Malignant Neoplasms

INTRODUCTION

Mainly a disease of older adults, cancer is second to cardiovascular disease as the leading cause of death in the United States (more than 560,000 deaths annually). More than 70% of patients who die of cancer are older than age 65. The most common cancers in men in the United States are prostate, lung, and colorectal, and the leading causes of cancer death are lung, prostate, colorectal, and liver. The most common cancers in women in the United States are breast, lung, and colorectal, and the leading causes of cancer death are lung, breast, and colorectal.

Cancer results from a malignant transformation (carcinogenesis) of normal cells. (See Histologic characteristics of cancer cells.) Cancer cells proliferate uncontrollably, thus establishing themselves at other tissues to form secondary foci (metastasis). Cancer cells in malignant tumors differ from those in benign tumors, and they serve no useful purpose. (See Comparing benign and malignant tumors, page 706.) Cancer cells metastasize via circulation through the blood or lymphatics, by unintentional transplantation from one site to another during surgery, and by local extension. (See How cancer metastasizes, page 707.)

Classified by their histologic origin, tumors derived from epithelial tissues are called carcinomas; from epithelial and glandular tissues, adenocarcinomas; from connective, muscle, and bone tissues, sarcomas; from glial cells, gliomas; from pigmented cells, melanomas; and from plasma cells, myelomas. Cancer cells derived from erythrocytes are known as erythroleukemia; from lymphocytes, leukemia; and from lymphatic tissue, lymphoma.

WHAT CAUSES CANCER?

Cancer develops from mutations within the genes of cells. Thus, cancer is a genetic disease. Cancer susceptibility genes are of two types. Some are oncogenes, which activate cell division and influence embryonic development, and some are tumor suppressor genes, which halt cell division.

These genes are typically found in normal human cells, but certain kinds of mutations may transform the normal cells. Inherited defects may cause a genetic mutation, whereas repeated exposure to a carcinogen may cause an acquired mutation. Current evidence indicates that carcinogenesis results from a complex interaction of carcinogens and accumulated mutations in several genes.

In animal studies of the ability of viruses to transform cells, some human viruses exhibit carcinogenic potential. For example, the Epstein-Barr virus, the cause of infectious mononucleosis, has been linked to Burkitt’s lymphoma and nasopharyngeal cancer.

High-frequency radiation, such as ultraviolet and ionizing radiation, damages deoxyribonucleic acid (DNA), possibly inducing genetically transferable abnormalities. Other factors, such as a person’s tissue type and hormonal status, interact to potentiate radiation’s carcinogenic effect. Examples of substances that
may damage DNA and induce carcinogenesis include:

alkylating agents—leukemia
aromatic hydrocarbons and benzopyrene (from polluted air)—lung cancer
asbestos—mesothelioma of the lung
tobacco—cancer of the lung, oral cavity and upper airways, esophagus, pancreas, kidneys, and bladder
vinyl chloride—angiosarcoma of the liver

Comparing benign and malignant tumors

Factor	Benign	Malignant
Differentiation	Well differentiated	Variable
Effect on body	Cachexia rare; usually not fatal but may obstruct vital organs, exert pressure, produce excess hormones; can become malignant	Cachexia typical, with such symptoms as anemia, loss of weight, and weakness; fatal if untreated
Growth	Slow expansion; push aside surrounding tissue but don’t infiltrate	Usually infiltrate surrounding tissues rapidly, expanding in all directions
Limitation	Commonly encapsulated	Seldom encapsulated; in many cases poorly delineated
Mitotic activity	Variable	Extensive
Morphology	Cells closely resemble cells of tissue of origin	Cells may differ considerably from those of tissue of origin
Recurrence	Rare after surgical removal	When removed only by surgery, commonly recur due to infiltration into surrounding tissues
Spread	No metastasis	Spread via blood and lymph systems; establish secondary tumors
Tissue destruction	Usually slight	Extensive due to infiltration and metastatic lesion

Diet can also be a factor, especially in the development of GI cancer as a result of a high animal fat diet. Additives composed of nitrates and certain methods of food preparation— particularly charbroiling—are also recognized factors

The role of hormones in carcinogenesis is still controversial, but it seems that excessive use of some hormones, especially estrogen, produces cancer in animals. Also, the synthetic estrogen diethylstilbestrol causes vaginal cancer in some daughters of women who were treated with it. It’s unclear, however, whether changes in human hormonal balance retard or stimulate cancer development.

Some forms of cancer and precancerous lesions result from genetic predisposition either directly (as in Wilms’ tumor and retinoblastoma) or indirectly (in association with inherited conditions such as Down syndrome or immunodeficiency diseases). Expressed as autosomal recessive, X-linked, or autosomal dominant disorders, their common characteristics include:

early onset of malignant disease
increased incidence of bilateral cancer in paired organs (breasts, adrenal glands, kidneys, and eighth cranial nerve [acoustic neuroma])
increased incidence of multiple primary malignancies in nonpaired organs
abnormal chromosome complement in tumor cells

IMMUNE RESPONSE

Other factors that interact to increase susceptibility to carcinogenesis are immunologic competence, age, nutritional status, hormonal balance, and response to stress. Presumably, the body develops cancer cells continuously, but the immune system recognizes them as foreign cells and destroys them. This defense mechanism, known as immunosurveillance, has two major components: humoral immune response and cell-mediated immune response.
Their interaction promotes antibody production, cellular immunity, and immunologic memory. Thus, the intact human immune system is responsible for spontaneous regression of tumors.

Theoretically, the cell-mediated immune response begins when T lymphocytes become sensitized by contact with a specific antigen. After repeated contacts, sensitized T cells release chemical factors called lymphokines, some of which begin to destroy the antigen. This reaction triggers the transformation of an additional population of T lymphocytes into “killers” of antigen-specific cells—in this case, cancer cells.

Similarly, the humoral immune response reacts to an antigen by triggering the release of antibodies from plasma cells and activating the serum-complement system, which destroys the antigen-bearing cell. However, an opposing immune factor, a “blocking antibody,” enhances tumor growth by protecting malignant cells from immune destruction.

Cancer may arise when any one of several factors disrupts the immune system:

Aging cells, when copying their genetic material, may begin to err, giving rise to mutations. The aging immune system may not recognize these mutations as foreign and thus may allow them to proliferate and form a malignant tumor.
Cytotoxic drugs decrease antibody production and destroy circulating lymphocytes.
Extreme stress or certain viral infections can depress the immune system.
Increased susceptibility to infection commonly results from radiation, cytotoxic drug therapy, and lymphoproliferative and myeloproliferative diseases, such as lymphatic and myelocytic leukemia. These cause bone marrow depression, which can impair leukocyte function.
Acquired immunodeficiency syndrome weakens cell-mediated immunity.
Cancer itself is immunosuppressive; advanced cancer exhausts the immune response. (The absence of immune reactivity is known as anergy.)

DIAGNOSTIC METHODS

A thorough medical history and physical examination should be done before diagnostic procedures. Useful tests for the early detection and staging of tumors include X-ray, endoscopy, isotope scan, computed tomography scan, and magnetic resonance imaging, but the single most important diagnostic tool is a biopsy for direct histologic study of tumor tissue. Biopsy tissue samples can be taken by curettage, fluid aspiration (pleural effusion), fine-needle aspiration biopsy (breast), dermal punch (skin or mouth), endoscopy (rectal polyps), and surgical excision (visceral tumors and nodes).

An important tumor marker, carcinogenic embryonic antigen (CEA), although nonspecific
and not diagnostic by itself, can signal malignancies of the large bowel, stomach, pancreas, lungs, and breasts. CEA titers range from normal (less than 5 ng) to suspicious (5 to 10 ng) to suspect (greater than 10 ng). CEA serves many valuable purposes:

as a baseline during chemotherapy to evaluate the extent of tumor spread
to regulate drug dosage
to prognosticate after surgery or radiation
to detect tumor recurrence

Although no more specific than CEA, alphafetoprotein—a fetal antigen uncommon in adults—can suggest testicular, ovarian, gastric, and hepatocellular cancers. Beta human chorionic gonadotropin may point to testicular cancer or choriocarcinoma. Other commonly used tumor markers include prostate-specific antigen to detect and monitor prostatic cancer, and CA-125, useful for monitoring ovarian, colorectal, and gastric cancers.

STAGING AND GRADING

Choosing effective therapeutic options depends on correct staging of malignant disease, commonly with the TNM staging system (tumor size, nodal involvement, metastatic progress). This classification system provides an accurate tumor description that’s adjustable as the disease progresses. TNM staging allows reliable comparison of treatments and survival rates among large population groups; it also identifies nodal involvement and metastasis to other areas.

Grading, another way to define a tumor, classifies the lesion according to corresponding normal cells, such as lymphoid or mucinous lesions; it compares tumor tissue to normal cells (differentiation); and it estimates the tumor’s growth rate. For example, a low-grade tumor typically has cells more closely resembling normal cells, whereas a high-grade tumor has poorly differentiated cells.

FIVE MAJOR THERAPIES

Cancer treatments include surgery, radiation, chemotherapy, biotherapy (also called immunotherapy), and hormonal therapy. Therapies may be used alone or in combination, depending on the type, stage, localization, and responsiveness of the tumor and on limitations imposed by the patient’s clinical status.

Surgery, the mainstay of cancer treatment, is often combined with other therapies. Surgery may be performed as a biopsy to obtain tissue for study; as continued surgery to remove the bulk of the tumor; or before chemotherapy or radiation to debulk the tumor in hope of a better outcome. Surgery can be curative as well. Other therapies may be used later to discourage proliferation of residual cells.

Surgery can also relieve pain, correct obstruction, and alleviate pressure. Current, less radical surgical procedures (such as lumpectomy instead of radical mastectomy) are often as effective as radical procedures and are better tolerated by patients.

Radiation therapy aims to destroy the dividing cancer cells while damaging nonmalignant cells as little as possible. Therapeutic radiation is either particulate or electromagnetic. Both types ionize matter and have cellular DNA as their target.

Radiation treatment approaches include external beam radiation and intracavitary and interstitial implants. The latter therapy requires personal radiation protection for all staff members who come in contact with the patient.

Normal and malignant cells respond to radiation differently, depending on blood supply, oxygen saturation, previous irradiation, and immune status. Generally, normal cells recover from radiation faster than malignant cells. The success of the treatment and damage to normal tissue also vary with the intensity of the radiation. Although a large single dose of radiation has greater cellular effects than fractions of the same amount delivered sequentially, a protracted schedule allows time for normal tissue to recover in the intervals between individual sublethal doses.

Radiation may be used palliatively to relieve or reduce pain, obstruction, malignant effusions, cough, dyspnea, ulcerations, and hemorrhage; it can also promote the repair of pathologic fractures after surgical stabilization and delay tumor spread.

Combining radiation and surgery can minimize radical surgery, prolong survival, and preserve anatomic function. For example, preoperative doses of radiation shrink a tumor, making it operable, while preventing further spread of the disease during surgery. After the wound heals, postoperative doses prevent residual cancer cells from multiplying or metastasizing.

Systemic adverse effects, such as weakness, fatigue, anorexia, nausea, vomiting, and anemia, may subside with antiemetics, steroids, frequent small meals, fluid maintenance, and
rest. They are seldom severe enough to require discontinuing radiation but may require a dosage adjustment. (For localized adverse effects, see Radiation’s adverse effects.)

