Oncologic Emergencies Flashcards

1
Q

Do patients with sepsis always present with a fever?

A

NO, especially in elderly patients

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2
Q

Sepsis/Septic Shock:

A

The result of an overwhelming bacterial, viral, or fungal infection to which the body does not provide an adequate immune response.

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3
Q

Risk factors that place a patient at higher risk of sepsis include:

A

Older age, poor performance status, prolonged neutropenia lasting longer than seven (7) days, portal entry risks (e.g., implanted IV catheter), stem cell transplantation, COPD, diabetes, autoimmune disorders, and pressure ulcers or wounds.

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4
Q

Phase 1 of sepsis

A

Local Inflammation

The patient may present with normal vitals and localized infection.

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5
Q

Phase 2 of sepsis

A

Systemic Infectious Inflammation

The patient may have subtle changes in vitals, with minimal organ dysfunction. This may present as chills, altered mental status, and/or warm extremities.

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6
Q

Phase 3 of sepsis

A

Shock

The patient’s blood pressure may drop, their mental status may worsen, and/or they may have cold extremities. They may also have tachypnea, fluid volume shifts, and organ dysfunction.

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7
Q

Symptoms of sepsis and septic shock can often be subtle. Initial symptoms often include:

A

Fever, shaking, chills, hypotension, tachycardia, tachypnea, and mental status changes. In elderly patients, fever may be the only symptom or be absent. Severe sepsis and septic shock can impact virtually every organ system in the body.

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8
Q

To help you remember which symptoms to be alert for, remember the acronym TIME.

A
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9
Q

Life-threatening reactions occur in about ___% of oncology drug infusions

A

5

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10
Q

What are high risk drugs for anaphylaxis?

A

High-risk drugs include asparaginase, taxanes, platinums, procarbazine, interferons, interleukins, and monoclonal antibodies

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11
Q

hypersensitivity

A

is a larger “umbrella” term for reactions which are the result of an immune-mediated response, can be localized or systematic, and are a reaction to an antigen or foreign substance.

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12
Q

what is the largest difference between anaphylactic reactions and other drug reactions?

A

Anaphylactic reactions typically involve more than one system of the body.

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13
Q

What patients are at higher risk for a anaphylactic reaction

A

Patients who may be at a higher risk can include: individuals assigned female at birth, people with a history of asthma, history of IV contrast reactions, untreated hematologic malignancies, and patients with a leukemia or lymphoma diagnosis with a lymphocyte count of less than 25,000/mm3. Other patients who may run a higher risk for anaphylaxis and hypersensitivity are younger patients receiving oxaliplatin or older patients receiving rituximab.

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14
Q

What can help prevent the risk of reaction?

A

Pre-medications, such as corticosteroids and histamine antagonists, are utilized to address some of the physiologic process that results in symptoms of hypersensitivity.

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15
Q

If anaphylaxis is suspected, the following actions should be initially taken.

A
  1. Stop the infusion and maintain IV line with normal saline or appropriate solution.
  2. Notify the physician/rapid response team.
  3. Place the patient in supine position to promote organ perfusion.
  4. Monitor vitals every two minutes until patient is stable.
  5. Epinephrine is the first-line medication to treat anaphylaxis and should be given without delay. There is no contraindication to epinephrine in the setting of anaphylaxis. Other medications will not stop the underlying mechanism of anaphylaxis, but rather treat the symptoms associated with anaphylaxis. These medications may include: antihistamines, corticosteroids, oxygen, and large-volume fluids.
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16
Q

Up to 15% of patients with cancer will experience a malignant spinal cord compression during the course of their disease. It is more common in patients who have been diagnosed with

A

breast, prostate, lung, non-Hodgkin’s lymphoma, multiple myeloma, and renal cell carcinoma.

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17
Q

Symptoms of MSCC (Malignant spinal cord compression)

A

The hallmark symptom is back pain, which can occur weeks to months before other symptoms. Pain may be localized, radicular (radiating), or referred. Symptoms can progress to motor weakness, sensory loss, autonomic dysfunction (e.g., loss of bladder control), and irreversible paralysis.

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18
Q

How are MSCCs treated?

A

Initial supportive therapy generally includes pain management and corticosteroids, which reduce inflammation, resulting in improved neurologic symptoms and pain. Conventional external beam radiation can be employed as a stand-alone therapy to treat and palliate MSCC. Surgery is considered a controversial intervention, and is more often utilized in radioresistant tumors.

