This article discusses 5 of the 10 oncologic emergencies recognized by the Oncology Nursing Society. The oncologic emergencies discussed are septic shock, syndrome of inappropriate antidiuretic hormone (SIADH), tumor lysis syndrome, disseminated intravascular coagulopathy (DIC), and spinal cord compression. These are among the most common and complex of oncologic emergencies.
An oncologic emergency is defined as a clinical condition resulting from a structural or metabolic change caused by cancer or its treatment that requires immediate medical intervention to prevent loss of life or quality of life.
It is the nurse who must identify, assess, intervene, and educate, thus ensuring the opportunity for a positive outcome in the management of oncologic emergencies. Therefore, it is important for nurses to have working knowledge of the signs, symptoms, and laboratory values associated with each oncologic emergency. Infusion therapy plays an important role in the treatment of patients with these life-threatening conditions.
Septic shock is a clinical condition characterized by hemodynamic instability, abnormal coagulation, and altered metabolism in response to infection. Septic shock is associated with gram-negative bacteria, usually caused by Escherichia coli and Klebsiella. Although septic shock can be associated with fungi such as Candida and Aspergillus, and gram-positive septic shock has increased with the use of central and indwelling lines, this article focuses on gram-negative septic shock.
Gram-negative septic shock manifests itself differently in patients with cancer because the causative organism most frequently arises from the patient’s own flora. A patient with cancer may be neutropenic, with a white blood cell (WBC) count less than 1000, or severely immunocompromised. These patients can become infected and die of a dental carie, a rectal abscess, or mucositis. Even the smallest source of infection in a patient with cancer must be evaluated and treated fully. One example of a seemingly insignificant event with great consequences is a flea bite that led to sepsis and death of a young woman who previously had received high-dose chemotherapy for leukemia.
The occurrence of septic shock has increased by 140% over the past two decades in patients with cancer, partly because patients with cancer are living longer. Cancer treatment has become more successful, and patients with cancer can be supported through intense or high-dose therapies.
Risk factors for septic shock include disruption of anatomic barriers with biopsies and invasive tests, indwelling lines, alteration in microbial flora from antacids and chronic antibiotic use, cross-contamination from medical personnel during repeated hospitalizations, and loss of normal defense mechanisms and immunity with lowering of the WBC from repeated chemotherapy treatments or steroid use. 1 As patients with cancer are hospitalized for repeated, intense therapy, the risk for septic shock rises.
When working with patients with cancer, the nursing staff must maintain a high index of suspicion for the development of septic shock. The only manifestation of impending shock may be the development of fever. The first temperature elevation to 100°F is significant. If the WBC is profoundly depressed, the symptoms associated with infection may be absent, including the lack of pus formation. Other symptoms of early septic shock include flushed warm skin, increased respirations, decreased oxygen pressure, anxiety, confusion, and progressive hypotension. Symptoms of full-blown septic shock include disorientation, weight gain, hypotension, rapid thready pulse, cool clammy skin, hypoxemia, decreased urine output, and subnormal temperature. 2
Endotoxins are a component of the bacterial cell membrane in gram-negative organisms. These compounds are released when the bacteria die or reproduce. When endotoxins released by pathogens damage the cell membrane, an immune response is activated. Endotoxins may activate the clotting cascade, releasing histamines, cytokines, and interleukins. When attempts to reverse shock are ineffective, vasodilation, capillary leak, and the third-spacing of fluid occurs. 3
Positive blood cultures are present in only 50% of patients with septic shock. Other common laboratory findings include decreased WBC, increased blood urea nitrogen and creatinine, and arterial blood gases, indicating respiratory alkalosis progressing to metabolic acidosis and blood values associated with excessive anticoagulation. Laboratory values may change before clinical symptoms are apparent, providing an opportunity for early intervention when recognized.
Treatment of septic shock involves correcting the underlying cause of infection and supporting the patient through the physiologic crises. Blood and urine cultures should be drawn immediately and fluids given to improve perfusion and increase blood pressure. Dopamine may be indicated for renal perfusion and for increasing peripheral vascular resistance. Broad-spectrum antibiotics must be initiated within 1 hour of septic shock symptoms. Electrolyte replacement and oxygen should be administered to support cellular function.
