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Oncology patients can present significant challenges for both healthcare providers and caregivers. Modern-day chemotherapies may cause potentially life-threatening oncological emergencies. Nurses working with oncology patients must recognize signs and symptoms of these oncological emergencies and be knowledgeable in treatment therapies aimed at reducing these risks (1). 

Overview of Oncological Emergencies

The lifespan of cancer survivors has increased over the years in direct response to advancements in both cancer diagnosis and treatment options. The risk for associated oncologic complications has also increased, demanding that oncologic healthcare providers develop a solid knowledge base for identifying potential emergent complications and take actions to minimize such issues.  

Nurses working with oncology patients are uniquely positioned to educate patients and their caregivers about these risk factors. Oncology nurses deliver patient care, participate in clinical trials, and advance cancer research. They can educate people on preventive strategies, early symptom recognition, and available treatment options, all of which are pivotal in enhancing both quantity (of life years) and quality of life.

The oncology nurse must be aware of the various oncological emergencies that can arise. Oncological emergencies can occur at any point in the care and management of a cancer diagnosis, from the time of acute care onset to end-of-life care. Proper training will ensure early identification of such emergencies and minimize life-threatening complications. (1) ​

Tumor Lysis Syndrome 

Tumor Lysis Syndrome (TLS) is one of the most common oncological emergencies. It is a condition that occurs when massive tumor cell lysis (or breakdown) releases large amounts of potassium, phosphate, and nuclide cells into the patient’s systemic circulation (2,3). A large number of cancer cells die within a very short period of time and release their content into the bloodstream, resulting in the sudden onset of hyperkalemia, hyperphosphatemia, secondary hypocalcemia, and acute kidney injury.  

Patients with a significant “tumor burden” (number of cancer cells, the size of a tumor, or the amount of cancer in the body) of cancer cells and tumors that typically have rapidly dividing cells, such as acute leukemia or high-grade lymphoma, as well as tumors that are highly responsive to therapy, are at most significant risk of developing TLS.  

The condition can also occur in patients receiving steroids, hormonal therapy, targeted therapy, or radiation therapy. Dehydrated patients and those with existing kidney dysfunction are at higher risk of developing TLS; kidney failure can occur if left untreated (4). 

In TLS, clinical signs and symptoms may develop before the initiation of chemotherapy or, more commonly, within 72 hours after the administration of cytotoxic therapy. These symptoms often appear very vague initially; some symptoms are initially thought to be related to the chemotherapy agents rather than as a possible complication.  

Symptoms may include the following (4): 

• Nausea with or without vomiting 

• Lack of appetite and fatigue 

• Dark urine reduced urine output or flank pain 

• Numbness, seizures, or hallucinations 

• Muscle cramps and spasms 

• Heart palpitations 

• Weakness and fatigue 

• Joint pain 

• Fainting/syncope 

Treatment for TLS consists of serial blood testing to monitor electrolyte imbalances. Additionally, intravenous fluids and ICU monitoring are needed to ensure kidney function; temporary hemodialysis may be warranted in the acute treatment phase. 

Strict intake/output monitoring is essential to treat decreases in urine output and the threat of fluid overload. Allopurinol and rasburicase have been used to reduce serum uric acid levels. A renal diet, low in potassium and phosphorus) may be prescribed. 

Oncology patients at high risk for TLS should undergo blood testing and monitoring before and during therapy to ensure an early diagnosis and treatment intervention. 

 Patient and caregiver education should include dietary instructions (avoiding foods high in potassium and phosphorus, such as bananas, oranges, tomatoes, and certain prepared/processed foods), home monitoring for adequate fluid intake and output, and signs/symptom recognition (5). 

Febrile Neutropenia 

Febrile neutropenia is the development of fever, often with other signs of infection; in a patient with neutropenia, there is an abnormally low number of neutrophil granulocytes (a type of white blood cell) in the blood. It is not only the most common life-threatening complication of cancer therapy; its treatment is one of the most urgent oncological emergencies (6).   