Radiation’s adverse effects

Area radiated	Effect	Management
Abdomen and pelvis	Cramps, diarrhea, nausea	Administer loperamide and diphenoxylate with atropine. Provide a low-residue diet. Maintain fluid and electrolyte balance. Administer antiemetics as ordered.
Chest	Esophagitis	Give pain medication. Provide total parenteral nutrition or tube feedings. Maintain fluid balance.
	Lung tissue irritation, persistent nonproductive cough	Explain the importance of not smoking and of avoiding people with upper respiratory infections. Provide steroid therapy as indicated. Provide humidifier if necessary. Administer cough suppressants as indicated.
	Pericarditis, myocarditis	Give antiarrhythmics, such as procainamide, disopyramide, and phosphate, as indicated. Monitor for heart failure.
Head and neck	Alopecia	Gently comb and groom scalp. Use a soft head covering.
	Dental caries	Apply fluoride to teeth prophylactically, encourage use of fluoride mouth rinses, and provide gingival care.
	Mucositis	Provide a non-alcohol-based mouthwash with viscous lidocaine; cool carbonated drinks; ice pops; and a soft, nonirritating diet. Use soft toothbrushes or swabs. Avoid spicy food and alcohol.
	Xerostomia (dry mouth)	Encourage good oral hygiene. Consider prescribing an oral saliva replacement. Moist foods are better tolerated than dry foods.
Kidneys	Nephritis, lassitude, headache, edema, dyspnea, hypertensive nephropathy, azotemia, anemia	Maintain fluid and electrolyte balance, and watch for signs of renal failure (such as decreased urine output, peripheral edema). Consider prescribing erythropoietin.

Radiation therapy requires frequent blood counts (particularly of white blood cells and platelets), especially if the target site involves areas of bone marrow production. Radiation also requires special skin care, such as covering the irradiated area with loose cotton clothing and avoiding deodorants, colognes, and other topical agents during treatment. (See How to prepare the patient for external radiation therapy, page 710.)

Chemotherapy includes a wide array of drugs, which may induce regression of a tumor and its metastasis. It’s particularly useful in controlling residual disease and, as an adjunct to surgery or radiation therapy, it can induce long remissions and sometimes effect cures, especially in patients with childhood leukemia, Hodgkin’s lymphoma, choriocarcinoma, or testicular cancer. As a palliative treatment, chemotherapy aims to improve the patient’s quality of life by temporarily relieving pain and other symptoms.

Some major chemotherapeutic agents include:

alkylating agents and nitrosoureas, which inhibit cell growth and division by reacting with DNA
antimetabolites, which prevent cell growth by competing with metabolites in the production of nucleic acid
antitumor antibiotics, which block cell growth by binding with DNA and interfering with DNA-dependent ribonucleic acid synthesis
plant alkaloids, which prevent cellular reproduction by disrupting cell mitosis
steroid hormones, which inhibit the growth of hormone-susceptible tumors by changing their chemical environment

How to prepare the patient for external radiation therapy

Show the patient where radiation therapy takes place, and introduce him to the radiation therapist.
Tell him to remove all metal objects (pens, buttons, jewelry) that may interfere with therapy. Explain that the areas to be treated will be marked with indelible ink and that he must not scrub these areas because it’s important to radiate the same areas each time.
Reinforce the practitioner’s explanation of the procedure, and answer any questions as honestly as you can. If you don’t know the answer to a question, refer the patient to the practitioner.
Teach the patient to watch for and report any adverse effects. Because radiation therapy may increase susceptibility to infection, warn him to avoid people with colds or other infections during therapy. However, emphasize the benefits (such as outpatient treatment) instead of the adverse effects.
Reassure the patient that treatment is painless and won’t make him radioactive. Stress that he’ll be under constant surveillance during radiation administration and should call out if he needs anything.

The adverse effects of chemotherapy vary. Antineoplastic agents, toxic to cancer cells, can also cause transient changes in normal tissues, especially among proliferating body cells. Antineoplastic agents typically suppress bone marrow, causing anemia, leukopenia, and thrombocytopenia; irritate GI epithelial cells, causing nausea and vomiting; and destroy the cells of the hair follicles and skin, causing alopecia and dermatitis. Some chemotherapy drugs can also have permanent effects such as peripheral neuropathy.

Some I.V. chemotherapy drugs are irritants; others are vesicants. Irritants can cause pain at the injection site and along the vein but usually don’t cause tissue necrosis. However, vesicants, when extravasated, may cause deep cutaneous necrosis requiring debridement and skin grafting. (Note: Most drugs with the potential for direct tissue injury are now given through a central venous catheter.)

Therefore, all patients undergoing chemotherapy need special care:

Increase the patient’s fluid intake before and throughout chemotherapy.
Inform the patient of possible temporary hair loss, and reassure him that his hair should grow back after therapy ends. Suggest a wig or other head covering, and encourage the patient to purchase it before the hair loss.
Check skin for petechiae, ecchymoses, chemical cellulitis, and secondary infection during treatment.
Minimize tissue irritation and damage by checking needle placement before and during infusion if you administer the drug by a peripheral vein. Tell the patient to report any discomfort during infusion. If a vesicant extravasates, stop the infusion, aspirate the drug from the needle, and give the appropriate antidote if available.

Chemotherapeutic drugs can be given orally, subcutaneously, I.M., I.V., intracavitarily, intrathecally, intraperitoneally, topically, intralesionally, and by arterial infusion, depending on the drug and its pharmacologic action; usually, administration is intermittent to allow for bone marrow recovery between doses. Dosages are calculated according to the patient’s body surface area, with adjustments for general condition, degree of myelosuppression, and weight changes.

Because many patients approach chemotherapy with apprehension, allow them to express their concerns, and provide simple, truthful information. Explain that not all patients who undergo chemotherapy experience nausea and vomiting and, for those who do, antiemetic drugs, relaxation therapy, and diet can minimize these problems.

Biotherapy (also known as immunotherapy) utilizes agents called biological response modifiers. Biological agents are usually combined with chemotherapeutic drugs or radiation therapy. Much of the work done in biotherapy is still experimental. However, the Food and
Drug Administration has approved several new drugs, which are providing promising results. For example, rituximab—a monoclonal antibody—is effective for treatment of relapsed or refractory B-cell non-Hodgkin’s lymphoma.

The main biotherapy agent classifications include interferons, interleukins, hematopoietic growth factors, and monoclonal antibodies. Interferons have antiviral, antiproliferative, and immunomodulary effects. The interleukins exert their effects on the T lymphocytes. Monoclonal antibodies such as rituximab provide the most tumor-specific therapy for cancer by selectively binding to tumor cell surfaces.

Although not used to treat cancer directly, hematopoietic growth factors are used to increase the patient’s blood counts when chemotherapy or radiation causes a decrease.

The adverse effects of biotherapeutic agents mimic the body’s normal immune response with flulike symptoms being the most common.

Hormonal therapy is based on studies showing that certain hormones affect the growth of certain cancer types. For example, the gonadotropin-releasing hormone analogue leuprolide is used to treat prostate cancer. With long-term use, this hormone inhibits testosterone release and tumor growth; tamoxifen, an antiestrogen hormonal agent, blocks estrogen receptors in breast tumor cells that require estrogen to thrive. Additionally, tamoxifen can be given prophylactically to women at high risk for breast cancer.

Hormone-receptive tumors may be treated with aromatase inhibitors (anastrozole, exemestane, letrozole, testolactone), which inhibit the conversion of adrenal androgens to estrogens, thereby inhibiting the growth of hormonedependent tumors.

Some adverse effects of these hormonal agents include hot flashes, sweating, impotence, decreased libido, nausea and vomiting, and blood dyscrasias (with tamoxifen).

MAINTAINING NUTRITION AND FLUID BALANCE

Tumors grow at the expense of normal tissue by competing for nutrients; consequently, the cancer patient commonly suffers protein deficiency. Cancer treatments themselves produce fluid and electrolyte disturbances, such as vomiting and anorexia. Maintaining adequate nutrition, fluid intake, and electrolyte balance should be a major focus in cancer care.

Obtain a comprehensive dietary history to pinpoint nutritional problems and their past causes such as diabetes; help plan the diet accordingly.
Ask the dietitian to provide a liquid diet high in proteins, carbohydrates, and calories if the patient can’t tolerate solid foods. If the patient has stomatitis, provide soft, bland, nonirritating foods.
Encourage the patient’s family to bring foods from home, if he requests.
Make mealtime as relaxed and pleasant as possible. Encourage the patient to dine with visitors or other patients. Allow choices from a varied menu.
With the practitioner’s approval, you may suggest that the patient drink a glass of wine before dinner to stimulate the appetite and aid relaxation.
Encourage the patient to drink eight 8-oz (236.6 ml) glasses of noncaffeinated liquids per day. Urge him to drink juice or other caloric beverages instead of water.
Suggest frequent, small meals if he can’t tolerate normal ones.
Avoid strong-smelling foods.

IF THE PATIENT CAN’T EAT

The patient who has had recent head, neck, or GI surgery or who has pain when swallowing can receive nourishment through a nasogastric (NG) tube. If the patient still needs to use the tube after he’s discharged, teach him how to insert it, how to test its position in his stomach by aspirating stomach contents, and how to use it to feed himself.

If an NG tube isn’t appropriate, other alternatives are gastrostomy, jejunostomy and, occasionally, esophagostomy. These procedures make it possible for you to feed the patient prescribed protein formulas and semiliquids, such as cream soups and eggnog; they also make it easier for the patient to feed himself.

Warn the patient that if spilled gastric or intestinal juices come in contact with the abdominal skin, they’ll cause excoriation if they aren’t washed off immediately. Always flush the tube well with water following each feeding.

Also, to provide adequate hydration, instill about 4 to 6 oz (118 to 177.5 ml) of water or another clear liquid between meals.

After jejunostomy, begin with small feedings, slowly and carefully increasing the amounts. Provide additional fluids and calories during these days of limited food intake by supplementing jejunostomy feedings with I.V. fat emulsions.

TOTAL PARENTERAL NUTRITION

Commonly considered an important component of cancer care if the patient can’t tolerate enteral nutrition, total parenteral nutrition (TPN) can improve a severely debilitated patient’s protein balance. In doing so, TPN characteristically strengthens and conditions the patient, allowing him to better tolerate treatment.

TPN can produce a slight weight gain in the patient receiving radiation therapy, provide optimum nutrition for wound healing, and help the patient combat infection after radical surgery.

PAIN CONTROL

Typically, cancer patients have a great fear of pain. Therefore, pain control is critical at every stage of managing cancer—from localized cancer to advanced metastasis. In cancer patients, pain may result from inflammation of or pressure on pain-sensitive structures, tumor infiltration of nerves or blood vessels, or metastatic extension to bone. Chronic and unrelenting pain can wear down the patient’s tolerance to treatment, interfere with eating and sleeping, and cause anger, despair, and anxiety.

Opioid analgesics—either alone or in combination with nonopioid analgesics, antianxiety agents, or tricyclic antidepressants—are the mainstay of pain relief in patients with advanced cancer. In terminal stages of cancer, effective opioid dosages may be quite high because drug tolerance invariably develops. Provide such analgesics generously. Anticipate the need for pain relief, and provide it on a schedule that doesn’t allow pain to break through. Don’t wait to relieve pain until it becomes severe. Reassure the patient that you’ll provide pain medication whenever he needs it. (See Patientcontrolled analgesia system.)

Nonpharmacologic pain-relief techniques can be used alone or, more commonly, in combination with drug therapy. Popular techniques include cutaneous stimulation, relaxation, biofeedback, distraction, and guided imagery.

Surgical excision of the tumor can relieve pressure on sensitive tissues and pain caused by inflamed necrotic tissue; treatment with antibiotics can combat inflammation; radiation therapy can shrink metastatic tissue and control bone pain. When a tumor invades nerve tissue, effective pain control requires anesthetics, destructive nerve blocks, electronic nerve stimulation with a dorsal column or transcutaneous electrical nerve stimulator, rhizotomy, or chordotomy.

THE HOSPICE APPROACH

A holistic approach to patient care modeled after St. Christopher’s Hospice in London, hospice care provides comprehensive physical, psychological, social, and spiritual care for terminally ill patients. Although some hospices are located in inpatient settings, most hospice programs serve terminally ill patients in the more familiar and relaxed surroundings of their own home.