Chemotherapy may have a role in chemo-sensitive tumors, but is not generally used to manage acute MSCC because of the slower and more unpredictable response.

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19
Q

Cytokine Release Syndrome

A

A systemic inflammatory response, triggered by infections and certain drugs.

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20
Q

What are the patient risk factors for CRS

A

Patient-specific factors can include: CAR T-cell therapy, first infusion of rituximab, chemotherapy-naïve patients receiving a monoclonal antibody, and leukemia/lymphoma patients with high lymphocyte counts.

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21
Q

Mild symptoms of CRS

A

Mild symptoms of CRS can present as flu-like symptoms, including fever, fatigue, headache, rash, arthralgia, and myalgia. Symptoms typically occur within 2-3 days following infusion of a high-risk drug, and last 7-8 days.

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22
Q

Severe symptoms of CRS

A

More severe symptoms are the result of uncontrolled systemic inflammation, which causes capillary leaks, disseminated intravascular coagulation, and multi-system organ failure.

Hypotension that does not respond to fluid resuscitation, hypoxia requiring oxygen support, coagulopathy, renal dysfunction, cardiac dysfunction, and neurologic toxicity (confusion, hallucinations, seizures, and cranial nerve palsies) may be observed in more severe cases of CRS.

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23
Q

What lab values indicate CRS

A

Laboratory abnormalities include cytopenias, elevated liver enzymes, elevated CRP, and elevated creatinine.

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24
Q

CRS treatment

A

Early interventions may include: antipyretics, oxygen therapy, anti-cytokine therapy, symptomatic treatment of organ toxicities, and ruling out other processes, such as sepsis.

More intensive interventions may include more aggressive oxygen therapy, corticosteroids, vasopressors, and hemodynamic monitoring. ICU admission may be necessary in some cases.

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25
Q

Syndrome of Inappropriate Antidiuretic Hormone (SIADH):

A

The body creates inappropriate, unregulated production and secretion of antidiuretic hormones.

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26
Q

The most common malignancies associated with SIADH include

A

bronchogenic (most commonly small cell lung) and head and neck

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27
Q

Which chemotherapies can cause SIADH

A

Anti-neoplastic agents can cause SIADH including vincristine, vinblastine, cyclophosphamide, ifosfamide, high-dose melphalan, thiotepa, cisplatin, carboplatin, and docetaxel.

28
Q

SIADH physiology

A

In the case of a malignant tumor causing SIADH, the cells of the tumor can independently synthesize, store, and release ADH. This unregulated ADH results in water conservation in the kidney, concentrated urine, plasma hypo-osmolality, and dilutional serum hyponatremia.

29
Q

Symptoms of SIADH

A

More mild symptoms can include: thirst, anorexia, nausea, cramps, headache, and fatigue.

As the level of hyponatremia increases in severity, symptoms becomes more prominent and can include weight gain, delirium, hypoactive reflexes, seizures, and coma. If plasma sodium is below 115mEq/L, cerebral edema can develop and result in increased intracranial pressure, which is why so many neurologic symptoms are associated with severe hyponatremia.

30
Q

SVC Syndrome

A

A group of symptoms that are the result of mechanical obstructions or compression of the superior vena cava (SVC), or the greater veins emptying into the SVC.

31
Q

The four main mechanisms of SVC syndrome are:

A
  1. Occlusion by a mass
  2. Tumor invasion through the vessel wall
  3. Thrombus occurring around a central venous catheter
  4. Thrombus occurring within the SVC syndrome independent of a venous device
32
Q

The majority of SVC syndrome cases, greater than 80%, are related to a _____

A

malignancy. Lung cancer (SCLC and NSCLC) and primary mediastinal large B-cell lymphoma are the most common malignancies.

33
Q

Beginning signs of SVC

A

Mild symptoms may include subtle signs of edema, dyspnea, non-productive cough, feelings of fullness in the head, and chest discomfort. Patients may report the symptoms being worse after being supine for a period of time, for example, when getting out of bed in the morning, or when stooped or bending forward. Patients may exhibit face, neck, or arm swelling, and may notice shirt collars fit tighter (Stokes sign). Women may notice swelling in their breasts and have difficulty removing rings. The symptoms may dissipate after standing or sitting upright

34
Q

Later signs of SVC

A

Later signs of SVC syndrome include: dysphagia (increases risk of aspiration) and hoarseness as a result of cranial nerve entrapment. Increased intercranial pressure may lead to visual disturbances, dizziness, syncope, and mental status changes. Cyanosis of face and upper torso, chest pain, orbital edema, congestive heart failure, increased blood pressure, and stridor can also be later signs of SVC syndrome.