In many oncology cases, the actual cause of this condition cannot be determined, so it is marked as a fever of unknown origin (FUO). The actual definition of FUO is neutropenic cases with a fever greater than 38.3 C (100.9F) without any clinically or microbiologically defined infection. Documented infections only comprise approximately 30% of cases.  

Infection is the primary cause of morbidity and mortality in patients with cancer who present with fever and neutropenia. Most infections are bacterial, but viral or fungal etiology is possible. Common bacterial pathogens include gram-positive infections such as Staphylococcus, Streptococcus, and Enterococcus. In a cancer-related immunocompromised state, patients have a weakened immune to fend off infections. The GI tract or sinuses’ mucosal lining may be damaged, leading the host open to invasion from an infectious pathogen.  

Symptoms that indicate febrile neutropenia may include the following (7): 

• Fever, tachycardia, and hypotension 
• History of recent chemotherapy 
• History of prior episodes of neutropenia after chemotherapy 
• A fever, which is a temperature of 100.5°F (38°C) or higher 
• Chills or sweating 
• Sore throat, sores in the mouth, or a toothache 
• Abdominal pain 
• Pain or burning when urinating, or urinating often 
• A cough or shortness of breath 
• Any redness, swelling, or pain (especially around a cut, wound, or catheter) 
• Pretreatment hemoglobin <12 g/dL  

Risk factors for febrile neutropenia include preexisting bone marrow problems, autoimmune diseases, poor nutrition, preexisting organ dysfunction (heart, liver, kidney disease), and certain medications (blood pressure medications, certain epilepsy medications, and some antibiotics). 

Neutropenia is confirmed with a blood test (neutrophil level). A typical absolute neutrophil count (ANC) result is between 2,500 and 6,000 (8). The range of neutrophil numbers in mild neutropenia is 1,000-1,500; the number in moderate neutropenia is 500-1,000, and the count in severe neutropenia is less than 500. 

For patients with a diagnosis of febrile neutropenia, the most important determining factor of patient outcomes is the timing of IV antibiotic administration. Early administration of antibiotics has been shown to reduce mortality and hospital length in these patients. Although antibiotics will not affect the actual neutrophil counts, they will treat the suspected underlying infection (9). 

Oncology patient education on febrile neutropenia should include the following: 

• Avoid exposure to persons with respiratory infections; avoid crowded places. 

• They take their temperature daily, especially if they develop chills, sweats, or feverish symptoms. 

• Proper oral hygiene, including daily brushing and flossing to decrease the risk of dental inflammation/ infection. 

Neutropenic precautions may be instituted in a hospital setting. Such isolation aims to prevent contaminants and infectious potential from entering the patient’s room. Staff should wear PPE when entering the room; fresh fruits and vegetables should not be included in patient meals, and flowers should not be brought. Handwashing is paramount before entering a neutropenic isolation room (10,11). 

Superior Vena Cava Syndrome 

The superior vena cava is a central vein in your upper body; it carries blood from your head, neck, upper chest, and arms to the heart. Superior vena cava syndrome (SVCS) happens when the superior vena cava is partially blocked or compressed. Cancer (specifically lung cancer and non-Hodgkin’s lymphoma) is usually the leading cause of SVCS. Such tumors in the chest cavity can press on/ block the superior vena cave, block lymph nodes in the area, or cause blood clots in the chest cavity veins. Lung cancer accounts for nearly 80 percent of SVCS occurrences (12). 

Symptoms of SVCS can cause severe breathing problems; it is considered one of the various oncological emergencies. However, most patients do well with treatment if recognized quickly. 

Common symptoms of SVCS include: 

• Swelling of the face, neck, upper body, and arms 

• Trouble breathing or shortness of breath, coughing 

• A hoarse voice, difficulty speaking, or trouble swallowing 

• Paralysis of vocal cords 

• Swollen veins in your chest and neck or swollen arms 

• Coughing up blood, chest pain 

• A blue tinge to the face, which is caused by a decrease in oxygenation to the area 

• Horner’s syndrome (a condition where a nerve pathway may be disrupted by a tumor, resulting in a decreased pupil size, a drooping eyelid, and decreased sweating on the affected side of your face. Treatment for SVCS may alleviate the symptoms) 

SVCS is diagnosed by chest X-ray, CT (computer tomography) scan or MRI studies (magnetic resonance imaging), and ultrasound studies of venous blood flow to the affected area. Surgical interventions, such as stent placement for blocked blood flow, may be necessary. Corticosteroids are used to reduce inflammation of the area, and diuretics may be ordered if there is evidence of fluid retention/ overload (13). 

