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Oncologic emergencies Flashcards

1
Q

Types of body systems effected by oncologic emergencies

A

– Metabolic, neurologic, cardiovascular, respiratory, genitourinary,
gastrointestinal, hematological

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2
Q

Causes of oncologic emergencies

A

– Increased tumor size

– Tumors may secrete substances that mimic substances in the body

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3
Q

How do oncologic emergencies usually present

A

May be first s/s of cancer

May be sign cancer has advanced

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4
Q

What are the treatment goals in an oncologic emergency

A

• Immediate intervention to prevent loss of life or quality of life
• STAT aggressive supportive measures followed by definitive treatment
of the underlying malignancy

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5
Q

3 types of metabolic emergencies

A

Tumor lysis syndrome
SIADH
Hypercalcemia

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6
Q

Risk factors of tumor lysis syndrome

A 
acute leukemias most common 
Testicle cancer
Small cell lung CA
Breast CA
aggressive lymphoma
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7
Q

What happens in tumor lysis syndrome

A

Either as a result or treatment or as a result of worsening tumor, cells lyse and release contents which exceeds capacity for kidneys elimination

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8
Q

How does tumor lysis syndrome present

labs and manifestations

A

Increased K, cramps, N/D paralysis, paresthesias, ECG changes
Hyperphosphatemia: Oliguria/anuria/azotemia
Hypocalcemia: Tinnitus, twitching, seizures, parathesias and hypotension
Hyperuremia: N/V, AMS, edmea

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9
Q

Interventions for tumor lysis syndrome

A

Aggressive IV hydration, to regulate electrolyte levels and perfuse kidney
Allapurinol 300 mg PO: prevent uric acid synthesis
Rasburicase: 30 min infusion for TLS
Hemodialysis for acute episodes

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10
Q

SIADH

A

Too much antidieuretic hormone the prevalence of 1-2% of persons with cancer

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11
Q

Risk factors of SIADH and medications that can cause this

A

Small-cell lung cancer (60%), pancreatic, prostate, brain cancers
• Is adverse effect of cyclophosphamide (Cytoxan), vincristine, cisplatin

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12
Q

What happens in the body during SIADH

A

Water intoxication
ADH is secreted without response to usual feedback mechanism
Kidneys continue to retrun water to the body which dilutes the Na levels

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13
Q

SIADH symptoms when it is slow onset

A 
• Subtle mental and cognitive changes, i.e. memory loss, apathy, impaired abstract
thinking
• Fatigue, myalgia
• Headache
• Thirst
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14
Q

SIADH symptoms when it is rapid/severe onset

A

Asterixis (flap/tremor of hand when wrist extended)
Confusion
Seizures, coma

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15
Q

Diagnostic findings of SIADH

A

Serum Na <130 mmoL/L
Urine Na >20 mmoL/L
Urine osmolality exceeds that of plasma

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16
Q

SIADH Interventions

A

Treat the tumor—combination chemotherapy; RT
Fluid Restriction (<1000mL or <500 mL if there is a poor response
Declomycin in divided doses is given for refractory low Na
3%hypertonic Na by slow infusion to treat Neurosymptoms (seizure/coma)
Furosemide (Lasix) w/ normal saline infusion

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17
Q

how common is Hypercalcemia and what is the survival rate

A

• Is most common metabolic emergency; experienced by 25% of persons
with cancer
• 50% of patients diagnosed will die within one month of onset
• Mean survival 1-6 months

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18
Q

What is the cause of hypercalcemia

& special consideration

A

Altered calcium metabolism in bones kindeys, intestines esp in the presence of metastatic disease
Parathyroid hromone like substance screted by cancer cells (paraneoplastic syndrome)

Renal func/dehydration/physical activity

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19
Q

What are the diagnostic criteria fo hypercalcemia

A

Calcium levels of >11
K, Na, PO4 decreased
BUN/Creatinine Increased

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20
Q

What are the clinical manifestations of hypercalcemia

A 
Loss of appetite
Nausea and vomiting
Constipation and abdominal pain
Increased thirst and frequent urination
Fatigue, weakness, and muscle pain
Confusion, disorientation, and difficulty thinking
Headaches
Depression
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21
Q

Systems issues with hypercalcemia

A 
Kidney stones
Irregular heartbeat
Myocardial Infarction
 Loss of consciousness
 Coma
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22
Q

What do you assess in hypercalcemia

A

Assess levels of dehydration, renal function and CV status

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23
Q

What medications do you give for hypercalcemia

A

IV rehydration: IV hydration with NS 3L/24 hrs
Loop diuretics to enhance secretion of Ca
Bisphosphonates: decrease Ca levels (safest)
-IV aredia/zometa
Gallium nitrate: to prevent bone breakdown
calcitonin: band-aid response, shouldn’t be given as the primary treatment, usually given with biphosphates
Hemodialysis: if ca cannot be corrected with meds

