■ Keep a diary or calendar of headaches and possible precipitating events.

■ Avoid factors that can trigger a headache:

■ Foods containing amines (cheese, chocolate), nitrites (meats such as hot dogs), vinegar, onions, monosodium glutamate

■ Fermented or marinated foods

■ Alcohol (particularly red wine)

■ Emotional stress

■ Fatigue

■ Drugs such as ergot-containing preparations (ergotamine tartrate [Ergomar]) and monoamine oxidase inhibitors (e.g., rasagiline [Azilect])

■ Learn the purpose, action, dosage, and side effects of drugs taken.

■ Self-administer sumatriptan (Imitrex) subcutaneously if prescribed.

■ Use stress management techniques such as relaxation.

■ Participate in regular exercise.

■ Contact health care provider if any of the following occurs:

■ Symptoms become more severe, last longer than usual, or are resistant to medication.

■ Nausea and vomiting (if severe or not typical), change in vision, or fever occurs with the headache.

■ Problems occur with any drugs.

Heart failure

Description

Heart failure (HF) is an abnormal clinical syndrome involving impaired cardiac pumping and/or filling of the heart. This results in the inability of the heart to provide sufficient blood to meet the oxygen needs of the tissues. In clinical practice, the terms acute and chronic HF have replaced the term congestive HF (CHF) because not all HF involves pulmonary congestion.

HF is associated with numerous types of cardiovascular diseases, particularly long-standing hypertension, coronary artery disease (CAD), and MI.

■ HF is a major health problem in the United States. In contrast to other cardiovascular diseases, HF is increasing in incidence and prevalence. This is because of improved survival after cardiovascular events and the increased aging population. HF is the most common reason for hospital admission in older adults.

■ CAD and hypertension are the primary risk factors for HF. Other factors, including advanced age, diabetes, cigarette smoking, obesity, and high serum cholesterol, contribute to the development of HF.

Pathophysiology

HF may be caused by any interference with the normal mechanisms regulating cardiac output (CO). CO depends on (1) preload, (2) afterload, (3) myocardial contractility, and (4) heart rate (HR). Any changes in these factors can lead to decreased ventricular function and subsequent HF.

■ Major causes of HF may be divided into two subgroups: (1) primary causes, consisting of underlying cardiac diseases, such as CAD and cardiomyopathy; and (2) precipitating causes, such as anemia, pulmonary disease, and hypervolemia (see the complete listing of causes in Tables 35-1 and 35-2, Lewis et al, Medical-Surgical Nursing, ed. 9, p. 767).

Heart failure is classified as systolic or diastolic failure. Systolic failure results from an inability of the heart to pump effectively. It is caused by impaired contractile function (e.g., MI), increased afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart disease). The hallmark of systolic dysfunction is a decrease in the left ventricular ejection fraction (EF).

Diastolic failure is the inability of the ventricles to relax and fill during diastole. Decreased filling results in decreased stroke volume and CO and venous engorgement in both the pulmonary and systemic vascular systems. The diagnosis of diastolic failure is based on the presence of HF symptoms with a normal EF. Diastolic failure is usually the result of left ventricular hypertrophy from chronic hypertension, aortic stenosis, or hypertrophic cardiomyopathy.

Mixed systolic and diastolic failure is seen in disease states such as dilated cardiomyopathy, in which poor systolic function (weakened muscle function) is further compromised by dilated left ventricular walls that are unable to relax.

The patient with ventricular failure of any type has low systemic arterial BP, low CO, and poor renal perfusion. Whether a patient arrives at this point acutely (from an MI) or chronically (from worsening cardiomyopathy or hypertension), the body’s response to this low CO is to mobilize compensatory mechanisms to maintain CO and BP. The main compensatory mechanisms include (1) sympathetic nervous system activation, (2) neurohormonal responses, (3) ventricular dilation, and (4) ventricular hypertrophy.

HF is usually manifested by biventricular failure, although one ventricle may precede the other in dysfunction.

■ Left-sided failure is the most common form of initial heart failure. Left-sided failure causes blood to back up into the left atrium and pulmonary veins. The increased pulmonary pressure causes fluid leakage from the pulmonary capillary bed into the interstitium and then the alveoli, which is manifested as pulmonary congestion and edema.