Patient education regarding SVCS should include temperature monitoring at home, reporting any signs and symptoms of infection, difficulty breathing, coughing up blood, changes in voice, and signs of Horner syndrome (14). ​

Malignant Pericardial Effusion 

Malignant pericardial effusions (MPEs) are most often caused by lung, breast, melanoma, lymphoma, and leukemia. Lymph vessels may become blocked, which causes inflammation and possible infection. The extra fluid may then cause pressure on the heart, keeping it from pumping blood normally (15). 

The diagnosis of cancer as the cause of pericarditis requires imaging (e.g., a CT scan or cardiac magnetic resonance [CMR] imaging), cytology of pericardial fluid, and ultimately, biopsies confirming malignant infiltration within the pericardial tissue (16). Cancer cells can travel into nearby structures as well as spread throughout the bloodstream. Radiation and chemotherapy further increase the risk of viral or bacterial infections. Malignant cardiac involvement is thought to occur in approximately 10% of patients with known cancer. 

Symptoms may occur slowly or rapidly, depending on fluid accumulation rate, and may include the following: 

• Chest pain 

• Cough 

•  Palpitations and orthopnea 

•  Fatigue 

• Anxiety and confusion 

• Dyspnea on exertion 

• Lightheadedness or fainting ( syncope) 

• Enlargement of the neck veins 

Depending on the severity of the effusion, the patient may experience tachycardia, decreased heart sounds, neck vein distension, peripheral edema, and pericardial friction. If the outflow worsens into cardiac tamponade, the patient may show signs of low-output shock. Symptoms of cardiac tamponade may include severe shortness of breath, weakness, lightheadedness, and cough. Beck’s triad, the three strongly diagnostic indicators associated with cardiac tamponade, include muffled or distant heart sounds, fast heart rate, and low blood pressure (17). 

The treatment of malignant pericardial effusions must be individualized with consideration to the patient’s condition, tumor type, and the success rates and risks of various treatment options. 

A percutaneous pericardiocentesis achieves the initial relief of symptoms. After the pericardial effusion is drained, local sclerotherapy and/or chemotherapy usually alleviate the effusion without recurrence in most cases. Recurrent pericardial effusions may be treated with serial pericardiocentesis, sclerosing agents, and a percutaneous balloon pericardiotomy (18). 

Nursing education for patients at risk of an MPE includes contacting their healthcare provider for any issues of breathing difficulties, unusual weakness or fatigue, and palpitations/ irregular heartbeats. As with many oncological emergencies, many symptoms can also be attributed to the side effects of ongoing chemotherapy and radiation, so it is essential to keep providers appraised of any new symptom development.  

Syndrome of Inappropriate Antidiuretic Hormone 

Syndrome of inappropriate antidiuretic hormone (SIADH) is a group of symptoms that develops when there is too much antidiuretic hormone (ADH) in the body (19). Increased levels of ADH lead to water retention, electrolyte imbalances, and a low level of sodium in the blood (called hyponatremia or water intoxication) (19). 

The following cancers are at high risk for the development of SIADH (19): 

• small cell lung cancer/ non–small cell lung cancer 
• primary brain tumors, head and neck cancers 
• stomach cancer, duodenum cancer, pancreatic cancer 
• bladder cancer, prostate cancer 
• uterine cancer (19)
  

In addition, some cancer treatments can also heighten the risk for SIADH; these treatments include chemotherapy drugs such as cyclophosphamide, ifosfamide, and vincristine. Finally, some pain medications associated with cancer care, including opiate pain medicines such as morphine, can also lead to SIADH. Suffice it to say that SIADH is considered one of the high-priority oncological emergencies.  