The goal of the hospice care team is to help the patient achieve as full a life as possible, with minimal pain, discomfort, and restriction. Of the many medications provided for pain control, morphine is considered the drug of choice.

Hospice care also emphasizes a coordinated team effort to help the patient and family members overcome the severe anxiety, fear, and depression that occur with terminal illness. To that end, hospice staffs encourage family members to help with the patient’s care, thereby providing the patient with warmth and security and helping the family caregivers begin the grieving process before the patient dies.

Everyone involved in this method of care must be committed to high-quality patient care, unafraid of emotional involvement, and comfortable with personal feelings about death and dying. Good hospice care also requires open communication among team members, not just for evaluating patient care, but also for helping the staff cope with their own feelings.

PSYCHOLOGICAL ASPECTS

The diagnosis of cancer evokes a profound emotional response, which patients express in different ways. Some face this difficult reality from the outset of diagnosis and treatment. Many use denial as a coping mechanism and simply refuse to accept the truth, but this stance becomes increasingly difficult for them to maintain. As evidence of the tumor becomes inescapable, the patient may develop clinical depression. Family members may express denial in attempts to cope by encouraging unproven methods of cancer treatment, which can delay effective care. Some patients cope by intellectualizing about their disease, enabling them to obscure the reality of the cancer and regard it as unrelated to themselves. Generally, intellectualization is a more productive coping behavior than denial because the patient is receiving treatment. Be aware of the possible behavioral responses so you can identify them and then interact supportively with the patient and his family. For many malignancies, you can offer realistic hope for long-term survival or
remission; even in advanced disease, you can offer short-term achievable goals. To help a patient cope with cancer, make sure you understand your own feelings about it. Then listen sensitively to the patient so you can offer genuine understanding and support. When caring for a patient with terminal cancer, increase your effectiveness by seeking out someone to help you through your own grieving.

Patient-controlled analgesia system

The patient-controlled analgesia (PCA) system is an option for pain treatment in cancer care. It’s typically used in the postoperative clinical setting, where I.V. pain management is needed for acute intervention, and is also used in non-surgical cancer patients to control severe pain. This system permits the patient to selfadminister a premeasured dose of analgesic by pressing a button at the bedside that activates a pump fitted with a prefilled syringe containing the analgesic. Small, intermittent doses of the analgesic administered I.V. maintain blood levels that ensure comfort and minimize the risk of oversedation. The practitioner or the nursing staff presets doses and time intervals (usually 8 to 10 minutes) that allow the patient to determine his comfort level. The syringe is locked inside the pump as a safety feature, and the system will only dispense the analgesic when the correct (preset) time interval has elapsed.

Clinical studies report that patients on PCA tend to titrate analgesic drugs effectively and maintain comfort without oversedation. They also tend to use less of the drug than the amount normally given by I.M. injection.

PCA provides other significant advantages:

Patients are alert and active during the day.
Patients no longer need to suffer pain while awaiting their injections.
Patients are free from pain caused by injections.
The nursing staff is free for other clinical duties.

HEAD, NECK, AND SPINE

Malignant brain tumors

Primary malignant brain tumors account for about 10% to 30% of adult cancers. These tumors may occur at any age. The most common tumor types in adults are gliomas and meningiomas, which usually occur supratentorially (above the covering of the cerebellum). In children, incidence is generally highest before age 12, affecting 3 out of every 100,000 children; more than 1,200 new cases occur each year. The most common types in children are astrocytomas, medulloblastomas, ependymomas, and brain stem gliomas. In children, brain tumors of the central nervous system (CNS) account for 20% of all childhood cancers; they’re similar in incidence to leukemias.

CAUSES AND INCIDENCE

The cause of most brain tumors is unknown, but exposure to ionizing radiation is a known environmental risk. Additionally, most malignant tumors of the brain are of metastatic origin; 20% to 40% of patients with nonbrain primary cancer develop brain metastasis. (See Comparing brain tumors, pages 714 and 715.)

SIGNS AND SYMPTOMS

Brain tumors cause CNS changes by invading and destroying tissues and by secondary effect—mainly compression of the brain, cranial nerves, and cerebral vessels; cerebral edema; and increased intracranial pressure (ICP). Generally, clinical features result from increased ICP; these features vary with the type of tumor, its location, and the degree of invasion. (See What happens in increased ICP, page 716.) Onset of symptoms is usually insidious, and brain tumors are commonly misdiagnosed.

DIAGNOSIS

Comparing brain tumors

Tumor

Clinical features

Astrocytoma

▪ Second most common malignant glioma (about 10% of all gliomas)

▪ Occurs at any age; incidence higher in males

▪ Usually occurs in white matter of cerebral hemispheres; may originate in any part of the central nervous system

▪ Cerebellar astrocytomas usually confined to one hemisphere

General

▪ Headache; mental activity changes

▪ Decreased motor strength and coordination

▪ Seizures; scanning speech

▪ Altered vital signs

Localizing

▪ Third ventricle: changes in mental activity and level of consciousness, nausea, pupillary dilation and sluggish light reflex; later—paresis or ataxia

▪ Brain stem and pons: early—ipsilateral trigeminal, abducens, and facial nerve palsies; later—cerebellar ataxia, tremors, other cranial nerve deficits

▪ Third or fourth ventricle or aqueduct of Sylvius: secondary hydrocephalus

▪ Thalamus or hypothalamus: various endocrine, metabolic, autonomic, and behavioral changes

Ependymoma

▪ Rare glioma

▪ Most common in children and young adults

▪ Usually locates in fourth and lateral ventricles

General

▪ Similar to oligodendroglioma

▪ Increased intracranial pressure (ICP) and obstructive hydrocephalus, depending on tumor size

Glioblastoma multiforme (spongioblastoma multiforme)

▪ Peak incidence at 50 to 60 years; twice as common in males; most common glioma (accounts for 60% of all gliomas)

▪ Unencapsulated, highly malignant; grows rapidly and infiltrates the brain extensively; may become enormous before diagnosed

▪ Usually occurs in cerebral hemispheres, especially frontal and temporal lobes (rarely in brain stem and cerebellum)

▪ Occupies more than one lobe of affected hemisphere; may spread to opposite hemisphere by corpus callosum; may metastasize into cerebrospinal fluid (CSF), producing tumors in distant parts of the nervous system

General

▪ Increased ICP (nausea, vomiting, headache, papilledema)

▪ Mental and behavioral changes

▪ Altered vital signs (increased systolic pressure, widened pulse pressure, respiratory changes)

▪ Speech and sensory disturbances

▪ In children, irritability, projectile vomiting

Localizing

▪ Midline: headache (bifrontal or bioccipital); worse in the morning; intensified by coughing, straining, or sudden head movements

▪ Temporal lobe: psychomotor seizures

▪ Central region: focal seizures

▪ Optic and oculomotor nerves: visual defects

▪ Frontal lobe: abnormal reflexes, motor responses

Medulloblastoma

▪ Rare glioma

▪ Incidence highest in children ages 4 to 6

▪ Affects males more commonly than females

▪ Commonly metastasizes via CSF

General

▪ Increased ICP Localizing

▪ Brain stem and cerebrum: papilledema, nystagmus, hearing loss, flashing lights, dizziness, ataxia, paresthesia of face, cranial nerve palsies (V, VI, VII, IX, X, primarily sensory), hemiparesis, suboccipital tenderness; compression of supratentorial area produces other general and focal signs and symptoms

Meningioma

▪ Most common nongliomatous brain tumor (15% of primary brain tumors)

▪ Peak incidence among 50-year-olds; rare in children; more common in females (ratio 3:2)

▪ Arises from the meninges

▪ Common locations include parasagittal area, sphenoidal ridge, anterior part of the base of the skull, cerebellopontine angle, spinal canal

▪ Benign, well-circumscribed, highly vascular tumors that compress underlying brain tissue by invading overlying skull

General

▪ Headache

▪ Seizures (in two thirds of patients)

▪ Vomiting

▪ Changes in mental activity

▪ Similar to schwannomas Localizing

▪ Skull changes (bony bulge) over tumor

▪ Sphenoidal ridge, indenting optic nerve: unilateral visual changes and papilledema

▪ Prefrontal parasagittal: personality and behavioral changes

▪ Motor cortex: contralateral motor changes

▪ Anterior fossa compressing both optic nerves and frontal lobes: headaches and bilateral vision loss

▪ Pressure on cranial nerves causing varying symptoms

Oligodendroglioma

▪ Third most common glioma (accounts for less than 5% of all gliomas)

▪ Occurs in middle adult years; more common in women

▪ Slow-growing

General

▪ Mental and behavioral changes

▪ Decreased visual acuity and other vision disturbances

▪ Increased ICP Localizing

▪ Temporal lobe: hallucinations, psychomotor seizures

▪ Central region: seizures (confined to one muscle group or unilateral)

▪ Midbrain or third ventricle: pyramidal tract symptoms (dizziness, ataxia, paresthesia of the face)

▪ Brain stem and cerebrum: nystagmus, hearing loss, dizziness, ataxia, paresthesia of the face, cranial nerve palsies, hemiparesis, suboccipital tenderness, loss of balance

Schwannoma (acoustic neurinoma, neurilemoma, cerebellopontine angle tumor)

▪ Accounts for about 10% of all intracranial tumors

▪ Higher incidence in women

▪ Onset of symptoms between ages 30 and 60

▪ Affects the craniospinal nerve sheath, usually cranial nerve (CN) VIII; also, CN V and VII and, to a lesser extent, CN VI and X on the same side as the tumor

▪ Benign, but commonly classified as malignant because of its growth patterns; slow-growing—may be present for years before symptoms occur

General

▪ Unilateral hearing loss with or without tinnitus

▪ Stiff neck and suboccipital discomfort

▪ Secondary hydrocephalus

▪ Ataxia and uncoordinated movements of one or both arms due to pressure on brain stem and cerebellum

Localizing

▪ CN V: early—facial hypoesthesia or paresthesia on side of hearing loss; unilateral loss of corneal reflex

▪ CN VI: diplopia or double vision

▪ CN VII: paresis progressing to paralysis (Bell’s palsy)

▪ CN X: weakness of palate, tongue, and nerve muscles on same side as tumor

Other diagnostic tools include a patient history, a neurologic assessment, skull X-rays, a brain scan, a CT scan, MRI, and cerebral angiography. An EEG may reveal focal abnormalities. Lumbar puncture shows increased pressure and protein levels, decreased glucose levels and, occasionally, tumor cells in cerebrospinal fluid (CSF).

PATHOPHYSIOLOGY What happens in increased ICP

Intracranial pressure (ICP) is the force exerted within the intact skull by intracranial volume: about 10% blood, 10% cerebrospinal fluid (CSF), and 80% brain tissue and water. The rigid skull allows little space for expansion of these substances. When ICP increases dramatically, brain damage can result.

The brain compensates for increases by regulating the volume of the three substances by limiting blood flow to the head, displacing CSF into the spinal canal, and increasing absorption or decreasing production of CSF. When compensatory mechanisms become overworked, small changes in volume lead to large changes in pressure.

TREATMENT

Treatment includes surgical excision of a resectable tumor; surgical reduction of a nonresectable tumor; relief of cerebral edema, decrease of ICP, and other symptoms; and prevention of further neurologic damage.

The mode of therapy depends on the tumor’s histologic type, radiosensitivity, and location and may include surgery, radiation, chemotherapy, or decompression of increased ICP with diuretics, corticosteroids, or possibly ventriculoatrial or ventriculoperitoneal shunting of CSF.

A glioma usually requires resection by craniotomy, followed by radiation therapy and chemotherapy. The combination of nitrosoureas (carmustine [BCNU], lomustine [CCNU], or procarbazine), or methylating agents such as temozolomide, and postoperative radiation is more effective than radiation alone. Concurrent temozolomide and radiation therapy daily for 6 weeks has been shown to substantially improve survival.