35
Q

Hypercalcemia of malignancy risk factors

A

Patients who have widespread bone metastases (any type of malignancy); tumors that secrete humoral factors into circulation (breast, lung, renal cell, squamous cell cancers, ovarian, vulva, endometrium, liver, pancreatic, lymphomas, and adult T-cell leukemia); and increased synthesis of vitamin D are at high risk for HCM. Other conditions that can potentiate or increase the severity of HCM include: anorexia, nausea, vomiting, renal failure, use of thiazide diuretics, mucositis, dysphagia, and fever.

36
Q

How does HCM occur?

A
  1. Tumor stimulation of osteoclasts or parathyroid hormone results in an increase of bone resorption
  2. Tumor invasion of the bone, results in increased bone resorption
  3. Decreased renal clearance of calcium
  4. Increase of gut absorption of calcium
37
Q

Hypercalcemia of malignancy (HCM) symptoms

A

Symptoms are often vague or non-specific, which leads to later diagnosis of HCM. HCM affects multiple systems, but renal and neurologic symptoms are often noticed first. HCM can manifest as polyuria, polydipsia, nocturia, dehydration, kidney stones, and renal failure. Patients may report drowsiness, weakness, irritability, cognitive dysfunction, visual disturbances, seizures, stupor, muscle weakness, bone pain, ataxia, nausea and vomiting, constipation, and pruritis. In extreme cases, there may be electrocardiogram (ECG) changes or coma.

38
Q

How do you assess for HCM

A

To assess for HCM, monitor electrolytes, serum calcium, intact parathyroid hormone (iPTH), and ECG results. Nurses can assess neurologic status, urinary changes, back pain, cognitive changes, and gait changes. Use the CTCAE to grade for hypercalcemia.

39
Q

How do you treat HCM

A

Treatment for HCM can include: hydration, bisphosphonates, loop diuretics, dialysis for renal failure, corticosteroids, dietary changes, and weight-bearing activities. Patients should avoid vitamin A and D, NSAIDs, H2 receptor antagonists, and thiazide diuretics.

40
Q

Tumor Lysis Syndrome (TLS):

A

Occurs when large numbers of cancer cells are quickly destroyed, causing electrolyte changes in the systemic circulation.

41
Q

Treatment-Related TLS

A

Numerous chemotherapies, biologic and hormonal agents, radiation, or surgery can all cause TLS immediately following a first cycle treatment, or a few days post-treatment.

42
Q

Disease-Related TLS

A

Hematologic malignancies can cause TLS more commonly than solid tumors: Non-Hodgkin’s Lymphoma (NHL), Acute Lymphoblastic Leukemia (ALL), Acute Myeloid Leukemia (AML). Bulky disease, tumors with higher cell proliferation, and high tumor burden can also increase patient risk for TLS.

43
Q

Patient-Related TLS

A

Patients who have pre-existing conditions like uremia or hyperuricemia, dehydration, renal insufficiency, acidic urine, decreased urinary flow, elevated lactate dehydrogenase levels, or elevated white blood counts (WBC) run a higher risk of developing TLS

44
Q

Once the rapid lysis of dying cancer cells occurs, there is a rapid release of ______

A

intracellular components (potassium, uric acid, and phosphorus) into the bloodstream. The kidneys cannot keep up with excretion of these components.

45
Q

Typically, TLS presents within ________ after treatment. It can present with non-specific symptoms, like nausea and vomiting, cramps, and fatigue, or with laboratory changes only.

A

24 hours to seven days

46
Q

How is TLS treated?

A

Prior to high-risk therapy, treatment with allopurinol or rasburicase can help with prevention.

Treatment of TLS includes hydration, often aggressive hydration, along with diuresis. Rasburicase is also used to manage TLS once present in a patient.

Calcium carbonate, sodium biocarbonate, hypertonic glucose, or insulin can be used to help treat hyperkalemia. Phosphate-binding agents, such as antacids, can be used for hyperphosphatemia. IV calcium gluconate or calcium chloride can be used to treat hypocalcemia, while hemodialysis is used for significant renal failure.