Symptoms of SIADH (often mild at first and worsening as the sodium level continues to decrease) include: 

Early symptoms 

• fatigue 
• anorexia 
• headache 
• nausea and vomiting 
• muscle cramps  

Late symptoms 

• worsening mental status 
• lethargy 
• extreme weakness and irritability 
• agitation and confusion 
• hallucinations and poor balance 
• seizures 
• coma
  

Administration of high-dose cyclophosphamide (a chemotherapy medication often used to treat types of leukemias and lymphomas) may be problematic in patients at risk for SIADH. Aggressive hydration prevents hemorrhagic cystitis, creating the potential for water retention and severe hyponatremia. Combination chemotherapy often includes cisplatin administration, usually administered with large volumes of fluids to avoid nephrotoxicity. In addition, chemotherapy-induced nausea can stimulate the release of ADH.  

Diagnostic lab work to confirm SIADH may include serum levels of potassium, sodium chloride, osmolality, and urine-specific gravity. Hyponatremia is considered the hallmark lab test for SIADH. The normal range is 136-145 mEq/L. Levels below 136 may indicate the presence of SIADH.  

Treatment for SIADH includes appropriate fluid replacement (which may consist of fluid restrictions (generally <500 mL/day in severe cases and 800 to 1000 mL/day in moderate cases). 

There should also be ongoing cardiac monitoring and serial laboratory testing to assess for possible electrolyte imbalances.  

Patient education should include recognizing early symptoms, including fatigue, headache, and nausea/vomiting. Fluid intake, output, and daily body weight should be monitored at home, and the healthcare provider should be notified of extreme variances in these areas. As many chemotherapy medications (and their premedication precautions) can cause SIADH, further treatment may need to be adjusted for the patient’s safety and well-being (20). 

Disseminated Intravascular Coagulation 

Disseminated intravascular coagulation (DIC) is the formation of abnormal clumps of thickened blood (clots) inside blood vessels. These abnormal clots use up the blood’s clotting factors, which can lead to massive bleeding elsewhere. Causes include inflammation, infection, and cancer. 

The treatment goal is to address the underlying cause and provide supportive care through intravenous fluids and blood transfusions. 

In some cases of DIC, tiny blood clots form in the blood vessels and prevent the regular blood supply to organs such as the liver, brain, or kidneys (33). In other cases of DIC, the clotting proteins in your blood are consumed. When this happens, there is a high risk of severe bleeding, even from a minor injury or without injury (21, 22). 

Bleeding, often from multiple locations on the body, is one of the more common symptoms of DIC. In addition to internal bleeding, bleeding from the mucosal tissue (in the mouth and nose) and other external areas may occur (34). Other symptoms may include decreased blood pressure, easy bruising, and the presence of petechiae (tiny round brown-purple spots due to bleeding under the skin).  

Risk factors for DIC may include the following (22,22): 

• Blood transfusion reaction 

• Cancer, especially certain types of leukemia 

• Inflammation of the pancreas (pancreatitis) 

• Infection in the blood, especially by bacteria or fungus 

• Liver disease 

• Pregnancy complications (such as placenta that is left behind after delivery) 

• Recent surgery or anesthesia 

• Severe tissue injury (as in burns and head injury) 

There is no specific treatment for DIC. Treatment goals are to determine the underlying cause and treat it appropriately. DIC is treated with plasma transfusions to replace blood clotting factors and anticoagulants to prevent further blood clotting (23). 

Acute DIC can develop over a few hours or days and lead to severe bleeding. Conversely, chronic DIC may develop over weeks or months and usually presents with the formation of blood clots more so than excessive bleeding. Blood clots forming and traveling to the lungs will have the patient present as a possible pulmonary embolus, with shortness of breath, cyanosis, and severe chest pain.  

Simple nursing procedures such as venipuncture or IV insertion may cause severe external bleeding; thus, pressure to puncture sites may be longer than usual. Stool softeners are often prescribed to lessen straining during bowel movements. Bleeding precautions should be initiated, including no razors, soft toothbrushes, limited needle sticks, and blood pressure readings.  