Surgical resection of low-grade cystic cerebellar astrocytomas brings long-term survival. Treatment of other astrocytomas includes repeated surgery, radiation therapy, and shunting of fluid from obstructed CSF pathways. Some astrocytomas are highly radiosensitive, but others are radioresistant.

Treatment of oligodendrogliomas and ependymomas includes resection and radiation therapy; for medulloblastomas, resection and possibly intrathecal infusion of methotrexate or another antineoplastic drug. Meningiomas require resection, including dura mater and bone (operative mortality may reach 10% because of large tumor size).

For schwannomas, microsurgical technique allows complete resection of the tumor and preservation of facial nerves. Although schwannomas are moderately radioresistant, postoperative radiation therapy is necessary.

The breakdown of the blood-brain barrier allows chemotherapeutic drugs to penetrate the cerebrum. Intrathecal and intra-arterial administration of drugs maximizes drug actions.

Palliative measures for gliomas, astrocytomas, oligodendrogliomas, and ependymomas include dexamethasone for cerebral edema; osmotic diuretics, such as urea and mannitol, to reduce brain swelling; analgesics to control pain; and antacids and histamine receptor antagonists for stress ulcers. These tumors and schwannomas may also require anticonvulsants such as phenytoin to prevent or control seizures.

SPECIAL CONSIDERATIONS

A patient with a brain tumor requires comprehensive neurologic assessment, teaching, and supportive care. During your first contact with the patient, perform a comprehensive assessment (including a complete neurologic evaluation) to provide baseline data and to help develop your care plan. Obtain a thorough health history concerning onset of symptoms. Help the patient and his family cope with the treatment, potential disabilities, and changes in lifestyle resulting from his tumor. Throughout hospitalization:

Carefully document seizure activity (occurrence, nature, and duration).
Maintain airway patency.
Monitor patient safety.
Administer anticonvulsive drugs as ordered. Encourage the patient to wear a medical identification bracelet or necklace that identifies his risk for seizures.
Check continuously for changes in neurologic status, and watch for an increase in ICP.

Monitor temperature carefully. Fever commonly follows hypothalamic anoxia but might also indicate meningitis. Use hypothermia blankets preoperatively and postoperatively to keep the patient’s temperature down and minimize cerebral metabolic demands.
Administer steroids and osmotic diuretics such as mannitol as ordered to reduce cerebral edema. Fluids may be restricted to 1,500 ml/24 hours. Monitor fluid and electrolyte balance to avoid dehydration.
Observe and report signs and symptoms of stress ulcers: abdominal distention, pain, vomiting, and tarry stools. Administer antacids as ordered.

Surgery requires additional nursing care. After craniotomy, continue to monitor general neurologic status and watch for signs of increased ICP, such as an elevated bone flap and typical neurologic changes. To reduce the risk of increased ICP, restrict fluids to
1,500 ml/24 hours. To promote venous drainage and reduce cerebral edema after supratentorial craniotomy, elevate the head of the patient’s bed about 30 degrees. Position him on his side to allow drainage of secretions and prevent aspiration. As appropriate, instruct the patient to avoid Valsalva’s maneuver or isometric muscle contractions when moving or sitting up in bed; these can increase intra-thoracic pressure and thereby increase ICP. Withhold oral fluids, which may provoke vomiting and consequently raise ICP.

After infratentorial craniotomy, keep the patient flat for 48 hours, but logroll him every 2 hours to minimize complications of immobilization. Prevent other complications by paying careful attention to ventilatory status and to cardiovascular, GI, and musculoskeletal functions.

Radiation therapy is usually delayed until after the surgical wound heals, but it can induce wound breakdown even then, so observe the wound carefully for infection and sinus formation. Because radiation may cause brain inflammation, watch for signs of rising ICP.
Because chemotherapy—BCNU, CCNU, procarbazine, and temozolomide—used as adjuncts to radiotherapy and surgery can cause delayed bone marrow depression, tell the patient to watch for and immediately report any signs of infection or bleeding that appear within 4 weeks after the start of chemotherapy. Before chemotherapy, give ondansetron or another antiemetic, as ordered, to minimize nausea and vomiting.
Teach the patient and his family signs of recurrence; urge compliance with treatment regimen.
Because brain tumors may cause residual neurologic deficits that disable the patient physically or mentally, begin rehabilitation early. Changes in cognitive function may also be observed and affect daily functional activities. Consult with occupational and physical therapists to encourage independence in daily activities and improve the quality of life. As necessary, provide aids for self-care and mobilization, such as bathroom rails for the wheelchair patient. If the patient is aphasic, arrange for consultation with a speech pathologist.
Legal advice is helpful in forming advance directives such as power of attorney in cases where continued physical or intellectual decline is likely.
Refer the patient for counseling and to national and local support groups to help him cope with this disorder.

Pituitary tumors

Pituitary tumors, which constitute 10% of intracranial malignant neoplasms, usually originate in the anterior pituitary (adenohypophysis). They occur in adults of both sexes, usually during the 3rd and 4th decades of life. The three tissue types of pituitary tumors are chromophobe adenoma (90%), basophil adenoma, and eosinophil adenoma.

The prognosis for patients depends on the extent to which the tumor spreads beyond the sella turcica.

CAUSES AND INCIDENCE

Although the exact cause is unknown, a predisposition to pituitary tumors may be inherited through an autosomal dominant trait. Pituitary tumors aren’t malignant in the strict sense but, because their growth is invasive, they’re considered a neoplastic disease.

Chromophobe adenoma may be associated with production of corticotropin, melanocytestimulating hormone, growth hormone (GH), and prolactin; basophil adenoma, with evidence of excess corticotropin production and, consequently, with signs of Cushing’s syndrome; eosinophil adenoma, with excessive GH.

Pituitary tumors develop in 1 in 10,000 people. About 15% of tumors located within the skull are pituitary tumors.

SIGNS AND SYMPTOMS

As pituitary adenomas grow, they replace normal glandular tissue and enlarge the sella turcica, which houses the pituitary gland. The resulting pressure on adjacent intracranial structures produces these typical clinical manifestations:

Neurologic:

frontal headache
visual symptoms, beginning with blurring and progressing to field cuts (hemianopsias) and then unilateral blindness
cranial nerve (III, IV, VI) involvement from lateral extension of the tumor, resulting in strabismus; double vision, with compensating head tilting and dizziness; conjugate deviation of gaze; nystagmus; lid ptosis; and limited eye movements
increased intracranial pressure (ICP) (secondary hydrocephalus)
personality changes or dementia, if the tumor breaks through to the frontal lobes
seizures
rhinorrhea, if the tumor erodes the base of the skull
pituitary apoplexy secondary to hemorrhagic infarction of the adenoma. Such hemorrhage may lead to both cardiovascular and adrenocortical collapse

Endocrine:

hypopituitarism, to some degree, in all patients with adenoma, becoming more obvious as the tumor replaces normal gland tissue (signs and symptoms include amenorrhea, decreased libido and impotence in men, skin changes [waxy appearance, decreased wrinkles, and pigmentation], loss of axillary and pubic hair, lethargy, weakness, increased fatigability, intolerance to cold, and constipation [because of decreased production of corticotropin and thyroid-stimulating hormone])
addisonian crisis, precipitated by stress and resulting in nausea, vomiting, hypoglycemia, hypotension, and circulatory collapse
diabetes insipidus, resulting from extension to the hypothalamus
prolactin-secreting adenomas (in 70% to 75%), with amenorrhea and galactorrhea
GH-secreting adenomas, with acromegaly
corticotropin-secreting adenomas, with Cushing’s syndrome

DIAGNOSIS

Skull X-rays with tomography show enlargement of the sella turcica or erosion of its floor; if GH secretion predominates, X-rays show enlarged paranasal sinuses and mandible, thickened cranial bones, and separated teeth.
Carotid angiogram shows displacement of the anterior cerebral and internal carotid arteries if the tumor mass is enlarging; it also rules out intracerebral aneurysm
Computed tomography scan may confirm the existence of the adenoma and accurately depict its size.
Cerebrospinal fluid (CSF) analysis may show increased protein levels.
Endocrine function tests may contribute helpful information, but results are commonly ambiguous and inconclusive.
Magnetic resonance imaging (MRI) differentiates healthy, benign, and malignant tissues as well as arteries and veins. MRI is an excellent modality for viewing the pituitary. (See MRI of the pituitary.)

TREATMENT

Surgical options include transfrontal removal of large tumors impinging on the optic apparatus and transsphenoidal resection for smaller tumors confined to the pituitary fossa.

Radiation is the primary treatment for small, nonsecretory tumors that don’t extend beyond the sella turcica or for patients who may be poor postoperative risks; otherwise, it’s an adjunct to surgery.

Postoperative treatment includes hormone replacement with cortisone, thyroid, and sex hormones; correction of electrolyte imbalance; and, as necessary, insulin therapy.

Drug therapy may include bromocriptine, an ergot derivative that shrinks prolactin- and GH-secreting tumors. Cyproheptadine, an antisero-tonin drug, can reduce increased corticosteroid levels in the patient with Cushing’s syndrome.

Adjuvant radiation therapy is used when only partial removal of the tumor is possible. Cryohy-pophysectomy (freezing the area with a probe inserted by transsphenoidal route) is a promising alternative to surgical dissection of the tumor.

SPECIAL CONSIDERATIONS

Conduct a comprehensive health history and physical assessment to establish the onset of neurologic and endocrine dysfunction and provide baseline data for later comparison.
Establish a supportive, trusting relationship with the patient and his family to assist them in coping with the diagnosis, treatment, and potential long-term changes. Make sure they understand that the patient needs lifelong evaluations and, possibly, hormone replacement.
Reassure the patient that some of the distressing physical and behavioral signs and
symptoms caused by pituitary dysfunction (for example, altered sexual drive, impotence, infertility, loss of hair, and emotional instability) will disappear with treatment.
Maintain a safe, clutter-free environment for the visually impaired or acromegalic patient. Re assure him that he’ll probably recover his sight.

Prevent vomiting, which increases ICP. Don’t allow a patient who has had transsphenoidal surgery to blow his nose. Watch for CSF drainage from the nose. Monitor for signs of infection from the contaminated upper respiratory tract. Make sure the patient understands that he’ll lose his sense of smell.
Regularly compare the patient’s postoperative neurologic status with your baseline assessment. (See Postcraniotomy care.)
Monitor intake and output to detect fluid and electrolyte imbalances.
Before discharge, encourage the patient to wear a medical identification bracelet or necklace that identifies his hormone deficiencies and their proper treatment.

Postcraniotomy care

Monitor vital signs (especially level of consciousness), and perform a baseline neurologic assessment from which to plan further care and assess the patient’s progress.
Maintain the patient’s airway; suction as necessary.
Monitor intake and output carefully.
Prevent aspiration and vomiting, which increases intracranial pressure.
Observe for cerebral edema, bleeding, and leakage of cerebrospinal fluid.
Provide a restful, quiet environment.
Monitor for postoperative pain or headache

Laryngeal cancer

The most common form of laryngeal cancer is squamous cell cancer (95%); rare forms include adenocarcinoma, sarcoma, and others. Such cancer may be intrinsic or extrinsic. An intrinsic tumor is on the true vocal cord and doesn’t tend to spread because underlying connective tissues lack lymph nodes. An extrinsic tumor is on some other part of the larynx and tends to spread early.

CAUSES AND INCIDENCE

In laryngeal cancer, major predisposing factors include smoking and alcoholism; minor factors include chronic inhalation of noxious fumes and familial tendency. Cancer of the larynx rarely occurs in nonsmokers.

