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www.TheOncologyNurse.com increase calcium excretion. Bisphosphonates act by blocking osteoclatic bone resorption. Pamidronate and zoledronic acid are most often used for the treatment of hypercalcemia of malignancy.5 Calcitonin, given subcutaneously or by intramuscular injection, can lower calcium levels, but to a more modest degree compared with bisphosphonates.4,5 Monitoring the patient’s renal function and electrolytes during rehydration is important to foresee any long-term complications. Control of the underlying cancer is important to maintain control of the hypercalcemia.4 Possible complications related to untreated hypercalcemia include renal failure, cardiac arrest, and coma.6 Ectopic adrenocorticotropic hormone syndrome. Ectopic ACTH (Cushing) syndrome is mostly seen in patients with small-cell lung cancer (SCLC). Cushing syndrome presents when the cancer has produced too much ACTH, which in turn stimulates the adrenal glands to produce excessive corticosteroids. Although not well understood, the mechanism for ectopic ACTH production appears to be the irregular transcription and overexpression of inactive precursor peptides of ACTH. Signs and symptoms of Cushing syndrome include proximal muscle weakness, hypokalemia, metabolic alkalosis, glucose intolerance, and hypertension.4,6 Treatment of Cushing syndrome in cludes management of the primary tumor and pharmacologic therapy. Ketoconazole is the most commonly used pharmacologic agent, because it has a rapid onset of action and inhibits corti-
hypoosmolality, and urine hyperosmolality.9 As a result, the serum sodium level decreases and weight gain without edema occurs.10 Patients who present with mild hyponatremia may be asymptomatic or have general symptoms of tiredness, headache, weakness, muscle cramps, or decreased appetite. Patients with moderate hyponatremia may present with confusion, nausea, vomiting, oliguria, increased thirst, lethargy and, less commonly, loss of deep-tendon reflexes. Severe symptoms of SIADH develop when serum sodium levels are between 100 mEq/L and 115 mEq/L and include seizure activity and coma.9,11 Treatment of the underlying cancer, correction of electrolyte abnormalities, and fluid restriction of 500 to 1000 mL/day are the mainstays of treatment. Infusion of 3% hypertonic saline may help to increase serum sodium levels. Recurrent SIADH may be the first sign of cancer progression.11 Individuals with moderate hyponatremia will require IV fluids, diuretics, and electrolyte replacement.11 Specific guidelines direct the amount of sodium replacement needed to prevent neurologic problems; rapidly correcting the sodium level can lead to osmotic demyelination syndrome, characterized by severe progressive extremity weakness and other neurologic symptoms.9,11 Demeclocycline, a tetracycline antibiotic, may be used if the preceding measures have failed to produce results. As a side effect, demeclocycline induces nephrogenic diabetes insipidus, resulting in dehydration caused by the inability to concentrate urine.10
An oncologic emergency is defined as a clinical condition that results from a structural or metabolic change caused by cancer or its treatment requiring immediate medical attention to prevent loss of life or permanent disability. costeroid production.4 Ketoconazole and chemotherapy can be used in conjunction to treat patients with SCLC. Ketoconazole can cause adrenal suppression, so the patient’s liver enzymes as well as adrenal gland function must be monitored throughout the course of treatment.4,8 Syndrome of inappropriate antidiuretic hormone hypersecretion. In the paraneoplastic SIADH, the tumor secretes a protein similar to antidiuretic hormone (ADH). This abnormal production of ADH is unresponsive to the normal feedback mechanism, resulting in water intoxication. SCLC is responsible for up to 75% of cases of SIADH.9 Individuals with SIADH resulting from malignancy present with excess fluid buildup, leading to dilutional hyponatremia, serum
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Hematologic paraneoplastic syndromes Trousseau syndrome. Trousseau syndrome is the earliest paraneoplastic syndrome described, and demonstrates the association between thrombosis and malignancy. This syndrome is a hypercoagulable state with migratory thrombophlebitis and develops primarily in patients with mucin-producing tumors, such as adenocarcinomas of the lung. Trousseau syndrome occurs in 40% to 50% of patients with solid tumors. It is believed that mucin-producing carcinomas and tissue factor are responsible for the release of highly glycosylated secretory products of epithelial cells into the bloodstream, initiating thromboembolic events.12 Trousseau syndrome is associated with the occur-
Table. Oncologic Emergencies Associated with Lung Cancer Urgency/emergency Superior vena cava syndrome
6-7
Cardiac effusion and cardiac tamponade
5-10
Pleural effusion
Spinal cord compression
Selected signs and symptoms
Incidence, %
Dyspnea; head fullness; chest pain; facial, neck, and arm swelling; stridor; positive distension of superficial veins of chest, neck, upper arms Dyspnea, cough, anxiety, jugular vein distension, tachycardia, pulsus paradoxis, substernal chest pain Dyspnea, dry cough, pleuritic chest pain, dullness on chest percussion, tracheal deviation
15-20
Thoracic: 10 Lumbosacral: 20 Cervical: 10
Back pain followed by weakness and sensory deficits. Paraesthesias and a decrease or loss of temperature and vibratory sensation may also be experienced
Source: Reference 4.
rence of deep vein thrombosis (DVT) and pulmonary emboli.4 Signs and symptoms of DVT include pain and swelling of the affected extremity. Early on, mild pain may occur at the affected area without swelling, and patients may remain asymptomatic. Those with superficial thrombophlebitis may have only erythema at the site. Patients with shortness of breath and chest pain need to be assessed for pulmonary emboli. They may present with anginal chest pain, and, as the syndrome progresses, this may change to pleuritic chest pain with dyspnea.13 Treatment typically includes anticoagulation using IV continuous infusion unfractionated heparin.4 Low-molecular-weight heparins have been approved by the US Food and Drug Administration for outpatient management of DVT and inpatient management of pulmonary embolus. Low-molecular-weight heparins are dosed based on the weight of the patient; these drugs have been found to have good bioavailability, a long half-life, and predictable anticoagulant activity.14 In addition, laboratory monitoring is not necessary.14 Oncologic emergencies An oncologic emergency is defined as a clinical condition that results from a structural or metabolic change caused by cancer or its treatment requiring immediate medical attention to prevent loss of life or permanent disability10,15 (Table). Superior vena cava syndrome. Superior vena cava syndrome (SVCS), caused by a gradual obstruction of the superior
vena cava, can be caused by tumor, thrombosis, radiation, fibrosis, or infection.4 The superior vena cava drains into the right atrium of the heart, and can become compressed by a lung tumor as it grows. The superior vena cava lies close to intrathoracic lymph nodes, and lung cancer that spreads to these lymph nodes causes them to enlarge. Enlarged lymph nodes compress the vein, which slows the blood flow, and may ultimately result in complete blockage. Sixty percent to 95% of cases of SVCS arise from bronchogenic carcinoma.16 The onset of SVCS is usually slow, but can occur rapidly in the face of a rapidly growing tumor or thrombosis.5 Because of the slow progression of SVCS, collateral circulation has time to develop. Dyspnea is the most common presenting symptom with SVCS, occurring in more than 60% of patients.4 Distension of the neck and chest wall veins, facial edema and redness, and edema of the upper extremities are the most common presenting signs.5 Other symptoms include cough, dysphasia, and chest pain. The severity of symptoms is a reflection of the rapidity of the obstruction, the degree of the obstruction, and whether collateral circulation has been able to develop.17 Diagnosis of SVCS can include chest film, computed tomography (CT), venogram, magnetic resonance imaging (MRI), and a venous ultrasound. The goals for treatment of SVCS are symptom relief and therapy for the primary Continued on page 14
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