Laboratory tests confirm the presence of DIC. Platelet counts decrease while PT/PTT and D-dimer levels increase. When clotting is the issue, heparin is the drug of choice for chronic DIC. Excessive blood loss may require transfusions, and antibiotics are prescribed when infection or sepsis are present.   

Patient education for DIC includes reporting any unusual bruising or bleeding, as well as the onset of weakness, dizziness, or fatigue. Preventive bleeding precautions should also be encouraged, such as using electric razors, soft bristle toothbrushes, and stool softeners regularly. ​

Hypercalcemia of Malignancy

Hypercalcemia is the most common life-threatening metabolic disorder associated with cancer. 

There are two main mechanisms by which cancer can lead to hypercalcemia. The first and most common is local action on bone, as may be seen in multiple myeloma or carcinomas (e.g., breast or prostate) that metastasize to bone. The second mechanism is tumors that secrete humoral factors that stimulate bone resorption (24). 

Squamous carcinomas are the most common malignancies that cause HCM, including squamous cell cancers of the lung, head and neck, and esophagus, breast cancer, renal cell carcinoma, lymphomas, and multiple myeloma.  

Patients experiencing hypercalcemia often complain of generalized/nonspecific symptoms, such as muscle weakness and fatigue. Others may complain of kidney stones, a direct result of high levels of calcium.  

 HCM is thought to to affect between 2% to 30% of oncology patients, but these rates vary depending on cancer type and disease stage. Approximately 50% of these patients will die within 30 days of a hypercalcemia diagnosis, even if the hypercalcemia is corrected, which suggests that hypercalcemia is a sign of hormonally advanced cancer (25). 

Normal serum levels of calcium: 8.6-10.3 mg/dl 

Levels of hypercalcemia: 

Mild 10.5-11.9 mg/dl 

 Moderate 12-13.9 mg/dl 

Severe >14 mg/dl 

Treatment of hypercalcemia includes IV hydration and loop diuretics. Normal saline IV fluid at 200-500 ml/hr increases the glomerular filtration rate and filtered amount of calcium. Loop diuretics block calcium resorption in the loop of Henle. The patient is also advised to discontinue any medications that affect serum calcium, including vitamin supplements, thiazides, and calcium antacids (26). 

IV bisphosphonate treatment should be started after or often in conjunction with aggressive hydration to treat HCM. Bisphosphonates have been very well studied in this population of patients and are considered to be quite safe and effective. They act by inhibiting bone resorption. They bind to the bone and reduce or prevent osteoclast activity, which, as discussed above, is a major factor in the development of HCM (27). 

Malignant hypercalcemia is preventable and can often be effectively treated. However, it often occurs as a late complication of cancer and indicates widespread disease, so successful treatment effects are likely to be short-lived. Therefore, its management involves combining compassionate end-of-life care with the correct treatment. 

Patient education should focus on the identification (and notification of the healthcare provider) of the early symptoms of hypercalcemia: fatigue, muscle weakness, anorexia, and constipation. Left untreated, these symptoms could worsen to include confusion, nausea, and vomiting, resulting in dehydration, renal failure, cardiac arrhythmia, and eventual coma.   ​

Extravasation of Chemotherapy 

Chemotherapy extravasation remains an accidental complication of chemotherapy administration and may result in severe damage to patients. It is defined as the unintentional infiltration of chemotherapy into the subcutaneous or sub-dermal tissue at the injection site and can result in tissue necrosis. The exact incidence of chemotherapy extravasation varies significantly due to the general lack of reporting and the absence of a centralized registry of chemotherapy extravasation events (28). 

Chemotherapy extravasation’s prevalence ranges from 0.1% to 6% when administered through peripheral intravenous access and from 0.26% to 4.7% when administered through a central venous access device (CVAD).  

Intravenously administered drugs can be classified into five categories according to their damage potential: Vesicant, Exfoliants, Irritants, Inflammitants, and Neutrals. The drug damage from extravasation can range from skin erythema to soft tissue necrosis:  

• Vesicants can result in tissue necrosis or the formation of blisters when accidentally infused into tissue surrounding a vein.  

• Exfoliants can cause inflammation and shedding (peeling off) of skin without causing underlying tissue death.  