Antiendotoxins are very expensive and available only at a few institutions. When used, antiendotoxins can break the cycle of histamine, cytokine, or interleukin release and DIC activation. Patient education and family support are imperative. Patients with cancer can endure severe septic shock and appear irreversibly ill, yet recover with skilled intervention. Honestly answering questions about physiologic condition, treatment, and realistic outcomes allows the patient and family to deal more powerfully with the issues at hand and work toward a positive outcome.
SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
SIADH occurs when antidiuretic hormone (ADH) is aberrantly secreted without response to the body’s usual feedback mechanisms, resulting in water intoxication. This occurs most frequently in patients with small cell lung cancer, pancreatic cancer, prostate cancer, and primary brain cancer. Infusions of Cytoxan, vincristine, or cisplatin as well as pulmonary infections can cause SIADH. 4
Antidiuretic hormone, manufactured in the supraoptic nuclei of the hypothalamus, is stored and released from the posterior pituitary. Hypotension, hypoxia, increased serum osmolality, and increased blood sodium signals the need for ADH, which is released and carried to distal and collecting tubules in the kidney. Antidiuretic hormone increases the permeability of collecting ducts and blood volume so that blood pressure and sodium levels are restored. 5Figure 1 shows the mechanism of the ADH secretion and visually summarizes the major influences on ADH secretion.
SIADH is a paraneoplastic syndrome as the tumor itself secretes a protein similar to ADH. This ADH-like protein secreted by the tumor is not responsive to the feedback mechanism in the body. Additionally, after chemotherapy administration, the posterior pituitary may be stimulated by the chemotherapy to release ADH. The kidneys continue to return water to the body, and the sodium continues to be diluted. As a result, the body’s sodium continues to fall, and weight gain occurs without edema (Figure 2).
The symptoms of SIADH include headache, thirst, muscle cramps, lethargy, confusion, nausea, and vomiting. Hyporeflexia, oliguria, seizures, hypotension, and weight gain without edema may occur if this condition is not reversed. Treatment involves controlling the underlying cause and correcting the electrolyte imbalance. Initially, fluids may be restricted to 500 to 1000 mL/day. Infusion of 3% hypertonic saline may increase serum sodium. The standard of care when the preceding measures have failed is 600 to 1200 mg of demeclocycline per day.
It is important to check for a trend in the chemistry panel of patients completing chemotherapy and to consider scheduling regular chemistry panels after discharge. The time spent in the hospital for chemotherapy is limited, and assessment for the predictable effects of chemotherapy and their management after discharge are part of an appropriate discharge plan.
TUMOR LYSIS SYNDROME
Tumor lysis syndrome is a potentially fatal metabolic complication of cancer caused by rapid necrosis of bulky tumors (Table 1). This condition occurs when a rapidly growing bulky tumor exists, including liquid tumors as acute lymphocytic leukemia, acute myelocytic leukemia, non-Hodgkin lymphoma, chronic myelocytic leukemia, and Burkitt lymphoma, and sudden death of tumor cells occurs, usually resulting from intensive treatment with high-dose chemotherapy. 7 The patient’s body is unable to adjust to the large number of metabolic by-products that end up in the bloodstream after a huge cell kill. The following is an example of a patient with this condition:
A 40-year-old man is newly diagnosed with acute lymphocytic leukemia and presents with enlarged cervical and axillary lymphadenopathy. He does not feel sick except for some shortness of breath and a persistent cough. He has his annual physical examination, and an abnormal blood count is noted. His WBC is found to be 150,000 K/mm3, that his body has adjusted slowly over time. The patient is sent to the hospital for immediate treatment because he has a life-threatening illness. Chemotherapy is administered immediately, and a huge cell kill occurs that threatens the patient’s life as the cell contents, phosphorus (the precusor of uric acid), and potassium are released into the bloodstream. This patient’s potassium could go from 3 to 7 mEq/L in 24 hours because the metabolites are too great for the body to handle.
Chemotherapy administration precipitates the release of multiple cell contents into the blood stream, posing a threat to the patient’s life. Abnormal laboratory values may include an elevated potassium, elevated uric acid, elevated phosphorus, decreased calcium (phosphorus and calcium are in an inverse relationship), and a rising blood urea nitrogen and creatine. 8 A potassium level can rise from 3 mEQ/L to 7 MEQ/L in hours.