Laryngeal cancer is classified according to its location:

supraglottis (false vocal cords)
glottis (true vocal cords)
subglottis (downward extension from vocal cords [rare])

The ratio of male to female incidence is 10:1. Most victims are between ages 50 and 65. The five-year survival rate is 65%.

SIGNS AND SYMPTOMS

In intrinsic laryngeal cancer, the dominant and earliest symptom is hoarseness that persists longer than 3 weeks; in extrinsic cancer, it’s a lump in the throat or pain or burning in the throat when drinking citrus juice or hot liquid. Later clinical effects of metastasis include dysphagia, dyspnea, cough, enlarged cervical lymph nodes, and pain radiating to the ear.

TREATMENT

Early lesions are treated with surgery or radiation; advanced lesions with surgery, radiation, and chemotherapy. In early stages, laser surgery can excise precancerous lesions; in advanced stages it can help relieve obstruction caused by tumor growth. Surgical procedures vary with
tumor size and can include cordectomy, partial or total laryngectomy, supraglottic laryngectomy, or total laryngectomy with laryngoplasty. Primary systemic therapy may be administered concurrently with radiation. Principal agents include cisplatin, fluorouracil, carboplatin, and the taxanes. The goal is to eliminate the cancer and preserve speech. If speech preservation isn’t possible, speech rehabilitation may include esophageal speech or prosthetic devices; surgical techniques to construct a new voice box are still experimental.

SPECIAL CONSIDERATIONS

Provide psychological support and good preoperative and postoperative care to minimize complications and speed recovery.

Before partial or total laryngectomy:

Instruct the patient to maintain good oral hygiene. If appropriate, instruct a male patient to shave off his beard.
Encourage the patient to express his concerns before surgery. Help him choose a temporary nonspeaking communication method (such as writing).
If appropriate, arrange for a laryngectomee to visit the patient. Explain postoperative procedures (suctioning, nasogastric [NG] feeding, laryngectomy tube care) and their results (breathing through neck, speech alteration). Also prepare him for other functional losses: He won’t be able to smell, blow his nose, whistle, gargle, sip, or suck on a straw.

After partial laryngectomy:

Give I.V. fluids and, usually, tube feedings in the initial postoperative period; then resume oral fluids. Keep the tracheostomy tube (inserted during surgery) in place until edema subsides.
Keep the patient from using his voice until he has medical permission (usually 2 to 3 days postoperatively). Then caution him to whisper until healing is complete.

After total laryngectomy:

As soon as the patient returns to his bed, place him on his side and elevate his head 30 to 45 degrees. When you move him, remember to support his neck.
The patient will probably have a laryngectomy tube in place until his stoma heals (about 7 to 10 days). This tube is shorter and thicker than a tracheostomy tube but requires the same care. Watch for crusting and secretions around the stoma, which can cause skin breakdown. To prevent crust formation, provide adequate room humidification. Remove crusting with petroleum jelly, antimicrobial ointment, and moist gauze.
Teach stoma care.
Watch for and report complications: fistula formation (redness, swelling, secretions on suture line), carotid artery rupture (bleeding), and tracheostomy stenosis (constant shortness of breath). A fistula may form between the reconstructed hypopharynx and the skin. This eventually heals spontaneously but may take weeks or months. Carotid artery rupture usually occurs in patients who have had preoperative radiation, particularly those with a fistula that constantly bathes the carotid artery with oral secretions.

Tracheostomy stenosis occurs weeks to months after laryngectomy; treatment includes fitting the patient with successively larger tracheostomy tubes until he can tolerate insertion of a large one. If the patient has a fistula, feed him through an NG tube; otherwise, food will leak through the fistula and delay healing. Monitor vital signs (be especially alert for fever, which indicates infection). Record fluid intake and output, and watch for dehydration.
Give frequent mouth care.
Suction gently, unless ordered otherwise. Don’t attempt deep suctioning, which could penetrate the suture line. Suction through both the tube and the patient’s nose because the patient can no longer blow air through his nose; suction his mouth gently.
After insertion of a drainage catheter (usually connected to a wound-drainage system or a GI drainage system), don’t stop suction without the practitioner’s consent. After catheter removal, check dressings for drainage.
Give analgesics as ordered.
If the patient has an NG feeding tube, check tube placement and elevate the patient’s head to prevent aspiration.
Reassure the patient that speech rehabilitation may help him speak again. Encourage contact with the International Association of Laryngectomees and other sources of support.
Support the patient through the grieving process. If the depression seems severe, consider a psychiatric referral.

Thyroid cancer

Papillary and follicular carcinomas are the most common types of thyroid cancer and are usually associated with a longer survival. Papillary carcinoma accounts for half of all thyroid cancers in adults; it’s most common in young
adult females and metastasizes slowly. It’s the least virulent form of thyroid cancer. Follicular carcinoma is less common but more likely to recur and metastasize to the regional nodes and through blood vessels into the bones, liver, and lungs. Medullary carcinoma originates in the parafollicular cells derived from the last branchial pouch and contains amyloid and calcium deposits. It can produce calcitonin, histaminase, corticotropin (producing Cushing’s syndrome), and prostaglandin E₂ and F₃ (producing diarrhea). Of the three types of medullary carcinoma, sporadic is the most common and isn’t inherited. Multiple endocrine neoplasia, type II (MEN2) is familial; it’s associated with pheo-chromocytoma and parathyroid gland tumors
and is completely curable when detected before it causes symptoms. Untreated, it progresses rapidly. Seldom curable by resection, anaplastic tumors resist radiation and metastasize rapidly. The familial type of medullary cancer is also inherited but only affects the thyroid gland. Thyroid lymphoma begins in the lymphocytes and can move to the thyroid gland.

CAUSES AND INCIDENCE

Predisposing factors to thyroid cancer include radiation exposure (especially childhood radiation therapy), prolonged thyroid-stimulating hormone (TSH) stimulation (through radiation or heredity), familial predisposition, or chronic goiter.

Thyroid cancer occurs in all age-groups with peak ages of 45 to 49 years in women and 65 to 69 years in men. It is more common in people who have had radiation treatment of the neck area. Thyroid nodules are four times more common in women with thyroid carcinomas, occurring two to three times more often in women than in men.

SIGNS AND SYMPTOMS

The primary sign of thyroid cancer is a painless nodule, a hard nodule in an enlarged thyroid gland, or palpable lymph nodes with thyroid enlargement. (See Early, localized thyroid cancer.) Eventually, the pressure of such a nodule or enlargement causes hoarseness, dysphagia, dyspnea, and pain on palpation. If the tumor is large enough to destroy the gland, hypothyroidism follows, with its typical symptoms of low metabolism (mental apathy and sensitivity to cold). However, if the tumor stimulates excess thyroid hormone production, it induces symptoms of hyperthyroidism (sensitivity to heat, restlessness, and hyperactivity). Other clinical features include diarrhea, anorexia, irritability, vocal cord paralysis, and symptoms of distant metastasis.

DIAGNOSIS

The first clue to thyroid cancer is usually an enlarged, palpable node in the thyroid gland, neck, lymph nodes of the neck, or vocal cords. A patient history of radiation therapy or a family history of thyroid cancer supports the diagnosis. However, tests must rule out nonmalignant thyroid enlargements, which are much more common. Thyroid scan differentiates between functional nodes (rarely malignant) and hypofunctional nodes (commonly malignant) by measuring how readily nodules trap isotopes compared with the rest of the thyroid gland. In thyroid cancer, the scintiscan shows a “cold,” nonfunctioning nodule. Other tests include needle biopsy, computed tomography scan, ultrasonic scan, chest X-ray, serum alkaline phosphatase, and serum calcitonin assay to diagnose medullary cancer. Calcitonin assay is a reliable clue to silent medullary carcinoma.

TREATMENT

Total or subtotal thyroidectomy, with modified node dissection (bilateral or unilateral) on the side of the primary cancer (papillary or follicular cancer)
Total thyroidectomy and radical neck excision (for medullary, giant, or spindle cell cancer)
Radiation (¹³¹I) with external radiation (for inoperable cancer and sometimes postoperatively in lieu of radical neck excision) or alone (for metastasis)
Adjunctive thyroid suppression, with exogenous thyroid hormones suppressing TSH production, and simultaneous administration of an adrenergic blocking agent such as propranolol, increasing tolerance to surgery and radiation
Chemotherapy for symptom-producing, widespread metastasis is limited, but doxorubicin is sometimes beneficial

SPECIAL CONSIDERATIONS

Before surgery, tell the patient to expect temporary voice loss or hoarseness lasting several days after surgery.

Plan meticulous postoperative care:

When the patient regains consciousness, keep him in semi-Fowler’s position, with his head nei ther hyperextended nor flexed, to avoid pressure on the suture line. Support his head and neck with sandbags and pillows; when you move him, continue this support with your hands.

Check serum calcium levels daily; hypocal cemia may develop if parathyroid glands are re moved. Watch for and report other complications: hemorrhage and shock (elevated pulse rate and hypotension), tetany (carpopedal spasm, twitch ing, and seizures), thyroid storm (high fever,
severe tachycardia, delirium, dehydration, and extreme irritability), and respiratory obstruction (dyspnea, crowing respirations, and retraction of neck tissues). (See What happens in thyroid storm.)
Keep a tracheotomy set, suction, and oxygen equipment handy in case of respiratory obstruction. Use continuous steam inhalation in the patient’s room until his chest is clear.
The patient may need I.V. fluids or a soft diet, but many patients can tolerate a regular diet within 24 hours of surgery.

PATHOPHYSIOLOGY What happens in thyroid storm

Normally, the hypothalamus stimulates the release of thyrotropinreleasing hormone (TRH), which causes the anterior pituitary gland to release thyroid-stimulating hormone (TSH). The thyroid gland then secretes triiodothyronine (T₃) and thyroxine (T₄).

In thyroid storm, however, the thyroid overproduces T₃ and T₄, and systemic adrenergic activity increases. This causes epinephrine overproduction and severe hypermetabolism, leading rapidly to GI, cardiovascular, and sympathetic nervous system decompensation.

Care of the patient after extensive tumor and node excision is identical to other postoperative care after radical neck surgery. Referral to a local or national support group can help relieve the patient’s stress. (See Preventing thyroid cancer.)

Malignant spinal neoplasms

Malignant spinal neoplasms may be any one of many tumor types similar to intracranial tumors; they involve the cord or its roots and, if untreated, can eventually cause paralysis. As primary tumors, they originate in the meningeal coverings, the parenchyma of the cord or its roots, the intraspinal vasculature, or the vertebrae. Primary spinal cord tumors represent 2% to 4% of all primary tumors of the central nervous system. They can also occur as metastatic foci from primary tumors.

CAUSES AND INCIDENCE

Primary tumors of the spinal cord may be extramedullary (occurring outside the spinal cord) or intramedullary (occurring within the cord itself). Extramedullary tumors may be intradural (meningiomas and schwannomas), which account for 70% to 80% of all primary malignant spinal cord neoplasms, or extradural (metastatic tumors from breasts, lungs, prostate, leukemia, or lymphomas), which account for 25% of these malignant neoplasms.

Intramedullary tumors, or gliomas (astrocytomas or ependymomas), are comparatively
rare, accounting for only about 10%. In children, they’re low-grade astrocytomas.

PREVENTION Preventing thyroid cancer

Teach your patient about the following measures that may help decrease thyroid cancer risk:

Proper nutrition

To reduce the risk of not only thyroid cancer, but most types of cancer, encourage your patient to eat lots of fruits and vegetables and to eat less animal fat.

Surgery

For patients who have an inherited gene, preventive surgery may alleviate the risk of thyroid cancer; however, it will not reduce the risk of tumors affecting the adrenal or parathyroid gland.