• Irritants can cause inflammation, pain, or irritation at the extravasation site without blister formation. 

• Inflammitants can cause mild to moderate inflammation, painless skin erythema, and elevation (flare reaction) at the extravasation site.  

• Neutral are drugs that neither cause inflammation nor damage upon extravasation.  

Risk factors are related to the chemotherapeutic agent infused, as well as patient factors. 

• Chemotherapeutic agent-associated risk factors include the drug’s vesicant properties, concentration, volume, and duration in which the infusion is extravasated.  

• Risk factors related to patients that increase the risk of chemotherapy extravasation include small and fragile veins, preexisting patient lymphedema, obesity, impaired level of consciousness, and having had multiple previous venipunctures. 

• Patients with preexisting  hardened and thickened vessels due to frequent venipuncture 

• High-flow pressure delivery of chemotherapy agents 

Iatrogenic causes (effects inadvertently produced by the healthcare provider) include any of the following scenarios: 

• Lack of training of nurses 

• Poor cannula size selection and IV poor location selection 

• Accidental puncturing of the vein  

• Unintentional movement of the cannula (due to patient movement or IV site being improperly secured) 

• Prolonged peripheral line infusions of vesicants 

Education and training for nurses and physicians remain the mainstay of safe chemotherapy administration and emphasize the importance of being preemptive instead of reactive to extravasation. Extravasation prevention includes ensuring knowledge of risk factors, signs and symptoms, and guidelines for prevention and management.  

Consideration of the appropriate vascular access is crucial for the prevention of chemotherapy extravasation: 

• Chemotherapy should be infused only through central venous access or an adequate peripheral vein.  

• Small/fragile veins should be avoided as they might not withstand the required flow and rate of infusion.  

• IV insertion sites should be avoided, including the dorsum of the hand, the antecubital fossa, and the radial and ulnar aspects of the forearm. 

• Before IV insertion and chemotherapy infusion, patients should be assessed for possible risk factors, including preexisting diabetes, steroid usage, previous lymph node dissection, previous venipunctures, and current level of consciousness (to assure immobility and compliance during catheter insertion). 

Patient education should include instructions to report any discomfort, pain, redness, or swelling at infusion sites. Patients should also be aware of the class of drugs and options of venous access and understand the higher risk of extravasation associated with it. 

Infusion Reactions (Hypersensitivity and Anaphylactic)  

Chemotherapy drugs aim to improve patient’s quality of life and life expectancy, but an increasing number of reactions, including anaphylaxis, preclude their use in targeted populations. Drug allergic reactions are unexpected and can be severe, including anaphylaxis, and prevent the use of first-line therapies, consequently impacting the patient’s survival and quality of life (29). 

Drug reactions can range from mild pruritus and hives to life-threatening anaphylaxis with hypotension, oxygen desaturation, and cardiovascular collapse, and deaths have been reported after re-exposure to allergic drugs. Patients presenting with delayed cutaneous reactions are a significant concern for Stevens-Johnson syndrome and toxic epidermal necrolysis, two life-threatening conditions that can lead to permanent disability, blindness, and a dramatic decrease in the quality of life for survivors. Drug hypersensitivity is an increasing health hazard, compromising the quality of life and the life expectancy of cancer patients.  

Stevens-Johnson syndrome (SJS) is a rare, severe disorder of the skin and mucous membranes, often due to a medication reaction (30). Symptoms may include a painful rash, blister formation, fever or malaise, mouth ulcers, and difficulty swallowing. As the disorder worsens, extensive skin damage predisposes a person to a severe loss of body fluids and exposure to bacterial infections. Shock and multisystem organ failure can occur, making SJS/TCN a life-threatening disease. Toxic epidermal necrolysis is the more severe end of the SJS spectrum, fatal in up to 50 percent of such cases. 

Hypersensitivity reactions (HSRs) once prevented patients from receiving first-line therapies. Rapid desensitization protocols have been developed in many cases, allowing patients to now receive first-line therapies safely (despite previous documented reactions) while under close physician observation (31). 

Adverse reactions to chemotherapeutic agents can range from mild to anaphylactic.  