■ Right-sided failure causes a backup of blood into the right atrium and venous circulation. Venous congestion in the systemic circulation results in peripheral edema, hepatomegaly, and jugular venous distention. The primary cause of right-sided failure is left-sided failure. Cor pulmonale (right ventricular dilation and hypertrophy caused by pulmonary pathologic conditions) can also cause right-sided failure (see Cor Pulmonale, p. 159).

The primary cause of right-sided HF is left-sided HF. In this situation, left-sided HF results in pulmonary congestion and increased pressure in the blood vessels of the lung (pulmonary hypertension). Eventually, chronic pulmonary hypertension (increased right ventricular afterload) results in right-sided hypertrophy and HF.

Manifestations

Acute decompensated heart failure

In acute decompensated HF (ADHF), an increase in the pulmonary venous pressure is caused by failure of the left ventricle (LV). This results in engorgement of the pulmonary vascular system. This early stage is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (PaO₂).

ADHF can manifest as pulmonary edema. This is an acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid. The most common cause of pulmonary edema is acute LV failure secondary to CAD.

■ Manifestations of pulmonary edema are distinct: the patient is usually anxious, pale, and possibly cyanotic, with clammy and cold skin.

■ The patient has dyspnea, respiratory rate greater than 30 breaths/min, and orthopnea. Wheezing and coughing with production of frothy, blood-tinged sputum may also occur.

■ Auscultation of the lungs may reveal bubbling crackles, wheezes, and rhonchi. The patient’s HR is rapid, and BP may be elevated or decreased depending on the severity of the HF.

Chronic heart failure

Manifestations of chronic HF depend on the patient’s age, underlying type and extent of heart disease, and which ventricle is failing to pump effectively. Table 43 lists manifestations of left-sided and right-sided failure. The patient with chronic HF usually has manifestations of biventricular failure.

■ Fatigue after usual activities is one of the earliest symptoms.

■ Dyspnea is a common sign. Shortness of breath occurs when the patient is in the recumbent position (orthopnea).

■ Paroxysmal nocturnal dyspnea (PND) occurs when the patient is asleep. The patient awakens in a panic, has feelings of suffocation, and has a strong desire to sit or stand up.

■ A cough is often associated with HF and may be the first clinical symptom. It begins as a dry, nonproductive cough that is not relieved by position change or over-the-counter cough medicine.

■ Other common signs include tachycardia; edema in the legs, liver, abdominal cavity, and lungs; nocturia; dusky skin; restlessness and confusion; angina; and weight changes.

Table 43

Manifestations of Heart Failure

Right-Sided Heart Failure	Left-Sided Heart Failure
Signs
■ RV heaves ■ Murmurs ■ Jugular venous distention ■ Edema (e.g., pedal, scrotum, sacrum) ■ Weight gain ■ ↑ HR ■ Ascites ■ Anasarca (massive generalized body edema) ■ Hepatomegaly (liver enlargement)	■ LV heaves ■ Pulsus alternans (alternating pulses: strong, weak) ■ ↑ HR ■ PMI displaced inferiorly and posteriorly (LV hypertrophy) ■ ↓ PaO₂, slight ↑ PaCO₂ (poor O₂ exchange) ■ Crackles (pulmonary edema) ■ S₃ and S₄ heart sounds ■ Pleural effusion ■ Changes in mental status ■ Restlessness, confusion
Symptoms
■ Fatigue ■ Anxiety, depression ■ Dependent, bilateral edema ■ Right upper quadrant pain ■ Anorexia and GI bloating ■ Nausea	■ Weakness, fatigue ■ Anxiety, depression ■ Dyspnea ■ Shallow respirations up to 32-40/min ■ Paroxysmal nocturnal dyspnea ■ Orthopnea (shortness of breath in recumbent position) ■ Dry, hacking cough ■ Nocturia ■ Frothy, pink-tinged sputum (advanced pulmonary edema)

LV, Left ventricle; PaCO2, partial pressure of CO₂ in arterial blood; PaO2, partial pressure of O₂ in arterial blood; PMI, point of maximal impulse; RV, right ventricle.

Complications

Pleural effusion results from increasing pressure in the pleural capillaries. Enlargement of the heart chambers in chronic HF can cause atrial fibrillation. Patients also are at risk for ventricular dysrhythmias.

