Box 17.1 SUPERIOR VENA CAVAL SYNDROME

    Diagnosis of SVC syndrome is made on a clinical basis. Radiologic imaging of the chest may demonstrate widening of the mediastinum. Pleural effusions are present in about 25% of cases, but may also be normal in as many as 16% of the cases. A computed tomography (CT) scan provides the best imaging and can help define the anatomy of the obstructing lesion. In patients without a diagnosis of cancer, a biopsy is mandatory to establish a diagnosis. If the only site of disease is the mediastinal mass, a needle biopsy, or preferentially a surgical biopsy, should be obtained by skilled providers. In patients with a known history of cancer, appropriate treatment may be initiated without a need for a biopsy.

    Emergent treatment includes stabilization of the cardiopulmonary system. The primary treatment modality depends on the tumor histology. For patients with lung cancer, radiation therapy is the treatment of choice. In patients with lymphoma, a combination of steroids, chemotherapy, and radiation may be used. Depending on the tumor type, chemotherapy may be indicated following initial stabilization.

SPINAL CORD COMPRESSION

Prompt recognition of the signs and symptoms associated with spinal cord compression and the initiation of urgent therapy can in some cases prevent catastrophic complications such as paralysis. Epidural compression of the spinal cord resulting in cord injury is the most common etiology. Less commonly, direct extension through the foramen may occur. Metastatic tumors involving the vertebral bodies are often responsible. Common cancers with metastasis to the bone include lung, prostate, and breast cancer, as well as multiple myeloma. Compression can occur at any point along the spinal cord. The thoracic spine is the most common site, representing 70% of lesions, followed by the lumbosacral spine at 20% and the cervical spine at 10%. It is important to recognize that multiple sites of compression may be present at the same time. The cord usually terminates at L1. The implications of compression of the thecal sac at the level of the cauda equina are similar to cord compression. The most common presenting symptom of spinal cord compression is pain. The pain may be either localized back pain or in some cases radicular pain caused by compression of a nerve root. Pain is usually present for days or even months prior to the development of neurologic symptoms. The importance of recognizing pain as the presenting symptom of cord compression cannot be overemphasized, since the development of neurologic symptoms is ominous and the outcome for patients with neurologic impairment is poor. Signs of cord compression on physical examination include numbness, weakness in the extremities, or loss of bladder or bowel function. Motor weakness or numbness with loss of sense to pinprick may be present. The upper limit of the sensory loss is often one or two vertebrae below the site of cord compression. Deep tendon reflexes may be brisk. In advanced cases of cord compression, an extensor plantar reflex may be present. Loss of motor and sensory function often precedes sphincter dysfunction.

    If cord compression is suspected, a magnetic resonance imaging (MRI) of the spine should be performed immediately to confirm or exclude the diagnosis (box 17.2). An MRI of the entire spine should be performed if possible to ascertain if there are multiple sites of disease. Myelography in addition to CT scanning may also be used when an MRI cannot be obtained. In patients with a known diagnosis of cancer, treatment should be initiated immediately. For patients without a diagnosis, a biopsy should be performed while initiating therapy. Spinal epidural abscess is an uncommon condition but should be considered in the differential; hence the importance of obtaining a definitive diagnosis in patients without a history of cancer.

Box 17.2 CORD COMPRESSION

    The goals of treatment are the relief of pain and preservation of neurologic function. Most commonly, treatment of cord compression includes the administration of steroids in addition to radiation therapy. Prompt therapy is critical because outcome for patients who are ambulatory at the time of diagnosis is good. Unfortunately for patients who have already developed paralysis at the time of diagnosis, only 10% of these patients will resume ambulation. The role of surgical intervention in the treatment of spinal cord compression has evolved over the last several years. Early studies did not demonstrate a benefit of decompressive laminectomy compared with radiation therapy alone. More recently a randomized trial demonstrated an improved outcome for patients receiving resection and radiation therapy compared with radiation therapy alone in terms of regaining and maintaining ambulation. Given the significant complications of the surgery, careful selection of patients with a good performance status and adequate life expectancy is needed. Surgery may be required for mechanical stabilization or to establish a definitive diagnosis. For patients with recurrent spinal cord compression, surgery and chemotherapy may be considered. Chemotherapy is often only useful in patients with tumors that respond well to chemotherapy. The need for immediate treatment must be emphasized because pretreatment neurologic status is the most important predictor for response to therapy.

BRAIN METASTASIS

Central nervous system involvement by cancer can be found in 25% of patients. Cancers which most commonly metastasize to the brain are lung cancer, breast cancer, and melanoma. Brain metastasis often occurs in the presence of systemic disease and results in significant morbidity. A biopsy should be performed when the diagnosis of brain metastases is in doubt. This is particularly true when dealing with a solitary CNS lesion, since the diagnosis may change.

    Presenting signs of central nervous system involvement include headache, nausea, vomiting, seizures, and focal neurologic deficits. Behavioral changes may also be noted in some patients. Abrupt presentations resembling a stroke may occur in the setting of hemorrhage associated with metastasis. This is most common in melanoma or hypervascular tumors such as germ cell tumors and renal cell cancers. Edema resulting from metastatic lesion results in increased intracranial pressure. On examination, patients may demonstrate decreased mental alertness. They may have papilledema and neck stiffness or cranial nerve findings. Muscular weakness is also common depending on the location of the lesion.