47
Q

ICP etiology

A
  1. Intracerebral masses
  2. Obstruction of cerebrospinal flow
  3. Cerebral tissue alterations
  4. Cerebral circulation alterations
48
Q

Common causes of ICP in cancer patients include:

A

primary brain tumors, metastatic brain lesions, intracranial bleeding, infection, and meningeal cancers.

49
Q

Symptoms of ICP

A

Symptoms can include: headaches, nausea, vomiting, photophobia, behavior or cognitive changes, restlessness, and seizures. Headaches may become more frequent and intense as ICP increases, and worsen with certain activities, such as position changes. Headaches may also be worse in the morning, and respond poorly to analgesics.

50
Q

Later symptoms of increased ICP include:

A

lethargy, pupil changes, Cushing’s triad (hypertension, bradypnea, brachycardia), loss of reflexes, papilledema, and vision changes.

51
Q

Interventions/Treatment for ICP

A

Beyond preventative measures, treatment is aimed at reducing ICP or preventing it from becoming worse. Keeping the patient’s head elevated at 30 degrees, allowing for jugular venous drainage, providing oxygen, and maintaining body temperature and blood pressure are important. It is important to keep a patient’s body temperature normal, because an increase in body temperature leads to an increase in cerebral blood flow, which results in increased ICP.

52
Q

Disseminated Intravascular Coagulation (DIC):

A

The inappropriate and exaggerated coagulation of blood, which results in thrombus formation and then bleeding due to depleted clotting factors.

53
Q

More than 90% of patients with _____ develop DIC at the time of diagnosis, or after initiation of induction therapy.

A

acute promyelocytic leukemia

54
Q

Malignancies most commonly associated with DIC include

A

leukemia, lung, breast, ovarian, renal, stomach, pancreatic, prostate, melanoma, or gallbladder cancers.

55
Q

Early signs of DIC

A

Early signs may be venous thrombosis in the smaller, superficial vessels. This causes redness and tenderness over the area of the thrombus.

56
Q

Late stage signs of DIC

A

Symptoms are often not detected until later stages of DIC, when more major hemorrhaging is occurring. This leads to an increase in fatalities.

Bleeding occurs in the later stages of DIC, and may occur from any opening or orifice of the body. This can include: epistaxis, purpura, petechiae, hematomas, and ecchymoses. Systemic symptoms can include fever, hypoxia, hypotension, acidosis, and proteinuria.

57
Q

Treatment of DIC

A

Treating the underlying cause of DIC plays an important role in intervention. The first step is to treat any infection, followed by treating any active bleeding. Platelets, plasma, Vitamin K, antifibrinolytics may be used to treat active bleeding. Thrombosis has the largest impact on mortality in patients with DIC and is treated with anticoagulants (heparin). Anticoagulants are not indicated in rapidly evolving DIC with bleeding or high bleeding risk.

58
Q

Cardiac Tamponade:

A

The abnormal, excessive accumulation of fluid in the pericardial sac, which exerts pressure on the heart, resulting in impaired venous blood return to the heart, decreased cardiac filling, and decreased cardiac output.

59
Q

Up to ___ of cancer patients may experience cardiac tamponade.

A

21%

60
Q

Malignancy is the most common cause of cardiac tamponade, leading up to 60% of all cases. It is especially prevalent in patients who have

A

lung, breast, lymphoma, leukemia, or melanoma cancer.

61
Q

Anti-cancer drugs, like ______ can cause cardiac tamponade. Other drugs, like anticoagulants, thrombolytics, and penicillin, can also increase the risk of cardiac tamponade. Radiation therapy in the chest area can also result in cardiac tamponade.

A

anthracyclines, alkylating agents, taxanes, 5-FU, and TKIs

62
Q

Early symptoms of cardiac tamponade

A

Dyspnea is the most common presenting symptom. Mild cardiac tamponade may be asymptomatic in patients. Early symptoms can include: dyspnea, weakness, cough, orthopnea, anxiety, and a feeling of fullness in the chest.

63
Q

Moderate symptoms of cardiac tamponade

A

Moderate symptoms can include: tachycardia, muffled heart sounds, progressive dyspnea, and elevated jugular venous pressure.

64
Q

Late symptoms of cardiac tamponade

A

Late symptoms include: dyspnea even at rest, mental status changes, hoarseness, hiccups, anxiety, sense of impending doom, dysphagia, and pulsus paradoxus.

65
Q
A