Radioactive iodine

The federal government recommends that people living within 10 miles of a nuclear power plant be provided potassium iodide tablets. These tablets can be taken before or right after exposure to nuclear fallout. They provide protection to the thyroid gland from iodine^-131. Exposure to this type of radiation is especially a risk for children, and these tablets are safe for them to take. Those who have Graves’ disease, autoimmune thyroiditis, or a goiter shouldn’t take potassium iodide tablets.

Spinal cord tumors are rare compared with intracranial tumors (ratio of 1:4). They occur equally in men and women, with the exception of meningiomas, which occur mostly in women. Spinal cord tumors can occur anywhere along the length of the cord or its roots.

SIGNS AND SYMPTOMS

Extramedullary tumors produce symptoms by pressing on nerve roots, the spinal cord, and spinal vessels; intramedullary tumors, by destroying the parenchyma and compressing adjacent areas. Because intramedullary tumors may extend over several spinal cord segments, their symptoms are more variable than those of extramedullary tumors.

The following clinical effects are likely with all malignant spinal cord neoplasms:

Pain—Most severe directly over the tumor, radiates around the trunk or down the limb on the affected side and is unrelieved by bed rest. It may worsen when lying down or with straining, coughing, or sneezing. Pain can be diffuse, occurring over all extremities. Generally, it progressively worsens and isn’t relieved by medication.
Motor symptoms—Asymmetric spastic muscle weakness, decreased muscle tone, exaggerated reflexes, and a positive Babinski’s sign. If the tumor is at the level of the cauda equina, muscle flaccidity, muscle wasting, weakness, and progressive diminution in tendon reflexes are characteristic.
Sensory deficits—Contralateral loss of pain, temperature, and touch sensation (Brown-Séquard’s syndrome). These losses are less obvious to the patient than functional motor changes. Caudal lesions invariably produce paresthesia in the nerve distribution pathway of the involved roots.
Bowel and bladder symptoms—Urine retention is an inevitable late sign with cord compression. Early signs include incomplete emptying or difficulty with the urine stream, which is usually unnoticed or ignored. Cauda equina tumors cause bladder and bowel incontinence due to flaccid paralysis.

DIAGNOSIS

X-rays show distortions of the intervertebral foramina; changes in the vertebrae or collapsed areas in the vertebral body; and localized enlargement of the spinal canal, indicating an adjacent block.
Myelography identifies the level of the lesion by outlining it if the tumor is causing partial obstruction; it shows anatomic relationship to the cord and the dura. If obstruction is complete, the injected dye can’t flow past the tumor. (This study is dangerous if cord compression is nearly complete because withdrawal or escape of cerebrospinal fluid [CSF]
will allow the tumor to exert greater pressure against the cord.)
Radioisotope bone scan demonstrates metastatic invasion of the vertebrae by showing a characteristic increase in osteoblastic activity.
Computed tomography scan shows cord compression and tumor location.
Frozen section biopsy at surgery identifies the tissue type.
Lumbar puncture may be normal, abnormal, or nonspecific. It may show clear yellow CSF as a result of increased protein levels if the flow is completely blocked. If the flow is partially blocked, protein levels rise, but the fluid is only slightly yellow in proportion to the CSF protein level. Cytology of the CSF may show malignant cells of metastatic carcinoma.

TREATMENT

Treatment of spinal cord tumors generally includes decompression or radiation. Laminectomy is indicated for primary tumors that produce spinal cord or cauda equina compression; it isn’t usually indicated for metastatic tumors. If the tumor is slowly progressive or if it’s treated before the cord degenerates from compression, symptoms are likely to disappear, and complete restoration of function is possible. In a patient with metastatic carcinoma or lymphoma who suddenly experiences complete transverse myelitis with spinal shock, functional improvement is unlikely, even with treatment, and his outlook is ominous. If the patient has incomplete paraplegia of rapid onset, emergency surgical decompression may save cord function. Steroid therapy with dexamethasone minimizes cord edema and temporarily relieves symptoms until surgery can be performed. Partial removal of intramedullary gliomas, followed by radiation, may alleviate symptoms for a short time. Metastatic extradural tumors can be controlled with radiation, analgesics and, in the case of hormone-mediated tumors (breast and prostate), appropriate hormone therapy. Transcutaneous electrical nerve stimulation (TENS) may control radicular pain from spinal cord tumors and is a useful alternative to opioid analgesics. In TENS, an electrical charge is applied to the skin to stimulate large-diameter nerve fibers and thereby inhibit transmission of pain impulses through small-diameter nerve fibers. Chemotherapy generally hasn’t proven effective against most spinal tumors, but may be recommended as salvage therapy in the setting of surgical and radiation failure.

SPECIAL CONSIDERATIONS

The care plan for patients with spinal cord tumors should emphasize emotional support and skilled intervention during acute and chronic phases, early recognition of recurrence, prevention and treatment of complications, and maintenance of quality of life.

On your first contact with the patient, perform a complete neurologic evaluation to obtain baseline data for planning future care and evaluating changes in his clinical status.
Care of the patient with a spinal cord tumor is basically the same as that for the patient with spinal cord injury and requires psychologic support, rehabilitation (including bowel and bladder retraining), and prevention of infection and skin breakdown. After laminectomy, care includes checking neurologic status frequently, changing position by logrolling, administering analgesics, monitoring frequently for infection, and aiding in early walking. Physical therapy may be needed to improve muscle strength and to improve the ability to function independently when permanent neurologic losses occur.
Help the patient and his family to understand and cope with the diagnosis, treatment, potential disabilities, and necessary changes in lifestyle.
Take safety precautions for the patient with impaired sensation and motor deficits. Use side rails if the patient is bedridden; if he isn’t, encourage him to wear flat shoes, and remove scatter rugs and clutter to prevent falls.
Encourage the patient to be independent in performing daily activities. Avoid aggravating pain by moving the patient slowly and by making sure his body is well aligned when giving personal care. Advise him to use TENS to block radicular pain.
Administer steroids and antacids, as ordered, for cord edema after radiation therapy. Monitor for sensory or motor dysfunction, which indicates the need for more steroids.
Enforce bed rest for the patient with vertebral body involvement until the practitioner says he can safely walk because body weight alone can cause cord collapse and cord laceration from bone fragments.
Logroll and position the patient on his side every 2 hours to prevent pressure ulcers and other complications of immobility.
If the patient is to wear a back brace, make sure he wears it whenever he gets out of bed.

THORAX

Lung cancer

Even though it’s largely preventable, lung cancer is the most common cause of cancer death in men and women. Lung cancer usually develops within the wall or epithelium of the bronchial tree. (See Tumor infiltration in lung cancer.) Its most common types are epidermoid (squamous cell) carcinoma, small-cell (oat cell) carcinoma, adenocarcinoma, and large-cell (anaplastic) carcinoma. Although the prognosis is usually poor, it varies with the extent of metastasis at the time of diagnosis and the cell type growth rate. Only about 13% of patients with lung cancer survive 5 years after diagnosis.

CAUSES AND INCIDENCE

Most experts agree that lung cancer is attributable to inhalation of carcinogenic pollutants by a susceptible host. Who’s most susceptible? Any smoker older than age 40, especially if he began to smoke before age 15, has smoked a whole pack or more per day for 20 years, or works with or near asbestos.

Pollutants in tobacco smoke cause progressive lung cell degeneration. Lung cancer is 10 times more common in smokers than in nonsmokers, with 85% to 95% of the cases caused by voluntary or involuntary (secondhand) smoking. Cancer risk is determined by the number of cigarettes smoked daily, the depth of inhalation, how early in life smoking began, and the nicotine content of cigarettes. Two other factors also increase susceptibility: exposure to carcinogenic industrial and air
pollutants (asbestos, uranium, arsenic, nickel, iron oxides, chromium, radioactive dust, and coal dust) and familial susceptibility.

SIGNS AND SYMPTOMS

Because early-stage lung cancer usually produces no symptoms, this disease is usually in an advanced state at diagnosis. These late-stage symptoms commonly lead to diagnosis:

Epidermoid and small-cell carcinomas— smoker’s cough, hoarseness, wheezing, dyspnea, hemoptysis, and chest pain
Adenocarcinoma and large-cell carcinoma— fever, weakness, weight loss, anorexia, and shoulder pain

In addition to their obvious interference with respiratory function, lung tumors may also alter the production of hormones that regulate body function or homeostasis. Clinical conditions that result from such changes are known as hormonal paraneoplastic syndromes:

Gynecomastia may result from large-cell carcinoma.
Hypertrophic pulmonary osteoarthropathy (bone and joint pain from cartilage erosion due to abnormal production of growth hormone) may result from large-cell carcinoma and adenocarcinoma.
Cushing’s and carcinoid syndromes may result from small-cell carcinoma.
Hypercalcemia may result from epidermoid tumors.

Metastatic signs and symptoms vary greatly, depending on the effect of tumors on intrathoracic and distant structures:

bronchial obstruction: hemoptysis, atelectasis, pneumonitis, dyspnea
cervical thoracic sympathetic nerve involvement: miosis, ptosis, exophthalmos, reduced sweating
chest wall invasion: piercing chest pain, increasing dyspnea, severe shoulder pain radiating down arm
esophageal compression: dysphagia
local lymphatic spread: cough, hemoptysis, stridor, pleural effusion
pericardial involvement: pericardial effusion, tamponade, arrhythmias
phrenic nerve involvement: dyspnea, shoulder pain, unilateral paralyzed diaphragm with paradoxical motion
recurrent nerve invasion: hoarseness, vocal cord paralysis
vena caval obstruction: venous distention and edema of face, neck, chest, and back

Distant metastasis may involve any part of the body, most commonly the central nervous system, liver, and bone.

DIAGNOSIS

Typical clinical findings may strongly suggest lung cancer, but firm diagnosis requires further evidence.

Chest X-ray usually shows an advanced lesion, but it can detect a lesion up to 2 years before symptoms appear. It also indicates tumor size and location.
Sputum cytology, which is 75% reliable, requires a specimen coughed up from the lungs and tracheobronchial tree, not postnasal secretions or saliva.
Spiral or helical computed tomography (CT) of the chest may help to delineate the tumor’s size and its relationship to surrounding structures.
Magnetic resonance imaging (MRI) is useful for differentiating vascular abnormalities from tumor.
Bronchoscopy can locate the tumor site. Bronchoscopic washings provide material for cytologic and histologic examination. The flexible fiber-optic bronchoscope increases the test’s effectiveness.
Percutaneous needle biopsy of the lungs uses biplane fluoroscopic visual control to detect peripherally located tumors. This allows firm diagnosis in 80% of patients.
Mediastinoscopy with tissue biopsy of accessible metastatic sites includes supraclavicular and mediastinal node and pleural biopsy. Directed needle biopsy may be performed in conjunction with CT scan.
Thoracentesis allows chemical and cytologic examination of pleural fluid.

Additional studies include preoperative mediastinoscopy or mediastinotomy to rule out involvement of mediastinal lymph nodes (which would preclude curative pulmonary resection).

Other tests to detect metastasis include bone scan, bone marrow biopsy (recommended in small-cell carcinoma), CT scan of the brain or abdomen, and positron emission tomography.

After histologic confirmation, staging determines the extent of the disease and helps in planning the treatment and predicting the prognosis.

TREATMENT

Recent treatment, which consists of combinations of surgery, radiation, and chemotherapy, may improve the prognosis and prolong survival. Nevertheless, because treatment usually begins at an advanced stage, it’s largely palliative.

Surgery is the preferred treatment for stage I, stage II, or selected stage III squamous cell cancer; adenocarcinoma; and large-cell carcinoma, unless the tumor is nonresectable or other conditions rule out surgery.

Surgery may include partial removal of a lung (wedge resection, segmental resection, lobectomy, or radical lobectomy) or total removal (pneumonectomy or radical pneumonectomy). A less invasive form of surgery that’s used for small (11/2” or less) tumors is video-assisted thoracic surgery (VATS). VATS requires small incisions and causes less pain than other types of surgery.