Left ventricular thrombus may occur with ADHF or chronic HF in which the enlarged LV and decreased CO combine to increase the chance of thrombus formation in the LV. This places the patient at risk for stroke.

Hepatomegaly may result as the liver becomes congested with venous blood. Hepatic congestion leads to impaired liver function; eventually liver cells die, and cirrhosis can develop. The decreased CO that accompanies chronic HF also results in decreased perfusion to the kidneys and can lead to renal insufficiency or failure.

Diagnostic studies

Diagnosing HF is often difficult because neither patient signs nor symptoms are highly specific, and both may mimic many other medical conditions (e.g., anemia, lung disease). Diagnostic tests for acute decompensated and chronic heart failure are presented in Table 44.

Table 44

Collaborative Care
Heart Failure

Both ADHF and Chronic HF	ADHF	Chronic HF
Diagnostic
■ History and physical examination ■ Determination of underlying cause ■ Serum chemistries, cardiac enzymes, BNP or NT-proBNP level (see Table 32-6, Lewis et al, Medical-Surgical Nursing, 9e, p. 699), liver function tests, thyroid function tests, CBC ■ Chest x-ray ■ 12-lead ECG ■ Hemodynamic monitoring ■ Echocardiogram ■ Nuclear imaging studies (see Table 32-6, Lewis et al, Medical-Surgical Nursing, 9e, pp. 701-702) ■ Cardiac catheterization	■ ABGs ■ Endomyocardial biopsy	■ Exercise stress testing
Collaborative Therapy
■ Treatment of underlying cause ■ Circulatory assist devices (e.g., ventricular assist device) ■ Daily weights ■ Sodium- and, possibly, fluid-restricted diet	■ High Fowler’s position ■ O₂ by mask or nasal cannula ■ BiPAP ■ Circulatory assist device: intraaortic balloon pump ■ Endotracheal intubation and mechanical ventilation ■ Vital signs, urine output at least q1hr ■ Continuous ECG and pulse oximetry monitoring ■ Hemodynamic monitoring (e.g., intraarterial BP, PAWP, CO) ■ Drug therapy (see Table 35-7, Lewis et al, Medical-Surgical Nursing, 9e, p. 774) ■ Possible cardioversion (e.g., atrial fibrillation) ■ Ultrafiltration	■ O₂ therapy at 2-6 L/min by nasal cannula if indicated ■ Rest-activity periods ■ Cardiac rehabilitation ■ Home health nursing care (e.g., telehealth monitoring) ■ Drug therapy (see Table 35-7, Lewis et al, Medical-Surgical Nursing, 9e, p. 774) ■ Cardiac resynchronization therapy with biventricular pacing and internal cardioverter-defibrillator ■ LVAD ■ Cardiac transplantation ■ Palliative and end-of-life care

ABGs, Arterial blood gases; ADHF, acute decompensated heart failure; BiPAP, bilevel positive airway pressure; BNP, b-type natriuretic peptide; CO, cardiac output; HF, heart failure; LVAD, left ventricular assist device; NT-proBNP, N-terminal prohormone of BNP; PAWP, pulmonary artery wedge pressure.

A primary diagnostic goal is to determine the underlying etiology. An endomyocardial biopsy (EMB) may be done in patients who develop unexplained, new-onset HF that is unresponsive to usual care. EF is used to differentiate systolic and diastolic HF. In general, b-type natriuretic peptide (BNP) levels correlate positively with the degree of left ventricular dysfunction.

Nursing and collaborative management: Acute decompensated heart failure

With the addition of new drugs and device therapies, the management of HF has dramatically changed in the past few years. Table 44 lists collaborative therapy for the patient with ADHF.

Patients with ADHF need continuous monitoring and assessment, which may be done in an intensive care unit (ICU) setting. Monitor ECG and oxygen saturation. The patient may have continuous hemodynamic monitoring. Supplemental oxygen helps increase the percentage of oxygen in inspired air. In severe pulmonary edema the patient may need noninvasive ventilatory support or intubation and mechanical ventilation.

■ If the patient is dyspneic, place in a high Fowler’s position with the feet horizontal in the bed or dangling at the bedside. This position helps decrease venous return because of the pooling of blood in the extremities.