24
Q

Name the neurologic emergencies

A 
Spinal cord compression
Related to brain tumors
• Increased intracranial pressure (ICP)
• Seizures
• Altered mental status
Paraneoplastic syndromes
25
Spinal cord compression risk factors
• “Liquid” tumors, i.e. lymphomas or multiple myeloma • Solid tumors with bony metastases, such as prostate, lung, breast, renal cell
26
What causes a spinal cord compression in an oncologic emergency
From rapidly growing mass pressing against spinal cord Results in collapse of vertebrae Most commonly caused by bone metastasis in the spine 30% of patients will have metastases in >1 area of the spine
27
How will a patient with spinal cord compression present
95% of patients present with back pain • Intense, localized and persistent • May radiate to lower back, buttocks, legs or arms • Sensory or motor: Numbness/difficulty walking if Lumbosacral – incontinence of bowel or bladder, urinary retention, leg pain or numbness (can become permanent w/o immediate tx)
28
How is spinal cord compression diagnostics
``` Radiological Spinal films CT with myelography **MRI is gold standard **** Biopsy of the lesion Surgical ```
29
Types Cardiovascular emergencies
Cardiac tamponade | SVC syndrome
30
Cardiac tamponade risk factors
Lung ca Breast ca Hematologic ca
31
What can cause cardiac tamponade
Can result from pressure of metastases outside of heart; | pericarditis secondary to radiation therapy
32
How much fluid causes cardiac tamponade
Normally 50 ml of fluid between visceral (serous) and fibrous parietal layers; tamponade can result from as little as 200 ml “Stress relaxation” over weeks to months with parietal stretch; sac can hold 2 L or more before tamponade occurs
33
what happens in Cardiac tamponade
Fluid collection → Compression → Decreased CO
34
cardiac tamponade most common clinical manifestation
Exertional dyspnea most common symptom; occurs in 80% of | patients
35
Beck’s triad cardiac tamponade
Beck’s triad of hypotension, increased jugular venous | pressure, decreased heart sounds in acute tamponade
36
Beck’s triad cardiac tamponade
Beck’s triad of hypotension, increased jugular venous | pressure, decreased heart sounds in acute tamponade
37
Clinical manifestations of cardiac tamponade
``` Exertional dyspnea Chest heaviness, distant heart sounds, tachycardia, pericardial friction rub Narrow pulse pressure Shortness of breath, anxiety Tachycardia Beck’s triad ```
38
Cardiac Tamponade | Diagnostics tests & what they show
``` Chest- X Ray: Enlarged cardiac silhouette with increased transverse diameter (water bottle heart) ECG: • Nonspecific ST and T wave changes • Tachycardia • Low QRS voltage • Atrial dysrhythmias Echocardiogram: dec filling/dec CO Pericardiocentesis: Tx & dx drain fluid and test is confirmation ```
39
Cardiac tamponade ecg shows
``` ECG • Nonspecific ST and T wave changes • Tachycardia • Low QRS voltage • Atrial dysrhythmias ```
40
How to treat cardiac tamponade
Pericardiocentesis with placement of indwelling drainage catheter Sclerosing therapy, balloon pericardotomy, or surgical window (stop the buildup of blood) Prognosis poor with paradoxical hemodynamic instability in postoperative period
41
Nursing interventions for after pericardiocentisis
Oxygen therapy IV hydration Vasopressor therapy
42
Causes of SVC syndrome
thrombosis caused by implantable IV devices, i.e. tunneled CV catheters, port catheters, pacemaker leads Mediastinal mass obstructing blood flow; most common causes are lung cancer, non-Hodgkin's lymphoma, metastatic breast cancer Previous radiation therapy to the mediastinum
43
What happens in they body to lead to SVC syndrome
Presence of mediastinal mass or thrombosis results in high venous pressures and upstream vessel engorgement Collateral vein dilation results in an effort to reduce this pressure
44
SVC Syndrome clinical manifestations common symptoms
``` Common Symptoms Facial edema Facial redness Periorbital edema Distention of veins in head, neck and chest Dyspnea at rest, cough ```
45
SVC Syndrome clinical manifestations rare symptoms
``` Rare symptoms Difficulty Swallowing Chest pain Hoarseness Cyanosis Hemoptysis ```
46
Superior Vena Cava Syndrome | Diagnostics
``` Chest x-ray Computed tomography (CT) scan Magnetic resonance imaging (MRI) Venography Ultrasound ```
47
Superior Vena Cava Syndrome | Interventions
``` ► Elevation of head: to dec pressure above SVC ► Corticosteroids: dec swelling ► Diuretics: dec fluid vol Thrombosis req intervention ► Thrombolysis ► Stents ► Bypass surgery tx based on symptoms ```
48
Type of respiratory emergencies
Airway obstruction Massive hemoptysis Toxic lung injury
49
Airway Obstruction clinical manifestations
``` Dyspnea Cough Wheezing Hemoptysis Stridor ```
50
Airway Obstruction diagnostics
Bronchoscopy | Biopsy
51
Airway Obstruction Intervention
``` Airway Securement Surgery if indicated (rare) Radiation Obstruction reduction techniques Stent Laser vaporization Photodynamic therapy Cryotherapy Endobronchial brachytherapy ```
52
Massive hemoptysis risk factors
Bronchogenic carcinoma Metastatic cancer to bronchus or trachea Platelet dysfunction
53
Massive hemoptysis definition
≥ 500mL of blood over a 24hour period or | A bleeding at a rate of ≥ 100mL/hour
54
Massive Hemoptysis | Intervention
``` Maintain airway patency Localize the source of bleeding Control the bleeding Pulmonary angiography and embolization Surgery ```
55
Toxic lung injury risk factors
``` Radiation Therapy • Cobalt Chemotherapy drugs • Arsenic trioxide • Bleomycin – 20% of patients receiving this therapy • Idarubicin Pre-existing lung disease (i.e. COPD) ```

Complex DMR (12 decks)

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