Symptoms may include any of  the following: 

• Ocular itching 

• Watery ( teary) eyes 

• Rhinorrhea ( runny nose) 

• Nasal congestion and sneezing 

• Coughing, wheezing, chest discomfort 

• Nausea, vomiting, abdominal discomfort 

• Chest/back pain 

• Feelings of anxiety or a sense of impending doom 

Severe infusion reactions should be discontinued immediately and treated appropriately. Repeated infusion reactions that occur despite premedication and slowed infusion rates leave few alternate treatment options. While some oncologists advocate discontinuing the chemotherapy agent, others may attempt a trial of specific drug desensitization. The decision to pursue either treatment is based on many factors, including the severity of the reaction, the disease process itself, and the availability of comparable treatment options. 

Infusion reactions (IRs) tend to occur with various anticancer medications. Symptoms range from mild flushing to severe anaphylaxis-type symptoms. Most IRs occur either within the first hour of the first or second administration. Continuous monitoring during infusion initiation is encouraged for early identification and treatment of any potential IRs (32). The more rapidly a reaction develops, the more severe it will likely be. 

Patient education for infusion reactions includes reporting all unusual symptoms (no matter how mild they appear initially) to healthcare providers throughout an infusion. Patients should be informed that they will be closely monitored throughout the infusion process (serial blood pressure and pulse checks). Discharge instructions may include routine temperature checks at home and indicators when to seek emergency care (difficulty breathing, chest pain, facial swelling (lips, tongue, and throat).  

In conclusion, oncology nurses must know all aspects of patient care, including possible oncological emergencies. Early identification and prompt treatment afford the patient the best outcomes. Modern advances in cancer treatment have prolonged the lives of many oncology patients. However, some treatments remain aggressive and have harmful effects. Thus, the ongoing management of a cancer patient is a delicate balance of compassionate end-of-life care and correct treatment. Thus, Ongoing cancer care education is paramount in enabling nurses to provide holistic patient care.  ​

Case Study on Oncological Emergencies

You are working in an outpatient infusion center. Your patient arrives for her first chemotherapy infusion. Mary, age 39, is diagnosed with breast cancer and is six weeks post-operative from a bilateral mastectomy. She expresses mild anxiety, with concern over possible side effects from the chemotherapy. Her vital signs are all within normal range. As you begin to look for a good IV insertion site, Mary states, “good luck; they had a hard time getting blood from me in the hospital.” You are able to secure an IV site in her left forearm, with confirmed blood return.  

Given your patient medical history, what assessment should be done prior to obtaining a peripheral IV site (to lower the risk of extravasation)? 

Does this patient have any contraindications for a peripheral IV site?  

What other options are available, both short and long-term, for IV access? 

Mary tolerates her first infusion without incident. She asks you if there are any special instructions she needs to follow until her next appointment. She is observed after the infusion is complete; vital signs remain normal, and she is anxious to go home.

What discharge instructions should Mary be given? 

What instructions should she receive, regarding monitoring for signs and symptoms of oncological emergencies?

When should she notify her medical provider?  

Are there any specific instructions regarding food and fluid intake? 

Six days later, Mary calls the outpatient infusion center, complaining of a fever of 101F, with complaints of a poor appetite and decreased urine output. She is advised to go to the local emergency room and is eventually admitted to the hospital with a diagnosis of FUO- fever of unknown origin. Blood tests confirm an additional diagnosis of febrile neutropenia.  

Describe laboratory testing to support a diagnosis of FUO. What blood tests confirm neutropenia? 

Discuss special isolation procedures (neutropenic precautions) that should be initiated for this patient. How to they differ from contact isolation?  

The patient’s condition improves, and she is discharged home after three days. She asks you what she can do to lower her risk of infection while she is home.

What are some risk factors in the development of febrile neutropenia? 

Describe the importance of early IV antibiotic intervention when treating a neutropenic oncology patient.  

What are some personal care behaviors this patient can do at home to lower the risk of infection and other oncological emergencies? 

When should this patient be instructed to contact her medical provider (regarding symptom onset)? 

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