One of the most important factors in the care of patients at risk for tumor lysis syndrome is identification of the risk before treatment. A patient presenting for induction chemotherapy who has an elevated WBC, a huge tumor burden, and a rapidly dividing tumor is at risk of tumor lysis syndrome. The ideal plan of care includes lowering the WBC to a more normal level before initiating chemotherapy. The WBC can be decreased through the use of Hydrea, an oral chemotherapy agent, or through a series of WBC leukophereses. Prophylaxis with administration of allopurinol before initiation of chemotherapy will prevent uric acid precursors from converting to uric acid by blocking the activity of the enzyme, xanthine oxidase. Allopurinol decreases the risk of uric acid crystallization in the kidneys. Alkalinizing the urine by adding sodium bicarbonate to intravenous fluids can increase the solubility of urine and prevent crystal formation.
Management of Tumor Lysis Syndrome
After the administration of chemotherapy, laboratory results need to be monitored frequently. Specimens should be drawn for laboratory analysis every 6 hours in the first 24 hours after chemotherapy administration. If the phosphorus elevates, Kayexalate (aluminum sulfate) may be administered to decrease phosphorus levels because Kayexalate binds to phosphorus and is excreted in the feces through the gastrointestinal tract. When severe electrolyte imbalances occur (eg, a potassium level exceeding 6, a uric acid level higher than 10, or a phosphorus level of 10, dialysis should be considered as an appropriate treatment method. A patient with tumor lysis syndrome is most appropriately placed in an intensive care unit.
The patient undergoing treatment for tumor lysis syndrome often walks into the hospital. The syndrome is as much a result of the treatment as of the underlying disease. The ethical and medical standard of care is to return the patient to his or her baseline health. The patient with tumor lysis syndrome may appear to be dying, but can recover with skilled intervention and early assessment. After subsequent chemotherapy administration, conditions probably will not allow tumor lysis syndrome to occur again because the WBC and tumor burden will be within more normal parameters.
DISSEMINATED INTRAVASCULAR COAGULATION
A hematologic disorder, DIC is characterized by rapid formation of fibrin clots in the microcirculation, consumption of the clotting factors, and clot degradation. 10 The patient is continually bleeding and clotting until the elements needed for clotting are consumed and the patient bleeds uncontrollably.
In patients with cancer, DIC is associated most often with acute myelocytic leukemia, sepsis, or a transfusion reaction. It is less frequently associated with breast, prostate, colon, or lung cancer.
When DIC occurs in leukemia, adenocarcinoma, or tissue injury, the clotting cascade is stimulated via the extrinsic pathway, and thromboplastin is released into the circulation. Disruption of the endothelial cell membrane stimulates the intrinsic pathway of the clotting cascade during shock or transfusion. The outcome is the same, whether DIC is initiated via the extrinsic or intrinsic pathway.
In acute myelocytic leukemia, especially in acute promyelocytic or M3 leukemia, a paraneoplastic syndrome occurs, in which a thrombin-like substance is secreted by the malignant cells. 11 This substance stimulates clotting and is unresponsive to the normal feedback mechanisms in the body. Consumption of the clotting factors is greater than the body’s ability to replace them, so coagulation is ineffective. The products of degradation accumulate in the bloodstream and act as anticoagulants. The following is an example of this physiologic condition:
A 36-year-old white woman comes to the emergency room of a community hospital with uncontrolled vaginal bleeding. After the hospital staff assesses her, they think she has been abused because she has numerous areas of ecchymosis and bruising over her body. She has had a heavy vaginal flow for 3 weeks, with a resultant hemoglobin of 3.7. Acute promylocytic leukemia and DIC are diagnosed in this otherwise healthy woman. After treatment of her leukemia, she left the hospital in general good health with normalized laboratory work.
The most significant symptom of DIC is bleeding (Figure 3). 1 When DIC occurs, there usually are multiple sites of bleeding. Petechiae, ecchymosis, purpura, and pallor can occur. Bleeding from the gums, nosebleeds, hematuria, oliguria abdominal distention, and guaiac-positive stools can occur, along with dyspnea, hemoptysis, and tachypnea as a result of acute or slow bleeding into the lungs. Restlessness, confusion, lethargy, and altered mental status can be signs of intracranial bleeding. Tachycardia and hypotension are indications of a compromised cardiovascular system.
Until the underlying cause of DIC (leukemia or sepsis) is treated, the condition will not improve. Normal coagulation and vital organs must be supported through this crisis. Platelets, fresh frozen plasma, cryoprecipitate, factor IX, factor X, or packed red blood cells may be administered. Amicar, which inhibits fibrinolysis, may be given, although the administration of Amicar poses a possible risk of fibrin deposits and thrombosis. Heparin has been used, perhaps more in the past, with the goal of slowing clot formation. The administration of heparin carries a possible risk of increased bleeding. Additionally, DIC is visually horrific and traumatic for patients and family members. Support and education of family members is extremely important as the healthcare team works to stem the tide of uncontrolled bleeding. The mortality rate from DIC is 50%.