    CT with contrast or MRI is effective in diagnosing brain metastasis. MRI is more sensitive than CT scan at identifying small lesions as well as leptomeningeal disease. Emergent treatment includes steroid administration. Steroids lead to a reduction in edema associated with the metastatic lesion and improvement in the patient’s condition. In patients with multiple brain metastases, whole brain radiation therapy should be initiated. For patients with a single brain metastasis and controlled systemic disease, surgical excision followed by radiation therapy may be considered for younger individuals. Tumors that are not responsive to radiation therapy should also be considered for resection. Stereotactic radiosurgery may be used in treating tumors that have recurred or are in an anatomically sensitive location.

PERICARDIAL EFFUSION AND TAMPONADE

The most common cancers associated with pericardial involvement include lung cancer, breast cancer, leukemia, and lymphoma. Malignant pericardial disease is common and may be present at autopsy in up to 10% of patients with cancer. Patients with symptomatic pericardial disease or tamponade may present with complaints of dyspnea, cough, or orthopnea. Other signs include sinus tachycardia, jugular venous distention, hepatomegaly, and peripheral edema. Chest radiograph often demonstrates an enlarged cardiac silhouette. The electrocardiogram (EKG) may demonstrate abnormalities such as low voltage or electrical alternans. Echocardiography should be performed to confirm the diagnosis. Treatment is pericardiocentesis. Placement of a pericardial window and, in some cases, pericardial stripping may be required. Acute pericardial tamponade with hemodynamic instability is a medical emergency and requires immediate drainage.

INTESTINAL OR URINARY TRACT OBSTRUCTION

Intestinal obstruction may be a complication associated with advanced cancers, particularly colorectal, gastric, and ovarian carcinoma. Other cancers such as melanoma, breast cancer, and lung cancer that have metastasized to the abdomen can also be associated with obstruction. There are often multiple sites of obstruction present simultaneously. Symptoms of obstruction typically include pain, which is colicky in nature, or abdominal distension. Physical examination may be notable for a palpable tumor mass or distension. Treatment includes decompression. Conservative management may be used in patients with advanced cancer. In other cases, surgical correction or stent placement may be used.

    Urinary tract obstruction occurs most commonly in patients with prostate, bladder, or gynecologic cancers. Other etiologies include extrinsic compression from lymphoma, and from sarcoma in the retroperitoneum. Less commonly, radiation therapy to the pelvis or retroperitoneum may result in fibrosis leading to obstruction. The most common symptom is flank pain. Patients with bilateral obstruction may develop renal failure. Treatment includes internal stent placement or percutaneous nephrostomy. In cases of bladder outlet obstruction, a suprapubic cystostomy tube may be needed for urinary drainage.

TUMOR LYSIS SYNDROME

Tumor lysis syndrome (TLS) is the collection of electrolyte abnormalities that occur as a result of the rapid release of intracellular contents into the blood stream. TLS is characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia, which may result in metabolic acidosis and acute renal failure (Figure 17.1). The release of intracellular potassium and organic as well as inorganic phosphate into the bloodstream from cells undergoing apoptosis results in the development of hyperkalemia and hyperphosphatemia, respectively. Prolonged and severe hyperphosphatemia may result in a marked decrease of the serum calcium concentration, but symptomatic hypocalcemia rarely develops. However, hypocalcemia may develop from overzealous alkalinization, and thus one needs to exercise caution when using IV fluids with bicarbonate.

    Patients with large tumor burdens are at an increased risk for TLS, especially if the tumor is chemotherapy sensitive. These disorders include acute myeloid and lymphoblastic leukemias, especially those with high circulating blast counts; Burkitt lymphomas; and other high-grade lymphoproliferative disorders. Large bulky solid tumors that undergo rapid cellular destruction also place patients at a significant risk for the development of TLS. TLS is more common in patients with elevated LDH levels and, although extremely rare, TLS has also been described after the use of nonchemotherapy agents such as interferon-α or with hormonal therapy for breast cancer. Additionally, patients with poor renal function including older patients with a lower glomerular filtration rate (GFR) due to age are at an increased risk of developing TLS. These patients are more susceptible to electrolyte disturbances as compared to patients with normal GFR.

HYPERURICEMIA

Xanthine oxidase catalyzes the breakdown of hypoxanthine and xanthine to uric acid. Purine nucleotides and deoxynucleotides are broken down within the liver. The pKa of uric acid is approximately 5.75 at 37°C. Therefore, in the serum, uric acid is present in the acid-soluble form. However, within the acidic environment of the renal tubules uric acid may be present in the nonionized less-soluble form. Renal insufficiency may develop due to the development of uric acid crystals in the renal tubules as well as the distal renal collecting system. Nephrolithiasis due to the development of uric acid stones is uncommon and usually develops only in patients with chronic hyperuricemia. Many medications, especially diuretics such as thiazides as well as antituberculous drugs, IV contrast dye, and certain cytotoxic agents, can aggravate hyperuricemia.

    The most important factor to prevent hyperuricemia is to recognize patients who are most at risk for its development and then initiate appropriate prophylactic measures (table 17.1). Drugs that elevate serum uric acid levels should be discontinued if at all possible, and intravenous hydration should be initiated preferably prior to the start of chemotherapy. Any preexisting intravascular volume deficits must be corrected. The main focus in the treatment of hyperuricemia is to maintain adequate urinary volume. Alkalinization of the urine will further decrease uric acid solubility, which is usually achieved by the addition of sodium bicarbonate (50–100 mEq/L) to the intravenous fluids. The admixture should be adjusted so that the urine pH is maintained above 7.0 without over alkalinizing the serum, as this will lead to hypocalcemia. The most important factor in decreasing uric acid levels is the maintenance of adequate urine output; alkalinization is a secondary factor. Although furosemide increases the renal tubular reabsorption of uric acid, this is offset by the preservation of increased urinary flow rates. Therefore, furosemide can be safely used in order to maintain a proper total body fluid balance.

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