■ Ultrafiltration is an option for the patient with volume overload. It can rapidly remove intravascular fluid volume while maintaining hemodynamic stability.

■ Circulatory assist devices are used to manage patients with worsening HF. The intraaortic balloon pump (IABP) increases coronary blood flow to the heart muscle and decreases the heart’s workload. Ventricular assist devices can be used to maintain the pumping action of the heart.

■ Assess patients with HF for depression and anxiety, and treatment plans should be initiated if appropriate.

Drug therapy

Drug therapy is essential in treating acute heart failure.

■ Diuretics: Diuretics are the mainstay of treatment in patients with volume overload. They act to decrease sodium reabsorption within the nephrons, thereby enhancing sodium and water loss. Decreasing venous return (preload) reduces the amount of volume returned to the LV during diastole. Decreasing intravascular volume with the use of loop diuretics (e.g., furosemide [Lasix], bumetanide [Bumex]) reduces venous return.

■ Vasodilators: IV nitroglycerin reduces preload, slightly reduces afterload (in high doses), and increases myocardial oxygen supply. Sodium nitroprusside (Nipride) reduces both preload and afterload, thus improving myocardial contraction, increasing CO, and reducing pulmonary congestion. IV nesiritide (Natrecor), a recombinant form of BNP, causes both arterial and venous dilation.

■ Morphine: Morphine sulfate reduces preload and afterload and is used in the treatment of ADHF and pulmonary edema. It dilates the pulmonary and systemic blood vessels, thereby decreasing pulmonary pressures and improving gas exchange.

■ Positive inotropics: Inotropic therapy increases myocardial contractility. Drugs include β-adrenergic agonists (e.g., dopamine [Intropin], dobutamine [Dobutrex], epinephrine, norepinephrine [Levophed]), phosphodiesterase inhibitors (inamrinone [Inocor], milrinone [Primacor]), and digitalis.

Digitalis is a positive inotrope that improves LV function but also increases myocardial oxygen consumption. Inotropic therapy is only recommended for use in the short-term management of patients with ADHF who have not responded to conventional pharmacotherapy (e.g., diuretics, vasodilators, morphine).

Collaborative care: Chronic heart failure

The main goals in the treatment of chronic HF are to treat the underlying cause and contributing factors, maximize CO, reduce symptoms, improve ventricular function, improve quality of life, preserve target organ function, and improve mortality and morbidity. The treatment of causes such as dysrhythmias, hypertension, valvular disorders, and CAD is discussed elsewhere in this book.

Nondrug therapy

■ Administration of O₂ improves O₂ saturation and assists in meeting tissue oxygen needs, thereby helping to relieve dyspnea and fatigue.

■ Physical and emotional rest conserves energy and decreases the need for additional O₂. A patient with severe HF may be on bed rest with limited activity. A patient with mild to moderate HF can be ambulatory with a restriction of strenuous activity.

Cardiac resynchronization therapy (CRT), unlike traditional pacing, coordinates right and left ventricular contractility through biventricular pacing. The ability to have normal simultaneous electrical conduction (synchrony) within the right and left ventricles increases left ventricular function and CO.

Mechanical options such as the IABP and ventricular assist devices (VADs) are available for patients with deteriorating conditions, especially those awaiting cardiac transplantation. Limitations of bed rest, infection, and vascular complications preclude long-term use of IABPs. VADs provide highly effective long-term support and have become standard care in many heart transplant centers.

Drug therapy

■ Diuretics: Diuretics reduce edema, pulmonary venous pressure, and preload. Thiazide diuretics (e.g., hydrochlorothiazide [Hydrodiuril]) inhibit sodium reabsorption in the distal tubule, thus promoting excretion of sodium and water. Loop diuretics such as furosemide (Lasix), bumetanide (Bumex), and torsemide (Demadex) are potent but can cause hypokalemia and ototoxicity. In chronic HF the lowest effective dose of diuretic should be used.

■ Angiotensin-converting enzyme (ACE) inhibitors: ACE inhibitors (e.g., captopril [Capoten], enalapril [Vasotec]) are the primary drugs of choice for blocking the renin-angiotensin-aldosterone system in HF patients with systolic failure. A reduction in systemic vascular resistance (SVR) with the use of ACE inhibitors causes a significant increase in CO. Although BP decreases, tissue perfusion is maintained or increased as a result of improved CO, and diuresis is enhanced by the suppression of aldosterone.

