Oncologic Emergencies

Emergencies in the cancer pt may be classified into three categories: effects

from tumor expansion, metabolic or hormonal effects mediated by tumor products,

and treatment complications.

STRUCTURAL/OBSTRUCTIVE ONCOLOGIC EMERGENCIES

The most common problems are: superior vena cava syndrome; pericardial effusion/ tamponade, spinal cord compression; seizures (Chap. 185) and/or increased intracranial pressure; and intestinal, urinary, or biliary obstruction. The

last three conditions are discussed in Chap. 88 in HPIM-16.

SUPERIOR VENA CAVA SYNDROME Obstruction of the superior

vena cava reduces venous return from the head, neck, and upper extremities.

About 85% of cases are due to lung cancer; lymphoma and thrombosis of central

venous catheters are also causes. Pts often present with facial swelling, dyspnea,

and cough. In severe cases, the mediastinal mass lesion may cause tracheal

obstruction. Dilated neck veins and increased collateral veins on anterior chest

wall are noted on physical exam. CXR documents widening of the superior

mediastinum; 25% of pts have a right-sided pleural effusion.

TREATMENT

Radiation therapy is the treatment of choice for non-small cell lung cancer;

addition of chemotherapy to radiation therapy is effective in small cell lung

cancer and lymphoma. Symptoms recur in 10–30% and can be palliated by

venous stenting. Clotted central catheters producing this syndrome should be

withdrawn, and anticoagulation therapy initiated. Catheter clots may be prevented

withwarfarin, 1 mg/d.

PERICARDIAL EFFUSION/TAMPONADE Accumulation of fluid in

the pericardium impairs filling of the heart and decreases cardiac output. Most

commonly seen in pts withlung or breast cancers, leukemias, or lymphomas;

pericardial tamponade may also develop as a late complication of mediastinal

radiation therapy. Common symptoms are dyspnea, cough, chest pain, orthopnea,

and weakness. Pleural effusion, sinus tachycardia, jugular venous distention,

hepatomegaly, and cyanosis are frequent physical findings. Paradoxical

pulse, decreased heart sounds, pulsus alternans, and friction rub are less common

with malignant than nonmalignant pericardial disease. Echocardiography

is diagnostic; pericardiocentesis may show serous or bloody exudate, and cytology

usually shows malignant cells.

TREATMENT

Drainage of fluid from the pericardial sac may be lifesaving until a definitive

surgical procedure can be performed.

SPINAL CORD COMPRESSION Primary spinal cord tumors occur

rarely, and cord compression is most commonly due to epidural metastases from

vertebral bodies involved withtumor, especially from prostate, lung, breast,

lymphoma, and myeloma primaries. Pts present with back pain, worse when

recumbent, withlocal tenderness. Loss of bowel and bladder control may occur.

On physical exam, pts have a loss of sensation below a horizontal line on the

trunk, called a sensory level, that usually corresponds to one or two vertebrae

below the site of compression. Weakness and spasticity of the legs and hyperactive

reflexes withupgoing toes on Babinski testing are often noted. Spine

radiographs may reveal erosion of the pedicles (winking owl sign), lytic or

sclerotic vertebral body lesions, and vertebral collapse. Collapse alone is not a

reliable indicator of tumor; it is a common manifestation of a more common

disease, osteoporosis. MRI can visualize the cord throughout its length and

define the extent of tumor involvement.

TREATMENT

Radiation therapy plus dexamethasone, 4 mg IV or PO q4h, is successful in

arresting and reversing symptoms in about 75% of pts who are diagnosed

while still ambulatory. Only 10% of pts made paraplegic by the tumor recover

the ability to ambulate.

EMERGENT PARANEOPLASTIC SYNDROMES

Most paraneoplastic syndromes have an insidious onset (Chap. 80). Hypercalcemia, syndrome of inappropriate antidiuretic hormone (SIADH), and adrenal insufficiency may present as emergencies.

HYPERCALCEMIA The most common paraneoplastic syndrome, it occurs

in about 10% of cancer pts, particularly those with lung, breast, head and

neck, and kidney cancer and myeloma. Bone resorption mediated by parathormone- related protein is the most common mechanism; IL-1, IL-6, TNF, and transforming growthfactor- _ may act locally in tumor-involved bone. Pts usually present withnonspecific symptoms: fatigue, anorexia, constipation, weakness.

Hypoalbuminemia associated withmalignancy may make symptoms

worse for any given serum calcium level because more calcium will be free

rather than protein bound.