Preoperative radiation therapy may reduce tumor bulk to allow for surgical resection. Preradiation chemotherapy helps improve response rates. Radiation therapy is ordinarily recommended for stage I and stage II lesions, if surgery is contraindicated, and for stage III lesions when the disease is confined to the involved hemithorax and the ipsilateral supraclavicular lymph nodes.

Generally, radiation therapy is delayed until 1 month after surgery, to allow the wound to heal, and is then directed to the part of the chest most likely to develop metastasis. High-dose radiation therapy or radiation implants may also be used.

Research has shown that chemotherapy combinations of paclitaxel, gemcitabine, docetaxel, irinotecan, etoposide, and vinorelbine are more active and better tolerated when combined with cisplatin or carboplatin. Many of these drugs are also being utilized as single agents for the treatment of small-cell and non-small-cell lung cancers.

In laser therapy, laser energy is directed through a bronchoscope to destroy local tumors.

SPECIAL CONSIDERATIONS

Comprehensive supportive care and patient teaching can minimize complications and speed recovery from surgery, radiation, and chemotherapy.

Before surgery:

Supplement and reinforce the information given to the patient by the health care team about the disease and the surgical procedure.
Explain expected postoperative procedures, such as insertion of an indwelling catheter, use of an endotracheal tube or chest tube (or both), dressing changes, and I.V. therapy.
Teach the patient how to perform coughing, deep diaphragmatic breathing, and range-of-motion (ROM) exercises.
Reassure the patient that analgesics will be provided and proper positioning will be implemented to control postoperative pain.
Inform the patient that he may take nothing by mouth beginning after midnight the night before surgery, that he’ll shower with a soaplike antibacterial agent the night or morning before surgery, and that he’ll be given preoperative medications, such as a sedative and an anticholinergic to dry secretions.

After thoracic surgery:

Maintain a patent airway, and monitor chest tubes to reestablish normal intrathoracic pressure and prevent postoperative and pulmonary complications.
Check vital signs every 15 minutes during the first hour after surgery, every 30 minutes during the next 4 hours, and then every 2 hours. Watch for and report abnormal respiration and other changes.
Suction the patient as needed, and encourage him to begin deep breathing and coughing as soon as possible. Check secretions often. Initially, sputum will be thick and dark with blood, but it should become thinner and grayish yellow within a day.
Monitor and record closed chest drainage. Keep chest tubes patent and draining effectively. Fluctuation in the water-seal chamber on inspiration and expiration indicates that the chest tube is patent. Watch for air leaks, and report them immediately. Position the patient on the surgical side to promote drainage and lung reexpansion.
Watch for and report foul-smelling discharge and excessive drainage on dressing. Usually, the dressing is removed after 24 hours, unless the wound appears infected.
Monitor intake and output. Maintain adequate hydration.
Watch for and treat infection, shock, hemorrhage, atelectasis, dyspnea, mediastinal shift, and pulmonary embolus.
To prevent pulmonary embolus, apply antiem-bolism stockings and encourage ROM exercises.

If the patient is receiving chemotherapy and radiation:

Explain possible adverse effects of radiation and chemotherapy. Watch for, treat and, when possible, try to prevent them.
Ask the dietary department to provide soft, nonirritating foods that are high in protein, and encourage the patient to eat high-calorie between-meal snacks.
Give antiemetics and antidiarrheals, as needed.
Schedule patient care activities in a way that helps the patient conserve his energy.
During radiation therapy, administer skin care to minimize skin breakdown. If the patient receives radiation therapy in an outpatient setting, warn him to avoid tight clothing, exposure to the sun, and harsh ointments on his chest. Teach him exercises to help prevent shoulder stiffness.

For patients who smoke, explain the benefits of quitting and encourage them to quit.
Refer smokers who want to quit to the American Cancer Society or smoking-cessation programs or suggest group therapy, individual counseling, or use of smoking-cessation products.
Encourage patients with recurring or chronic respiratory infections and those with chronic lung disease who detect any change in the character of a cough to see their practitioner promptly for evaluation.

Breast cancer

Breast cancer occurs more commonly in the left breast than the right and more commonly in the outer upper quadrant. Growth rates vary. Theoretically, slow-growing breast cancer may take up to 8 years to become palpable at 1 cm. It spreads by way of the lymphatic system and the bloodstream, through the right side of the heart to the lungs, and eventually to the other breast, the chest wall, liver, bone, and brain.

The estimated growth rate of breast cancer is referred to as doubling time, or the time it takes the malignant cells to double in number. Survival time for breast cancer is based on tumor size and spread; the number of involved nodes is the single most important factor in predicting survival time.

Breast cancer is classified by histologic appearance and location of the lesion, as follows:

adenocarcinoma—arising from the epithelium
intraductal—developing within the ducts (in cludes Paget’s disease)
infiltrating—occurring in parenchyma of the breast
inflammatory (rare)—reflecting rapid tumor growth, in which the overlying skin becomes edematous, inflamed, and indurated
lobular carcinoma in situ—reflecting tumor growth involving lobes of glandular tissue
medullary or circumscribed—large tumor with rapid growth rate

Breast cancer is also classified as invasive or noninvasive. Invasive tumor cells, which make up 90% of all breast cancers, break through the duct walls and encroach on other breast tissues. Noninvasive tumor cells remain confined to the duct in which they originated. (See Types of breast cancer.)

CAUSES AND INCIDENCE

The cause of breast cancer isn’t known, but its high incidence in women implicates estrogen.

Certain predisposing factors are clear; women at high risk include those who have a family history of breast cancer, particularly first-degree relatives (mother, sister, and maternal aunt).

Other women at high risk include those who:

have long menstrual cycles or began menses early (before age 12) or menopause late (after age 55)
have taken hormonal contraceptives
used hormone replacement therapy for more than 5 years
who took diethylstilbestrol to prevent miscarriage
have never been pregnant
were first pregnant after age 30 have had unilateral breast cancer
have had ovarian cancer—particularly at a young age
were exposed to low-level ionizing radiation
have genetic mutations, such as in BRCA1 and BRCA2 genes

Women at lower risk include those who:

were pregnant before age 20
have had multiple pregnancies
are Native American or Asian

Most breast cancer deaths occur in women age 50 and older (84% of cases), and 77% of new breast cancer cases occur in this age-group. However, breast cancer may develop any time after puberty. It occurs in men, but rarely; male cases of breast cancer account for less than 1% of all cases.

The 5-year survival rate for localized breast cancer has improved because of earlier diagnosis and the variety of treatments now available.
According to the most recent data, mortality rates continue to decline in White women and, for the first time, are also declining in younger Black women. Lymph node involvement is the most valuable prognostic predictor. With adjuvant therapy, 70% to 75% of women with negative nodes will survive 10 years or more compared with 20% to 25% of women with positive nodes.

SIGNS AND SYMPTOMS

Warning signals of possible breast cancer include:

a lump or mass in the breast (a hard, nontender stony mass is usually malignant)
change in symmetry or size of the breast
change in skin, thickening, scaly skin around the nipple, dimpling, edema (peau d’orange), or ulceration
change in skin temperature (a warm, hot, or pink area; suspect cancer in a nonlactating woman older than childbearing age until proven otherwise)
unusual drainage or discharge (A spontaneous discharge of any kind in a nonbreast-feeding, nonlactating woman warrants thorough investigation; so does any discharge produced by breast manipulation [greenish black, white, creamy, serous, or bloody]. If a breast-fed infant rejects one breast, this may suggest possible breast cancer.)
change in the nipple, such as itching, burning, erosion, or retraction
pain (not usually a symptom of breast cancer unless the tumor is advanced, but it should be investigated)
bone metastasis, pathologic bone fractures, and hypercalcemia
edema of the arm

DIAGNOSIS

The most reliable method of detecting breast cancer is the clinical breast examination, followed by immediate evaluation of any abnormality. Other diagnostic measures include mammography, ultrasound, needle biopsy, and surgical biopsy. Mammography is indicated for any woman whose physical examination suggests breast cancer. It should be done as a baseline on women between ages 35 and 39 and annually on all women older than age 40, on those who have a family history of breast cancer, and on those who have had unilateral breast cancer (to check for new disease).

The value of mammography is questionable for women under age 35 (because of the density
of the breasts), except for those women who are strongly suspected of having breast cancer. False-negative results can occur in as many as 30% of all tests. Consequently, with a suspicious mass, a negative mammogram should be disregarded, and a fine-needle aspiration or surgical biopsy should be done. Ultrasonography, which can distinguish a fluid-filled cyst from a tumor, can also be used instead of an invasive surgical biopsy.

Understanding IVDMIA

A prognostic tool for predicting breast cancer tumor recurrence recently received FDA approval. In vitro diagnostic multivariate index assay (IVDMIA) (such as MammaPrint) predicts the odds that an early-stage breast cancer will metastasize in 5 to 10 years. Using a biopsy sample taken from the tumor, the test analyzes the activity of 70 genes that affect whether or not an early-stage breast cancer will spread. It rates the patient as high risk or low risk for metastases. The test is intended for women younger than age 61 with stage I or II disease, who are lymph node-negative, and whose tumors are no larger than 5 cm.

Bone scan, brain scan, computed tomography scan, measurement of alkaline phosphatase levels, liver function studies, and liver biopsy can detect distant metastases. A hormonal receptor assay done on the tumor can determine if the tumor is estrogen or progesterone dependent. (This test guides decisions to use therapy that blocks the action of the estrogen hormone that supports tumor growth.) (See Understanding IVDMIA.) Additionally, molecular testing for human epidermal growth factor receptor 2 (HER2) is recommended for determination of tumor status.

TREATMENT

In choosing therapy, the patient and practitioner should take into consideration the stage of the disease, the woman’s age and menopausal status, and the disfiguring effects of the surgery. Treatment of breast cancer may include one or any combination of the following:

Surgery involves either mastectomy or lumpectomy. A lumpectomy may be done on an outpatient basis and may be the only surgery needed, especially if the tumor is small and there’s no evidence of axillary node involvement. In many cases, radiation therapy is combined with this surgery.

A two-stage procedure, in which the surgeon removes the lump and confirms that it’s malignant and then discusses treatment options with the patient, is desirable because it allows the patient to participate in her plan of treatment. Sometimes, if the tumor is diagnosed as clinically malignant, such planning can be done before surgery. In lumpectomy and dissection of the axillary lymph nodes, the tumor and the axillary lymph nodes are removed, leaving the breast intact. A simple mastectomy removes the breast but not the lymph nodes or pectoral muscles. Modified radical mastectomy removes the breast and the axillary lymph nodes. Radical mastectomy, the performance of which has declined, removes the breast, pectoralis major and minor muscles, and the axillary lymph nodes.

The spread of breast cancer to regional lymph nodes is considered a vital prognostic indicator. Sentinel lymph-node biopsy, a reliable and minimally invasive procedure, is used to identify and sample the sentinel lymph node closest to the breast tumor. During the patient’s surgery, the axillary node is injected with dye to help with identification and then sent to the pathologist to assess for cancer spread. If the node is negative, the patient can be spared an axillary node dissection, which carries its own risks and the potential for long-term complications.

Reconstructive breast surgery can be performed at the same time as mastectomy or it can be planned for a later date. Several options are available for breast reconstruction, including the insertion of breast implants or a transverse rectus abdominis musculocutaneous flap.

Chemotherapy, involving various cytotoxic drug combinations, is used as either adjuvant or primary therapy, depending on several factors, including the TNM staging of the cancer, as well as estrogen receptor and HER2 status. The most commonly used antineoplastic drugs are cyclophosphamide, fluorouracil, methotrexate, doxorubicin, vincristine, and paclitaxel. A common drug combination used in both premenopausal and postmenopausal women is cyclophosphamide, doxorubicin, and paclitaxel.