Assessment is a critical element in the care of patients at risk for DIC. A daily visual inspection of every body orifice is necessary. A patient can exsanguinate from her vagina and be too weak to report the bleeding. Slow bleeding can occur down the back of the throat or from the nose. Maintenance of the central venous line is of critical importance. Blood draws should be coordinated to minimize potential line contamination. The risk of potential injury, especially from increased pressure to the central nervous system, must be managed carefully.
SPINAL CORD COMPRESSION
Spinal cord compression occurs as a result of tumor invasion of the vertebrae and collapse of the vertebrae on the spinal cord, tumor invasion of the spinal canal with resulting increased pressure on the cord, or primary tumors of the spinal cord. This condition is most commonly associated with metastatic cancers such as cancer of the breast, lung, prostate, or renal system as well as myeloma, lymphoma, melanoma, gastric cancer, or sarcoma. Primary cancers of the spinal cord less commonly associated with spinal cord compression are ependymoma, astrocytoma, and gliomas. Of spinal cord compressions, 10% occur in the cervical region, 20% in the lumbosacral region, and 70% in the thoracic region.
Most spinal cord compressions are extradural. The greater part of the extradural involvement occurs as a result of metastatic disease that spreads hematogenously from the venous plexus to the vertebral body. As the disease spreads, it causes interruption of blood flow to affected tissues, edema of the tissues and nerves, and neural distortion followed by ischemia and tissue death. When nerve tissue dies, regeneration is not always possible, and function is quickly and most often permanently lost. Figure 4 details the physiologic landmarks of the spinal cord.
There are three main locations of spinal cord compression. Extramedullary compression usually is caused by swhannomas or meningiomas in the subarachnoid space. Intramedullary compression usually is caused by astrocytomas or gliomas. Extravertebral compression may be caused by lymphoma or metastatic disease. The chief symptom associated with spinal cord compression is back pain. Respiratory distress may occur if the compression is in the cervical spine. Hypotonicity, ataxia, hyporeflexia, weakness in the lower extremities, or paraplegia occurs if spinal cord compression progresses without treatment. 13 Urinary and fecal incontinence as well as urinary retention are associated with progressive nerve compromise resulting from compression. Parathesias, loss of temperature sensation, loss of vibration sensation, and loss of sensation to light touch may be experienced.
Management of spinal cord compression requires rapid intervention to prevent permanent quality of life loss. 14 Initially, 10 to 100 mg of intravenous Decadron should be administered, followed by 4 mg given four times daily. Standard treatment for spinal cord compression is external beam radiation therapy to the spine, treating at least two vertebrae above and below the site of compression. The usual dose is 2,000 to 4,000 cGy. Radiation therapy shrinks the tumor, decreasing the pressure on the spinal nerves. Surgical decompression may be appropriate for removal of the tumor, the involved vertebral lamina, and the spinous processes. This usually is offered for tumors resistant to radiation therapy or for a single site.
Spinal cord compression usually carries a poor prognosis, with a life expectancy of 3 months or less. However, the quality of life during this time can be greatly affected by skilled healthcare. Quick assessment and rapid intervention when subtle neurologic changes occur are paramount in the prevention of spinal cord compression. Attention to reports of persistent back pain by a patient with cancer can lead to diagnosis before function is lost. Once a diagnosis of spinal cord compression has been made, the goal is to preserve and maximize function.
The other oncologic emergencies recognized by the Oncology Nursing Society are increased intracranial pressure, cardiac tamponade, superior vena cava syndrome, hypercalcemia, and anaphylaxis. A working knowledge that assists in the recognition and appropriate treatment of oncologic emergencies is critical for nurses who work with patients who have cancer. Rapid intervention may be the factor that determines whether the patient spends the final days of his or her life as a relatively independent individual or as a paraplegic. More and more attention is being given to these physiologic conditions as patients with cancer are living longer because of more aggressive and effective treatments, and because of advanced supportive therapies. This knowledge will benefit any healthcare professional working with a patient who has cancer.
The author thanks Becky Tiemann, Administrative Assistant, and Kathy McDonald, RN, MPH, CIC, for reviewing the manuscript.