■ Nitrates: Nitrates (e.g., nitroglycerin) cause vasodilation by acting directly on the smooth muscle of the vessel wall. Nitrates are of particular benefit in the management of myocardial ischemia related to HF because they promote vasodilation of the coronary arteries.

■ BiDil: A combination drug containing isosorbide dinitrate and hydralazine (BiDil) is used for the treatment of HF in African Americans who are already being treated with standard therapy.

■ β-Adrenergic blockers: β-Adrenergic blockers including carvedilol (Coreg), metoprolol (Toprol-XL), and bisoprolol (Zebeta) directly block the negative effects of the sympathetic nervous system on the failing heart.

■ Positive inotropes: Positive inotropes are used to improve cardiac contractility. Digitalis preparations (e.g., digoxin [Lanoxin]) increase the force of cardiac contraction (inotropic action). They also decrease conduction speed within the myocardium and slow the HR (chronotropic action). This allows for more complete emptying of the ventricles, reducing the volume remaining in the ventricles during diastole. CO increases because of increased stroke volume from improved contractility.

Nutritional therapy

Diet teaching and weight management are essential to the patient’s control of chronic HF. You or a dietitian should obtain a detailed diet history to determine not only what foods the patient eats but also when, where, and how often they dine out.

The edema associated with chronic HF is often treated by dietary restriction of sodium. Teach the patient what foods are low and high in sodium and ways to enhance food flavors without the use of salt (e.g., substituting lemon juice, various spices). The degree of sodium restriction depends on the severity of the HF and the effectiveness of diuretic therapy.

■ A commonly prescribed diet for a patient with mild HF is a 2-g sodium diet. All foods high in sodium should be eliminated. (For sample menu plans for sodium-restricted diets see Table 35-8, Lewis et al, Medical-Surgical Nursing, ed. 9, p. 778).

Fluid restrictions are not commonly prescribed for mild to moderate HF. However, in moderate to severe HF, fluid restrictions are usually implemented.

■ Instruct patients to weigh themselves at the same time each day, preferably before breakfast, while wearing the same type of clothing. For a weight gain of 3 lb (1.4 kg) over 2 days or a 5-lb (2.3-kg) gain over 1 week, the primary health care provider should be called.

Nursing management: Chronic heart failure

Goals

The patient with HF will have a decrease in symptoms (e.g., shortness of breath, fatigue), decreased peripheral edema, increased exercise tolerance, adherence with medical regimen, and no complications related to HF.

See NCP 35-1 for the patient with HF, Lewis et al, Medical-Surgical Nursing, ed. 9, pp. 780 to 781.

Nursing diagnoses

■ Activity intolerance

■ Excess fluid volume

■ Decreased cardiac output

■ Impaired gas exchange

Nursing interventions

Help to aggressively identify and treat risk factors for HF to prevent or slow the progression of the disease. For example, teach a patient with hypertension or hyperlipidemia measures to manage BP or cholesterol with medication, diet, and exercise. Patients with valvular disease should have valve replacement planned before lung congestion develops.

Acute intervention.

Many people with HF will experience one or more episodes of ADHF. When they do, they are usually managed in an intensive care unit, an intermediate care unit with continuous cardiac monitoring capability, or a specialized HF unit.

■ Successful HF management depends on several important principles: (1) HF is a progressive disease, and treatment plans are established along with quality-of-life goals; (2) symptom management is controlled by the patient with self-management tools (e.g., daily weights, drug regimens, diet and exercise plans); (3) salt and, at times, water must be restricted; (4) energy must be conserved; and (5) support systems are essential to the success of the entire treatment plan.

■ Reduction of anxiety is an important nursing function, since anxiety may increase the sympathetic nervous system (SNS) response and further increase myocardial workload. Reducing anxiety may be facilitated by a variety of nursing interventions and the use of sedatives (e.g., benzodiazepines, morphine sulfate).

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Tags: Clinical Companion to Medical-Surgical Nursing

Oct 26, 2016 | Posted by admin in NURSING | Comments Off

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