Tamoxifen, an estrogen antagonist, or select aromatose inhibitors are the adjuvant treatments of choice for postmenopausal patients with positive estrogen receptor status. They have also been found to reduce the risk of breast cancer in women at high risk.
For individuals with HER2-positive receptors, monoclonal antibodies such as trastuzumab are indicated for adjuvant therapy.

Peripheral stem cell therapy is an option, but it’s rarely used for advanced breast cancer.
Primary radiation therapy before or after tumor removal is effective for small tumors in early stages with no evidence of distant metastasis; it’s also used to prevent or treat local recurrence. Presurgical radiation to the breast in inflammatory breast cancer helps make tumors more surgically manageable.
Estrogen, progesterone, androgen, or antiandrogen aminoglutethimide therapy may also be given to breast cancer patients. The success of these drug therapies—along with growing evidence that breast cancer is a systemic, not local, disease—has led to a decline in ablative surgery.

SPECIAL CONSIDERATIONS

To provide good care for a patient with breast cancer, begin with a history, assess the patient’s feelings about her illness, and determine what she knows about it and what she expects. Preoperatively, make sure you know what kind of surgery is scheduled, so you can prepare her properly. If a mastectomy is scheduled, in addition to the usual preoperative preparation (for example, skin preparations and not allowing the patient anything by mouth), provide the following information:

Teach her how to deep-breathe and cough to prevent pulmonary complications and how to rotate her ankles to help prevent thromboembolism.
Tell her she can ease her pain by lying on the affected side or by placing a hand or pillow on the incision. Preoperatively, show her where the incision will be. Inform her that she’ll receive pain medication and that she need not fear addiction. Remember, adequate pain relief encourages coughing and turning and promotes general well-being. Positioning a small pillow anteriorly under the patient’s arm provides comfort.
Encourage her to get out of bed as soon as possible (even as soon as the anesthesia wears off or the first evening after surgery).
Explain that, after mastectomy, an incisional drain or suction device will be used to remove accumulated serous or sanguineous fluid, thereby promoting healing.

Postoperative care:

Inspect the dressing anteriorly and posteri orly, reporting bleeding promptly.
Measure and record the amount of drainage; also note the color. Expect drainage to be bloody during the first 4 hours and afterward to become serous.
Check circulatory status (blood pressure, pulse, respirations, and bleeding).
Monitor intake and output for at least 48 hours after general anesthesia.
Inform the patient to not let anyone draw blood, start an I.V., give an injection, or take a blood pressure on the affected side because these activities will also increase the chances of developing lymphedema.
Inspect the incision. Encourage the patient and her partner to look at her incision as soon as possible, perhaps when the first dressing is removed.
Advise the patient to ask her practitioner about reconstructive surgery or to call the local or state medical society for the names of plastic reconstructive surgeons who regularly perform surgery to create breast mounds. In many cases, reconstructive surgery may be planned before the mastectomy.
Instruct the patient about breast prostheses. The American Cancer Society’s Reach to Recovery group can provide instruction, emotional support and counseling, and a list of area stores that sell prostheses.
Give psychological and emotional support. Most patients fear cancer and possible disfigurement and worry about loss of sexual function. Explain that breast surgery doesn’t interfere with sexual function and that the patient may resume sexual activity as soon as she desires after surgery.
Also explain to the patient that she may experience phantom breast syndrome (a phenomenon in which a tingling or a pins-and-needles sensation is felt in the area of the amputated breast tissue) or depression following mastectomy. Listen to the patient’s concerns, offer support, and refer her to an appropriate organization such as the American Cancer Society’s Reach to Recovery, which offers caring and sharing groups to help breast cancer patients in the hospital and at home.

Postoperative arm and hand care

Hand exercises for the patient who’s prone to lymphedema can begin on the day of surgery. Plan arm exercises with the physician because he can anticipate potential problems with the suture line.

Have the patient open her hand and close it tightly six to eight times every 3 hours while she’s awake.
Elevate the arm on the affected side on a pillow above the heart level.
Encourage the patient to wash her face and comb her hair—an effective exercise.
Measure and record the circumference of the patient’s arm 2½” (5.7 cm) from her elbow. Indicate the exact place you measured. By remeasuring a month after surgery, and at intervals during and following radiation therapy, you can determine whether lymphedema is present. The patient may complain that her arm is heavy—an early symptom of lymphedema.
When the patient is home, she can elevate her arm and hand by supporting it on the back of a chair or a couch.

ABDOMEN AND PELVIS

Gastric cancer

Gastric cancer can be classified as polypoid, ulcerating, ulcerating and infiltrating, or diffuse, according to gross appearance. The parts of the stomach affected by gastric cancer, listed in order of decreasing frequency, are the pylorus and antrum, the lesser curvature, the cardia, the body of the stomach, and the greater curvature. (See Sites of gastric cancer.)

Gastric cancer infiltrates rapidly to regional lymph nodes, omentum, liver, and lungs by the following routes: walls of the stomach, duodenum, and esophagus; lymphatic system; adjacent organs; bloodstream; and peritoneal cavity.

CAUSES AND INCIDENCE

The cause of gastric cancer is unknown. It’s commonly associated with gastritis with gastric atrophy, which may result from gastric cancer and may not be a precursor state. Predisposing factors include environmental influences, such as smoking and high alcohol intake. Genetic factors have also been implicated because this disease occurs more commonly among people with type A blood than among those with type O; similarly, it’s more common in people with a family history of gastric cancer. E-cadhern mutations have been found in approximately 25% of families with an autosomal dominant form of gastric cancer. Dietary factors also seem related, including types of food preparation, physical properties of some foods, and certain methods of food preservation (especially smoking, pickling, or salting). There’s a strong correlation between infection with Helicobacter pylori and distal gastric cancer.

Gastric cancer is common throughout the world and affects all races; however, unexplained geographic and cultural differences in incidence occur—for example, a higher mortality in Japan, Iceland, Chile, and Austria. In the United States, during the past 25 years, incidence has decreased by 50%; the resulting death rate is one third what it was 30 years ago. Incidence is higher in males older than 40. Hispanic, Native, and African Americans are twice as likely to develop gastric cancer than Whites. The prognosis depends on the stage of the disease at the time of diagnosis. Gastric cancer is frequently diagnosed at an advanced stage. The overall 5-year survival rate is about 19%.

SIGNS AND SYMPTOMS

Early clues to gastric cancer are chronic dyspepsia and epigastric discomfort, followed in later stages by weight loss, anorexia, feeling of fullness after eating, anemia, and fatigue. If the cancer is in the cardia, the first sign or symptom may be dysphagia and, later, vomiting (commonly coffee-ground vomitus). Affected patients may also have blood in their stools.

The course of gastric cancer may be insidious or fulminating. Unfortunately, the patient typically treats himself with antacids or histamine blockers until the symptoms of advanced stages appear.

DIAGNOSIS

Diagnosis depends primarily on reinvestigations of any persistent or recurring GI changes and complaints. To rule out other conditions producing similar symptoms, diagnostic evaluation must include the testing of blood, stools, and stomach fluid samples.

Diagnosis of gastric cancer generally requires these studies:

Barium X-rays of the GI tract with fluoroscopy show changes (tumor or filling defect in the outline of the stomach, loss of flexibility and dis-tensibility, and abnormal gastric mucosa with or without ulceration).
Gastroscopy with fiber-optic endoscopy helps rule out other diffuse gastric mucosal abnormalities by allowing direct visualization and gastroscopic biopsy to evaluate gastric mucosal lesions.
Photography with fiber-optic endoscope provides a permanent record of gastric lesions that can later be used to determine disease progression and effect of treatment.
A gastric acid stimulation test determines whether the stomach is able to properly secrete acid.

Certain other studies may rule out specific organ metastasis: computed tomography scans, chest X-rays, liver and bone scans, and liver biopsy.

TREATMENT

In many cases, surgery is the treatment of choice. Excision of the lesion with appropriate margins is possible in more than one third of patients. Even in patients whose disease isn’t considered surgically curable, resection offers palliation and improves potential benefits from chemotherapy and radiation.

The nature and extent of the lesion determine what kind of surgery is most appropriate. Common surgical procedures include subtotal gastric resection (subtotal gastrectomy) and total gastric resection (total gastrectomy). When carcinoma involves the pylorus and antrum, gastric resection removes the lower stomach and duodenum (gastrojejunostomy or Billroth II). If metastasis has occurred, the omentum and spleen may also have to be removed.

If gastric cancer has spread to the liver, peritoneum, or lymph glands, palliative surgery may
include gastrostomy, jejunostomy, or a gastric or partial gastric resection. Such surgery may temporarily relieve vomiting, nausea, pain, and dysphagia, while allowing enteral nutrition to continue.

Chemotherapy for GI cancers may help to control symptoms and prolong survival. Adenocarcinoma of the stomach (see Adenocarcinoma of the stomach) has responded to several agents, including fluorouracil, paclitaxel, doxorubicin, cisplatin, methotrexate, etoposide, docetaxel, oxaliplatin, irinotecan, and mitomycin. Antiemetics can control nausea, which increases as the cancer advances. In the more advanced stages, sedatives and tranquilizers may be necessary to control overwhelming anxiety. Opioids are commonly necessary to relieve severe and unremitting pain.

Radiation has been particularly useful when combined with chemotherapy in patients who have unresectable or partially resectable disease. It should be given on an empty stomach and shouldn’t be used preoperatively because it may damage viscera and impede healing.

Treatment with antispasmodics and antacids may help relieve GI distress. Histamine₂-receptor antagonists can treat GI ulcers.

SPECIAL CONSIDERATIONS

Before surgery, prepare the patient for its effects and for postsurgical procedures such as insertion of a nasogastric (NG) tube for drainage and I.V. lines.
Reassure the patient who’s having a partial gastric resection that he may eventually be able to eat normally. Prepare the patient who’s having a total gastrectomy for slow recovery and only partial return to a normal diet.
Include the family in all phases of the patient’s care.
Emphasize the importance of changing position every 2 hours and of deep breathing.
After surgery, give meticulous supportive care to promote recovery and prevent complications.
After any type of gastrectomy, pulmonary complications may result, and oxygen may be needed. Regularly assist the patient with turning, coughing, and deep breathing. Turning the
patient hourly and administering analgesic opioids, as ordered, may prevent pulmonary problems. Incentive spirometry may also be needed for complete lung expansion. Proper positioning is important as well; semi-Fowler’s position facilitates breathing and drainage.
After gastrectomy, little (if any) drainage comes from the NG tube because no secretions form after stomach removal. Without a stomach for storage, many patients experience dumping syndrome. Intrinsic factor is absent from gastric secretions, leading to malabsorption of vitamin B₁₂. To prevent vitamin B₁₂ deficiency, the patient must take a replacement vitamin for the rest of his life as well as an iron supplement.
During radiation treatment, encourage the patient to eat high-calorie, well-balanced meals. Offer fluids such as ginger ale to minimize such radiation adverse effects as nausea and vomiting.

PREVENTION Preventing gastric cancer

Although gastric cancer can’t entirely be prevented, encourage your patient to make these lifestyles changes to reduce the risk of its occurring.

Limit nitrates

Nitrates are known to contribute to gastric cancer. They’re found mainly in processed meats such as bologna, salami, and corned beef, and in cured meats, such as ham and bacon.

Limit smoked, pickled, and heavily salted foods

Smoked, pickled, and heavily salted foods have been linked to an increased risk of stomach cancer. Eating fewer of these foods may help reduce the risk of developing gastric cancer.

Stop smoking

Smoking greatly increases the risk of developing stomach cancer, especially cancer that occurs at the junction of the esophagus and stomach.

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Tags: Professional Guide to Diseases

Aug 27, 2016 | Posted by drzezo in PATHOLOGY & LABORATORY MEDICINE | Comments Off

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