TREATMENT

Saline hydration, antiresorptive agents (e.g., pamidronate, 60–90 mg IV over

4 h, or zoledronate, 4–8 mg IV) and glucocorticoids usually lower calcium

levels significantly within 1–3 days. Treatment effects usually last several

weeks. Treatment of the underlying malignancy is also important.

SIADH Induced by the action of arginine vasopressin produced by certain

tumors (especially small cell cancer of the lung), SIADH is characterized by

hyponatremia, inappropriately concentrated urine, and high urine sodium excretion

in the absence of volume depletion. Most pts with SIADH are asymptomatic.

When serum sodium falls to_115 meq/L, pts may experience anorexia,

depression, lethargy, irritability, confusion, weakness, and personality changes.

TREATMENT

Water restriction controls mild forms. Demeclocycline (150–300 mg PO tid

or qid) inhibits the effects of vasopressin on the renal tubule but has a slow

onset of action (1 week). Treatment of the underlying malignancy is also

important. If the patient has mental status changes with sodium levels _115

meq/L, normal saline infusion plus furosemide to increase free water clearance

may provide more rapid improvement. Rate of correction should not

exceed 0.5–1 meq/L per hour.

ADRENAL INSUFFICIENCY The infiltration of the adrenals by tumor

and their destruction by hemorrhage are the two most common causes. Symptoms

such as nausea, vomiting, anorexia, and orthostatic hypotension may be

attributed to progressive cancer or to treatment side effects. Certain treatments

(e.g., ketoconazole, aminoglutethimide) may directly interfere with steroid synthesis in the adrenal.

TREATMENT

In emergencies, a bolus of 100 mg IV hydrocortisone is followed by a continuous

infusion of 10 mg/h. In nonemergent but stressful circumstances,

100–200 mg/d oral hydrocortisone is the beginning dose, tapered to maintenance

of 15–37.5 mg/d. Fludrocortisone (0.1 mg/d) may be required in the

presence of hyperkalemia.

TREATMENT COMPLICATIONS

Complications from treatment may occur acutely or emerge only many years

after treatment. Toxicity may be related either to the agents used to treat the

cancer or from the response of the cancer to the treatment (e.g., leaving a perforation in a hollow viscus or causing metabolic complications such as the tumor lysis syndrome). Several treatment complications present as emergencies. Fever and neutropenia and tumor lysis syndrome will be discussed here; others are

discussed in Chap. 88 in HPIM-16.

FEVER AND NEUTROPENIA Many cancer pts are treated withmyelotoxic

agents. When peripheral blood granulocyte counts are _1000/_L, the risk

of infection is substantially increased (48 infections/100 pts). A neutropenic pt

who develops a fever (_38_C) should undergo physical exam with special attention

to skin lesions, mucous membranes, IV catheter sites, and perirectal area.

Two sets of blood cultures from different sites should be drawn, and a CXR

performed, and any additional tests should be guided by findings from the history

and physical exam. Any fluid collections should be tapped, and urine and/or fluids

should be examined under the microscope for evidence of infection.

TREATMENT

After cultures are obtained, all pts should receive IV broad-spectrum antibiotics

(e.g., ceftazidime, 1 g q8h). If an obvious infectious site is found, the

antibiotic regimen is designed to cover organisms that may cause the infection.

Usually therapy should be started with an agent or agents that cover both

gram-positive and -negative organisms. If the fever resolves, treatment should

continue until neutropenia resolves. If the pt remains febrile and neutropenic

after 7 days, amphotericin B should be added to the antibiotic regimen.

TUMOR LYSIS SYNDROME When rapidly growing tumors are treated

with effective chemotherapy regimens, the rapid destruction of tumor cells can

lead to the release of large amounts of nucleic acid breakdown products (chiefly

uric acid), potassium, phosphate, and lactic acid. The phosphate elevations can

lead to hypocalcemia. The increased uric acid, especially in the setting of acidosis,

can precipitate in the renal tubules and lead to renal failure. The renal

failure can exacerbate the hyperkalemia.

TREATMENT

Prevention is the best approach. Maintain hydration with 3 L/d of saline, keep

urine pH _ 7.0 withbicarbonate administration, and start allopurinol, 300

mg/m2 per day, 24 h before starting chemotherapy. Once chemotherapy is

given, monitor serum electrolytes every 6 h. If after 24 h, uric acid (_8 mg/

dL) and serum creatinine (_1.6 mg/dL) are elevated, rasburicase (recombinant

urate oxidase), 0.2 mg/kg IV daily, may lower uric acid levels. If serum

potassium _ 6.0 meq/L and renal failure ensues, hemodialysis may be required.

Maintain normal calcium levels.